Structured Review

Proteintech p23
AIL inhibits DNA damage repair of GC cells. (A) Transcriptome sequencing and pathway enrichment were performed on PDX tumor tissues from DMSO- and AIL-treated mice. (B) Differential gene expression analysis of the transcriptome sequencing. (C) AGS, SNU719 and SGC7901 cells were treated with AIL (0.5 µM) for 0, 12, and 24 hours, the cells were then lysed, and the expression levels of <t>P23</t> and XRCC1 were detected by western blotting. (D) Western blotting was performed to analyze the expression of HSP90, XRCC1, AKT and P23 in GC cell lines (AGS, SNU719 and SGC7901) after treatment with the specified concentrations of AIL for 24 hours. (E) AGS, SNU719 and SGC7901 cells were treated with 17-AAG (HSP90 inhibitor, 5 µM), CEL (P23 inhibitor, 2 µM) and AIL (1 µM) for 24 hours, and the expression of XRCC1 was detected by western blotting. (F) Representative images of P23, HSP90, and XRCC1 in PDX tumor tissue as detected via immunohistochemistry (100X). Scale bars, 200 µm. (G) Data were derived from experiments conducted in triplicate in (F). The PDX tumor tissues were compared with the control group, *P<0.05, **P<0.01, ***P<0.001.
P23, supplied by Proteintech, used in various techniques. Bioz Stars score: 93/100, based on 1 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
https://www.bioz.com/result/p23/product/Proteintech
Average 93 stars, based on 1 article reviews
Price from $9.99 to $1999.99
p23 - by Bioz Stars, 2024-04
93/100 stars

Images

1) Product Images from "Ailanthus Altissima-derived Ailanthone enhances Gastric Cancer Cell Apoptosis by Inducing the Repression of Base Excision Repair by Downregulating p23 Expression"

Article Title: Ailanthus Altissima-derived Ailanthone enhances Gastric Cancer Cell Apoptosis by Inducing the Repression of Base Excision Repair by Downregulating p23 Expression

Journal: International Journal of Biological Sciences

doi: 10.7150/ijbs.60674

AIL inhibits DNA damage repair of GC cells. (A) Transcriptome sequencing and pathway enrichment were performed on PDX tumor tissues from DMSO- and AIL-treated mice. (B) Differential gene expression analysis of the transcriptome sequencing. (C) AGS, SNU719 and SGC7901 cells were treated with AIL (0.5 µM) for 0, 12, and 24 hours, the cells were then lysed, and the expression levels of P23 and XRCC1 were detected by western blotting. (D) Western blotting was performed to analyze the expression of HSP90, XRCC1, AKT and P23 in GC cell lines (AGS, SNU719 and SGC7901) after treatment with the specified concentrations of AIL for 24 hours. (E) AGS, SNU719 and SGC7901 cells were treated with 17-AAG (HSP90 inhibitor, 5 µM), CEL (P23 inhibitor, 2 µM) and AIL (1 µM) for 24 hours, and the expression of XRCC1 was detected by western blotting. (F) Representative images of P23, HSP90, and XRCC1 in PDX tumor tissue as detected via immunohistochemistry (100X). Scale bars, 200 µm. (G) Data were derived from experiments conducted in triplicate in (F). The PDX tumor tissues were compared with the control group, *P<0.05, **P<0.01, ***P<0.001.
Figure Legend Snippet: AIL inhibits DNA damage repair of GC cells. (A) Transcriptome sequencing and pathway enrichment were performed on PDX tumor tissues from DMSO- and AIL-treated mice. (B) Differential gene expression analysis of the transcriptome sequencing. (C) AGS, SNU719 and SGC7901 cells were treated with AIL (0.5 µM) for 0, 12, and 24 hours, the cells were then lysed, and the expression levels of P23 and XRCC1 were detected by western blotting. (D) Western blotting was performed to analyze the expression of HSP90, XRCC1, AKT and P23 in GC cell lines (AGS, SNU719 and SGC7901) after treatment with the specified concentrations of AIL for 24 hours. (E) AGS, SNU719 and SGC7901 cells were treated with 17-AAG (HSP90 inhibitor, 5 µM), CEL (P23 inhibitor, 2 µM) and AIL (1 µM) for 24 hours, and the expression of XRCC1 was detected by western blotting. (F) Representative images of P23, HSP90, and XRCC1 in PDX tumor tissue as detected via immunohistochemistry (100X). Scale bars, 200 µm. (G) Data were derived from experiments conducted in triplicate in (F). The PDX tumor tissues were compared with the control group, *P<0.05, **P<0.01, ***P<0.001.

Techniques Used: Sequencing, Expressing, Western Blot, Immunohistochemistry, Derivative Assay

AIL regulates XRCC1 through P23 to inhibit DNA damage repair. (A) Western blotting was performed to detect the expression of P23, HSP90 and XRCC1 in AGS, SNU719 and SGC7901 cells after treatment with different concentrations of CEL (P23 inhibitor) for 24 hours. (B) GC1, GC2, and GC3 organoids were flow-sorted to separate P23(-) and P23(+) organoid strains. (C) qPCR was performed to detect P23 mRNA levels in P23(-) and P23(+) organoid strains. (D) qPCR analysis of XRCC1 expression in P23(-) and P23(+) organoid strains. (E) Western blot analysis of the expression of HSP90 and XRCC1 in AGS, SNU719 and SGC7901 cells treated with the specified concentrations of 17-AAG (HSP90 inhibitor) for 24 hours. (F) Representative images of GC organoids treated with DMSO (control group), 17-AAG (10 µM), CEL (2 µM), and AIL (1 µM) for 14 days. The number of cell clusters (G) and size of clusters (H) were counted. Data were derived from experiments conducted in triplicate. The treated organoids were compared with the control group, *P<0.05, **P<0.01, ***P<0.001.
Figure Legend Snippet: AIL regulates XRCC1 through P23 to inhibit DNA damage repair. (A) Western blotting was performed to detect the expression of P23, HSP90 and XRCC1 in AGS, SNU719 and SGC7901 cells after treatment with different concentrations of CEL (P23 inhibitor) for 24 hours. (B) GC1, GC2, and GC3 organoids were flow-sorted to separate P23(-) and P23(+) organoid strains. (C) qPCR was performed to detect P23 mRNA levels in P23(-) and P23(+) organoid strains. (D) qPCR analysis of XRCC1 expression in P23(-) and P23(+) organoid strains. (E) Western blot analysis of the expression of HSP90 and XRCC1 in AGS, SNU719 and SGC7901 cells treated with the specified concentrations of 17-AAG (HSP90 inhibitor) for 24 hours. (F) Representative images of GC organoids treated with DMSO (control group), 17-AAG (10 µM), CEL (2 µM), and AIL (1 µM) for 14 days. The number of cell clusters (G) and size of clusters (H) were counted. Data were derived from experiments conducted in triplicate. The treated organoids were compared with the control group, *P<0.05, **P<0.01, ***P<0.001.

Techniques Used: Western Blot, Expressing, Derivative Assay

AIL inhibits the binding of P23 and XRCC1 to HSP90 in GC cells. (A) The colocalization of HSP90 with P23 and XRCC1 was demonstrated with immunofluorescence in GC organoids treated with AIL (1 µM) for 24 hours. Scale bars, 100 µm. (B) Data were derived from experiments conducted in triplicate in (A). (C) Pull-down of selected proteins with HSP90 in the nucleus and cytoplasm of GC cells treated with AIL for 24 hours, and then the IP fractions were immunoblotted with HSP90, XRCC1, P23, Lamin B1 and GAPDH. (D) Graphical illustration of the functions of AIL in inhibiting tumor growth. The treated cells were compared with the control group, *P<0.05, **P<0.01, ***P<0.001.
Figure Legend Snippet: AIL inhibits the binding of P23 and XRCC1 to HSP90 in GC cells. (A) The colocalization of HSP90 with P23 and XRCC1 was demonstrated with immunofluorescence in GC organoids treated with AIL (1 µM) for 24 hours. Scale bars, 100 µm. (B) Data were derived from experiments conducted in triplicate in (A). (C) Pull-down of selected proteins with HSP90 in the nucleus and cytoplasm of GC cells treated with AIL for 24 hours, and then the IP fractions were immunoblotted with HSP90, XRCC1, P23, Lamin B1 and GAPDH. (D) Graphical illustration of the functions of AIL in inhibiting tumor growth. The treated cells were compared with the control group, *P<0.05, **P<0.01, ***P<0.001.

Techniques Used: Binding Assay, Immunofluorescence, Derivative Assay

Highly expressed P23 is associated with GC recurrence. (A) Representative images of high and low expression levels of P23 detected via IHC (100X) in recurrent GC tissues. Scale bars, 200 µm. (B) Recurrence time curves of 93 patients with GC recurrence, including 42 patients with high P23 expression and 51 patients with low P23 expression. *P<0.05, **P<0.01, ***P<0.001.
Figure Legend Snippet: Highly expressed P23 is associated with GC recurrence. (A) Representative images of high and low expression levels of P23 detected via IHC (100X) in recurrent GC tissues. Scale bars, 200 µm. (B) Recurrence time curves of 93 patients with GC recurrence, including 42 patients with high P23 expression and 51 patients with low P23 expression. *P<0.05, **P<0.01, ***P<0.001.

Techniques Used: Expressing


Structured Review

Proteintech p23
AIL inhibits DNA damage repair of GC cells. (A) Transcriptome sequencing and pathway enrichment were performed on PDX tumor tissues from DMSO- and AIL-treated mice. (B) Differential gene expression analysis of the transcriptome sequencing. (C) AGS, SNU719 and SGC7901 cells were treated with AIL (0.5 µM) for 0, 12, and 24 hours, the cells were then lysed, and the expression levels of <t>P23</t> and XRCC1 were detected by western blotting. (D) Western blotting was performed to analyze the expression of HSP90, XRCC1, AKT and P23 in GC cell lines (AGS, SNU719 and SGC7901) after treatment with the specified concentrations of AIL for 24 hours. (E) AGS, SNU719 and SGC7901 cells were treated with 17-AAG (HSP90 inhibitor, 5 µM), CEL (P23 inhibitor, 2 µM) and AIL (1 µM) for 24 hours, and the expression of XRCC1 was detected by western blotting. (F) Representative images of P23, HSP90, and XRCC1 in PDX tumor tissue as detected via immunohistochemistry (100X). Scale bars, 200 µm. (G) Data were derived from experiments conducted in triplicate in (F). The PDX tumor tissues were compared with the control group, *P<0.05, **P<0.01, ***P<0.001.
P23, supplied by Proteintech, used in various techniques. Bioz Stars score: 93/100, based on 1 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
https://www.bioz.com/result/p23/product/Proteintech
Average 93 stars, based on 1 article reviews
Price from $9.99 to $1999.99
p23 - by Bioz Stars, 2024-04
93/100 stars

Images

1) Product Images from "Ailanthus Altissima-derived Ailanthone enhances Gastric Cancer Cell Apoptosis by Inducing the Repression of Base Excision Repair by Downregulating p23 Expression"

Article Title: Ailanthus Altissima-derived Ailanthone enhances Gastric Cancer Cell Apoptosis by Inducing the Repression of Base Excision Repair by Downregulating p23 Expression

Journal: International Journal of Biological Sciences

doi: 10.7150/ijbs.60674

AIL inhibits DNA damage repair of GC cells. (A) Transcriptome sequencing and pathway enrichment were performed on PDX tumor tissues from DMSO- and AIL-treated mice. (B) Differential gene expression analysis of the transcriptome sequencing. (C) AGS, SNU719 and SGC7901 cells were treated with AIL (0.5 µM) for 0, 12, and 24 hours, the cells were then lysed, and the expression levels of P23 and XRCC1 were detected by western blotting. (D) Western blotting was performed to analyze the expression of HSP90, XRCC1, AKT and P23 in GC cell lines (AGS, SNU719 and SGC7901) after treatment with the specified concentrations of AIL for 24 hours. (E) AGS, SNU719 and SGC7901 cells were treated with 17-AAG (HSP90 inhibitor, 5 µM), CEL (P23 inhibitor, 2 µM) and AIL (1 µM) for 24 hours, and the expression of XRCC1 was detected by western blotting. (F) Representative images of P23, HSP90, and XRCC1 in PDX tumor tissue as detected via immunohistochemistry (100X). Scale bars, 200 µm. (G) Data were derived from experiments conducted in triplicate in (F). The PDX tumor tissues were compared with the control group, *P<0.05, **P<0.01, ***P<0.001.
Figure Legend Snippet: AIL inhibits DNA damage repair of GC cells. (A) Transcriptome sequencing and pathway enrichment were performed on PDX tumor tissues from DMSO- and AIL-treated mice. (B) Differential gene expression analysis of the transcriptome sequencing. (C) AGS, SNU719 and SGC7901 cells were treated with AIL (0.5 µM) for 0, 12, and 24 hours, the cells were then lysed, and the expression levels of P23 and XRCC1 were detected by western blotting. (D) Western blotting was performed to analyze the expression of HSP90, XRCC1, AKT and P23 in GC cell lines (AGS, SNU719 and SGC7901) after treatment with the specified concentrations of AIL for 24 hours. (E) AGS, SNU719 and SGC7901 cells were treated with 17-AAG (HSP90 inhibitor, 5 µM), CEL (P23 inhibitor, 2 µM) and AIL (1 µM) for 24 hours, and the expression of XRCC1 was detected by western blotting. (F) Representative images of P23, HSP90, and XRCC1 in PDX tumor tissue as detected via immunohistochemistry (100X). Scale bars, 200 µm. (G) Data were derived from experiments conducted in triplicate in (F). The PDX tumor tissues were compared with the control group, *P<0.05, **P<0.01, ***P<0.001.

Techniques Used: Sequencing, Expressing, Western Blot, Immunohistochemistry, Derivative Assay

AIL regulates XRCC1 through P23 to inhibit DNA damage repair. (A) Western blotting was performed to detect the expression of P23, HSP90 and XRCC1 in AGS, SNU719 and SGC7901 cells after treatment with different concentrations of CEL (P23 inhibitor) for 24 hours. (B) GC1, GC2, and GC3 organoids were flow-sorted to separate P23(-) and P23(+) organoid strains. (C) qPCR was performed to detect P23 mRNA levels in P23(-) and P23(+) organoid strains. (D) qPCR analysis of XRCC1 expression in P23(-) and P23(+) organoid strains. (E) Western blot analysis of the expression of HSP90 and XRCC1 in AGS, SNU719 and SGC7901 cells treated with the specified concentrations of 17-AAG (HSP90 inhibitor) for 24 hours. (F) Representative images of GC organoids treated with DMSO (control group), 17-AAG (10 µM), CEL (2 µM), and AIL (1 µM) for 14 days. The number of cell clusters (G) and size of clusters (H) were counted. Data were derived from experiments conducted in triplicate. The treated organoids were compared with the control group, *P<0.05, **P<0.01, ***P<0.001.
Figure Legend Snippet: AIL regulates XRCC1 through P23 to inhibit DNA damage repair. (A) Western blotting was performed to detect the expression of P23, HSP90 and XRCC1 in AGS, SNU719 and SGC7901 cells after treatment with different concentrations of CEL (P23 inhibitor) for 24 hours. (B) GC1, GC2, and GC3 organoids were flow-sorted to separate P23(-) and P23(+) organoid strains. (C) qPCR was performed to detect P23 mRNA levels in P23(-) and P23(+) organoid strains. (D) qPCR analysis of XRCC1 expression in P23(-) and P23(+) organoid strains. (E) Western blot analysis of the expression of HSP90 and XRCC1 in AGS, SNU719 and SGC7901 cells treated with the specified concentrations of 17-AAG (HSP90 inhibitor) for 24 hours. (F) Representative images of GC organoids treated with DMSO (control group), 17-AAG (10 µM), CEL (2 µM), and AIL (1 µM) for 14 days. The number of cell clusters (G) and size of clusters (H) were counted. Data were derived from experiments conducted in triplicate. The treated organoids were compared with the control group, *P<0.05, **P<0.01, ***P<0.001.

Techniques Used: Western Blot, Expressing, Derivative Assay

AIL inhibits the binding of P23 and XRCC1 to HSP90 in GC cells. (A) The colocalization of HSP90 with P23 and XRCC1 was demonstrated with immunofluorescence in GC organoids treated with AIL (1 µM) for 24 hours. Scale bars, 100 µm. (B) Data were derived from experiments conducted in triplicate in (A). (C) Pull-down of selected proteins with HSP90 in the nucleus and cytoplasm of GC cells treated with AIL for 24 hours, and then the IP fractions were immunoblotted with HSP90, XRCC1, P23, Lamin B1 and GAPDH. (D) Graphical illustration of the functions of AIL in inhibiting tumor growth. The treated cells were compared with the control group, *P<0.05, **P<0.01, ***P<0.001.
Figure Legend Snippet: AIL inhibits the binding of P23 and XRCC1 to HSP90 in GC cells. (A) The colocalization of HSP90 with P23 and XRCC1 was demonstrated with immunofluorescence in GC organoids treated with AIL (1 µM) for 24 hours. Scale bars, 100 µm. (B) Data were derived from experiments conducted in triplicate in (A). (C) Pull-down of selected proteins with HSP90 in the nucleus and cytoplasm of GC cells treated with AIL for 24 hours, and then the IP fractions were immunoblotted with HSP90, XRCC1, P23, Lamin B1 and GAPDH. (D) Graphical illustration of the functions of AIL in inhibiting tumor growth. The treated cells were compared with the control group, *P<0.05, **P<0.01, ***P<0.001.

Techniques Used: Binding Assay, Immunofluorescence, Derivative Assay

Highly expressed P23 is associated with GC recurrence. (A) Representative images of high and low expression levels of P23 detected via IHC (100X) in recurrent GC tissues. Scale bars, 200 µm. (B) Recurrence time curves of 93 patients with GC recurrence, including 42 patients with high P23 expression and 51 patients with low P23 expression. *P<0.05, **P<0.01, ***P<0.001.
Figure Legend Snippet: Highly expressed P23 is associated with GC recurrence. (A) Representative images of high and low expression levels of P23 detected via IHC (100X) in recurrent GC tissues. Scale bars, 200 µm. (B) Recurrence time curves of 93 patients with GC recurrence, including 42 patients with high P23 expression and 51 patients with low P23 expression. *P<0.05, **P<0.01, ***P<0.001.

Techniques Used: Expressing


Structured Review

Proteintech p23
AIL inhibits DNA damage repair of GC cells. (A) Transcriptome sequencing and pathway enrichment were performed on PDX tumor tissues from DMSO- and AIL-treated mice. (B) Differential gene expression analysis of the transcriptome sequencing. (C) AGS, SNU719 and SGC7901 cells were treated with AIL (0.5 µM) for 0, 12, and 24 hours, the cells were then lysed, and the expression levels of <t>P23</t> and XRCC1 were detected by western blotting. (D) Western blotting was performed to analyze the expression of HSP90, XRCC1, AKT and P23 in GC cell lines (AGS, SNU719 and SGC7901) after treatment with the specified concentrations of AIL for 24 hours. (E) AGS, SNU719 and SGC7901 cells were treated with 17-AAG (HSP90 inhibitor, 5 µM), CEL (P23 inhibitor, 2 µM) and AIL (1 µM) for 24 hours, and the expression of XRCC1 was detected by western blotting. (F) Representative images of P23, HSP90, and XRCC1 in PDX tumor tissue as detected via immunohistochemistry (100X). Scale bars, 200 µm. (G) Data were derived from experiments conducted in triplicate in (F). The PDX tumor tissues were compared with the control group, *P<0.05, **P<0.01, ***P<0.001.
P23, supplied by Proteintech, used in various techniques. Bioz Stars score: 93/100, based on 1 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
https://www.bioz.com/result/p23/product/Proteintech
Average 93 stars, based on 1 article reviews
Price from $9.99 to $1999.99
p23 - by Bioz Stars, 2024-04
93/100 stars

Images

1) Product Images from "Ailanthus Altissima-derived Ailanthone enhances Gastric Cancer Cell Apoptosis by Inducing the Repression of Base Excision Repair by Downregulating p23 Expression"

Article Title: Ailanthus Altissima-derived Ailanthone enhances Gastric Cancer Cell Apoptosis by Inducing the Repression of Base Excision Repair by Downregulating p23 Expression

Journal: International Journal of Biological Sciences

doi: 10.7150/ijbs.60674

AIL inhibits DNA damage repair of GC cells. (A) Transcriptome sequencing and pathway enrichment were performed on PDX tumor tissues from DMSO- and AIL-treated mice. (B) Differential gene expression analysis of the transcriptome sequencing. (C) AGS, SNU719 and SGC7901 cells were treated with AIL (0.5 µM) for 0, 12, and 24 hours, the cells were then lysed, and the expression levels of P23 and XRCC1 were detected by western blotting. (D) Western blotting was performed to analyze the expression of HSP90, XRCC1, AKT and P23 in GC cell lines (AGS, SNU719 and SGC7901) after treatment with the specified concentrations of AIL for 24 hours. (E) AGS, SNU719 and SGC7901 cells were treated with 17-AAG (HSP90 inhibitor, 5 µM), CEL (P23 inhibitor, 2 µM) and AIL (1 µM) for 24 hours, and the expression of XRCC1 was detected by western blotting. (F) Representative images of P23, HSP90, and XRCC1 in PDX tumor tissue as detected via immunohistochemistry (100X). Scale bars, 200 µm. (G) Data were derived from experiments conducted in triplicate in (F). The PDX tumor tissues were compared with the control group, *P<0.05, **P<0.01, ***P<0.001.
Figure Legend Snippet: AIL inhibits DNA damage repair of GC cells. (A) Transcriptome sequencing and pathway enrichment were performed on PDX tumor tissues from DMSO- and AIL-treated mice. (B) Differential gene expression analysis of the transcriptome sequencing. (C) AGS, SNU719 and SGC7901 cells were treated with AIL (0.5 µM) for 0, 12, and 24 hours, the cells were then lysed, and the expression levels of P23 and XRCC1 were detected by western blotting. (D) Western blotting was performed to analyze the expression of HSP90, XRCC1, AKT and P23 in GC cell lines (AGS, SNU719 and SGC7901) after treatment with the specified concentrations of AIL for 24 hours. (E) AGS, SNU719 and SGC7901 cells were treated with 17-AAG (HSP90 inhibitor, 5 µM), CEL (P23 inhibitor, 2 µM) and AIL (1 µM) for 24 hours, and the expression of XRCC1 was detected by western blotting. (F) Representative images of P23, HSP90, and XRCC1 in PDX tumor tissue as detected via immunohistochemistry (100X). Scale bars, 200 µm. (G) Data were derived from experiments conducted in triplicate in (F). The PDX tumor tissues were compared with the control group, *P<0.05, **P<0.01, ***P<0.001.

Techniques Used: Sequencing, Expressing, Western Blot, Immunohistochemistry, Derivative Assay

AIL regulates XRCC1 through P23 to inhibit DNA damage repair. (A) Western blotting was performed to detect the expression of P23, HSP90 and XRCC1 in AGS, SNU719 and SGC7901 cells after treatment with different concentrations of CEL (P23 inhibitor) for 24 hours. (B) GC1, GC2, and GC3 organoids were flow-sorted to separate P23(-) and P23(+) organoid strains. (C) qPCR was performed to detect P23 mRNA levels in P23(-) and P23(+) organoid strains. (D) qPCR analysis of XRCC1 expression in P23(-) and P23(+) organoid strains. (E) Western blot analysis of the expression of HSP90 and XRCC1 in AGS, SNU719 and SGC7901 cells treated with the specified concentrations of 17-AAG (HSP90 inhibitor) for 24 hours. (F) Representative images of GC organoids treated with DMSO (control group), 17-AAG (10 µM), CEL (2 µM), and AIL (1 µM) for 14 days. The number of cell clusters (G) and size of clusters (H) were counted. Data were derived from experiments conducted in triplicate. The treated organoids were compared with the control group, *P<0.05, **P<0.01, ***P<0.001.
Figure Legend Snippet: AIL regulates XRCC1 through P23 to inhibit DNA damage repair. (A) Western blotting was performed to detect the expression of P23, HSP90 and XRCC1 in AGS, SNU719 and SGC7901 cells after treatment with different concentrations of CEL (P23 inhibitor) for 24 hours. (B) GC1, GC2, and GC3 organoids were flow-sorted to separate P23(-) and P23(+) organoid strains. (C) qPCR was performed to detect P23 mRNA levels in P23(-) and P23(+) organoid strains. (D) qPCR analysis of XRCC1 expression in P23(-) and P23(+) organoid strains. (E) Western blot analysis of the expression of HSP90 and XRCC1 in AGS, SNU719 and SGC7901 cells treated with the specified concentrations of 17-AAG (HSP90 inhibitor) for 24 hours. (F) Representative images of GC organoids treated with DMSO (control group), 17-AAG (10 µM), CEL (2 µM), and AIL (1 µM) for 14 days. The number of cell clusters (G) and size of clusters (H) were counted. Data were derived from experiments conducted in triplicate. The treated organoids were compared with the control group, *P<0.05, **P<0.01, ***P<0.001.

Techniques Used: Western Blot, Expressing, Derivative Assay

AIL inhibits the binding of P23 and XRCC1 to HSP90 in GC cells. (A) The colocalization of HSP90 with P23 and XRCC1 was demonstrated with immunofluorescence in GC organoids treated with AIL (1 µM) for 24 hours. Scale bars, 100 µm. (B) Data were derived from experiments conducted in triplicate in (A). (C) Pull-down of selected proteins with HSP90 in the nucleus and cytoplasm of GC cells treated with AIL for 24 hours, and then the IP fractions were immunoblotted with HSP90, XRCC1, P23, Lamin B1 and GAPDH. (D) Graphical illustration of the functions of AIL in inhibiting tumor growth. The treated cells were compared with the control group, *P<0.05, **P<0.01, ***P<0.001.
Figure Legend Snippet: AIL inhibits the binding of P23 and XRCC1 to HSP90 in GC cells. (A) The colocalization of HSP90 with P23 and XRCC1 was demonstrated with immunofluorescence in GC organoids treated with AIL (1 µM) for 24 hours. Scale bars, 100 µm. (B) Data were derived from experiments conducted in triplicate in (A). (C) Pull-down of selected proteins with HSP90 in the nucleus and cytoplasm of GC cells treated with AIL for 24 hours, and then the IP fractions were immunoblotted with HSP90, XRCC1, P23, Lamin B1 and GAPDH. (D) Graphical illustration of the functions of AIL in inhibiting tumor growth. The treated cells were compared with the control group, *P<0.05, **P<0.01, ***P<0.001.

Techniques Used: Binding Assay, Immunofluorescence, Derivative Assay

Highly expressed P23 is associated with GC recurrence. (A) Representative images of high and low expression levels of P23 detected via IHC (100X) in recurrent GC tissues. Scale bars, 200 µm. (B) Recurrence time curves of 93 patients with GC recurrence, including 42 patients with high P23 expression and 51 patients with low P23 expression. *P<0.05, **P<0.01, ***P<0.001.
Figure Legend Snippet: Highly expressed P23 is associated with GC recurrence. (A) Representative images of high and low expression levels of P23 detected via IHC (100X) in recurrent GC tissues. Scale bars, 200 µm. (B) Recurrence time curves of 93 patients with GC recurrence, including 42 patients with high P23 expression and 51 patients with low P23 expression. *P<0.05, **P<0.01, ***P<0.001.

Techniques Used: Expressing


Structured Review

Proteintech p23
AIL inhibits DNA damage repair of GC cells. (A) Transcriptome sequencing and pathway enrichment were performed on PDX tumor tissues from DMSO- and AIL-treated mice. (B) Differential gene expression analysis of the transcriptome sequencing. (C) AGS, SNU719 and SGC7901 cells were treated with AIL (0.5 µM) for 0, 12, and 24 hours, the cells were then lysed, and the expression levels of <t>P23</t> and XRCC1 were detected by western blotting. (D) Western blotting was performed to analyze the expression of HSP90, XRCC1, AKT and P23 in GC cell lines (AGS, SNU719 and SGC7901) after treatment with the specified concentrations of AIL for 24 hours. (E) AGS, SNU719 and SGC7901 cells were treated with 17-AAG (HSP90 inhibitor, 5 µM), CEL (P23 inhibitor, 2 µM) and AIL (1 µM) for 24 hours, and the expression of XRCC1 was detected by western blotting. (F) Representative images of P23, HSP90, and XRCC1 in PDX tumor tissue as detected via immunohistochemistry (100X). Scale bars, 200 µm. (G) Data were derived from experiments conducted in triplicate in (F). The PDX tumor tissues were compared with the control group, *P<0.05, **P<0.01, ***P<0.001.
P23, supplied by Proteintech, used in various techniques. Bioz Stars score: 93/100, based on 1 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
https://www.bioz.com/result/p23/product/Proteintech
Average 93 stars, based on 1 article reviews
Price from $9.99 to $1999.99
p23 - by Bioz Stars, 2024-04
93/100 stars

Images

1) Product Images from "Ailanthus Altissima-derived Ailanthone enhances Gastric Cancer Cell Apoptosis by Inducing the Repression of Base Excision Repair by Downregulating p23 Expression"

Article Title: Ailanthus Altissima-derived Ailanthone enhances Gastric Cancer Cell Apoptosis by Inducing the Repression of Base Excision Repair by Downregulating p23 Expression

Journal: International Journal of Biological Sciences

doi: 10.7150/ijbs.60674

AIL inhibits DNA damage repair of GC cells. (A) Transcriptome sequencing and pathway enrichment were performed on PDX tumor tissues from DMSO- and AIL-treated mice. (B) Differential gene expression analysis of the transcriptome sequencing. (C) AGS, SNU719 and SGC7901 cells were treated with AIL (0.5 µM) for 0, 12, and 24 hours, the cells were then lysed, and the expression levels of P23 and XRCC1 were detected by western blotting. (D) Western blotting was performed to analyze the expression of HSP90, XRCC1, AKT and P23 in GC cell lines (AGS, SNU719 and SGC7901) after treatment with the specified concentrations of AIL for 24 hours. (E) AGS, SNU719 and SGC7901 cells were treated with 17-AAG (HSP90 inhibitor, 5 µM), CEL (P23 inhibitor, 2 µM) and AIL (1 µM) for 24 hours, and the expression of XRCC1 was detected by western blotting. (F) Representative images of P23, HSP90, and XRCC1 in PDX tumor tissue as detected via immunohistochemistry (100X). Scale bars, 200 µm. (G) Data were derived from experiments conducted in triplicate in (F). The PDX tumor tissues were compared with the control group, *P<0.05, **P<0.01, ***P<0.001.
Figure Legend Snippet: AIL inhibits DNA damage repair of GC cells. (A) Transcriptome sequencing and pathway enrichment were performed on PDX tumor tissues from DMSO- and AIL-treated mice. (B) Differential gene expression analysis of the transcriptome sequencing. (C) AGS, SNU719 and SGC7901 cells were treated with AIL (0.5 µM) for 0, 12, and 24 hours, the cells were then lysed, and the expression levels of P23 and XRCC1 were detected by western blotting. (D) Western blotting was performed to analyze the expression of HSP90, XRCC1, AKT and P23 in GC cell lines (AGS, SNU719 and SGC7901) after treatment with the specified concentrations of AIL for 24 hours. (E) AGS, SNU719 and SGC7901 cells were treated with 17-AAG (HSP90 inhibitor, 5 µM), CEL (P23 inhibitor, 2 µM) and AIL (1 µM) for 24 hours, and the expression of XRCC1 was detected by western blotting. (F) Representative images of P23, HSP90, and XRCC1 in PDX tumor tissue as detected via immunohistochemistry (100X). Scale bars, 200 µm. (G) Data were derived from experiments conducted in triplicate in (F). The PDX tumor tissues were compared with the control group, *P<0.05, **P<0.01, ***P<0.001.

Techniques Used: Sequencing, Expressing, Western Blot, Immunohistochemistry, Derivative Assay

AIL regulates XRCC1 through P23 to inhibit DNA damage repair. (A) Western blotting was performed to detect the expression of P23, HSP90 and XRCC1 in AGS, SNU719 and SGC7901 cells after treatment with different concentrations of CEL (P23 inhibitor) for 24 hours. (B) GC1, GC2, and GC3 organoids were flow-sorted to separate P23(-) and P23(+) organoid strains. (C) qPCR was performed to detect P23 mRNA levels in P23(-) and P23(+) organoid strains. (D) qPCR analysis of XRCC1 expression in P23(-) and P23(+) organoid strains. (E) Western blot analysis of the expression of HSP90 and XRCC1 in AGS, SNU719 and SGC7901 cells treated with the specified concentrations of 17-AAG (HSP90 inhibitor) for 24 hours. (F) Representative images of GC organoids treated with DMSO (control group), 17-AAG (10 µM), CEL (2 µM), and AIL (1 µM) for 14 days. The number of cell clusters (G) and size of clusters (H) were counted. Data were derived from experiments conducted in triplicate. The treated organoids were compared with the control group, *P<0.05, **P<0.01, ***P<0.001.
Figure Legend Snippet: AIL regulates XRCC1 through P23 to inhibit DNA damage repair. (A) Western blotting was performed to detect the expression of P23, HSP90 and XRCC1 in AGS, SNU719 and SGC7901 cells after treatment with different concentrations of CEL (P23 inhibitor) for 24 hours. (B) GC1, GC2, and GC3 organoids were flow-sorted to separate P23(-) and P23(+) organoid strains. (C) qPCR was performed to detect P23 mRNA levels in P23(-) and P23(+) organoid strains. (D) qPCR analysis of XRCC1 expression in P23(-) and P23(+) organoid strains. (E) Western blot analysis of the expression of HSP90 and XRCC1 in AGS, SNU719 and SGC7901 cells treated with the specified concentrations of 17-AAG (HSP90 inhibitor) for 24 hours. (F) Representative images of GC organoids treated with DMSO (control group), 17-AAG (10 µM), CEL (2 µM), and AIL (1 µM) for 14 days. The number of cell clusters (G) and size of clusters (H) were counted. Data were derived from experiments conducted in triplicate. The treated organoids were compared with the control group, *P<0.05, **P<0.01, ***P<0.001.

Techniques Used: Western Blot, Expressing, Derivative Assay

AIL inhibits the binding of P23 and XRCC1 to HSP90 in GC cells. (A) The colocalization of HSP90 with P23 and XRCC1 was demonstrated with immunofluorescence in GC organoids treated with AIL (1 µM) for 24 hours. Scale bars, 100 µm. (B) Data were derived from experiments conducted in triplicate in (A). (C) Pull-down of selected proteins with HSP90 in the nucleus and cytoplasm of GC cells treated with AIL for 24 hours, and then the IP fractions were immunoblotted with HSP90, XRCC1, P23, Lamin B1 and GAPDH. (D) Graphical illustration of the functions of AIL in inhibiting tumor growth. The treated cells were compared with the control group, *P<0.05, **P<0.01, ***P<0.001.
Figure Legend Snippet: AIL inhibits the binding of P23 and XRCC1 to HSP90 in GC cells. (A) The colocalization of HSP90 with P23 and XRCC1 was demonstrated with immunofluorescence in GC organoids treated with AIL (1 µM) for 24 hours. Scale bars, 100 µm. (B) Data were derived from experiments conducted in triplicate in (A). (C) Pull-down of selected proteins with HSP90 in the nucleus and cytoplasm of GC cells treated with AIL for 24 hours, and then the IP fractions were immunoblotted with HSP90, XRCC1, P23, Lamin B1 and GAPDH. (D) Graphical illustration of the functions of AIL in inhibiting tumor growth. The treated cells were compared with the control group, *P<0.05, **P<0.01, ***P<0.001.

Techniques Used: Binding Assay, Immunofluorescence, Derivative Assay

Highly expressed P23 is associated with GC recurrence. (A) Representative images of high and low expression levels of P23 detected via IHC (100X) in recurrent GC tissues. Scale bars, 200 µm. (B) Recurrence time curves of 93 patients with GC recurrence, including 42 patients with high P23 expression and 51 patients with low P23 expression. *P<0.05, **P<0.01, ***P<0.001.
Figure Legend Snippet: Highly expressed P23 is associated with GC recurrence. (A) Representative images of high and low expression levels of P23 detected via IHC (100X) in recurrent GC tissues. Scale bars, 200 µm. (B) Recurrence time curves of 93 patients with GC recurrence, including 42 patients with high P23 expression and 51 patients with low P23 expression. *P<0.05, **P<0.01, ***P<0.001.

Techniques Used: Expressing


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Proteintech p23
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Proteintech p23
P23, supplied by Proteintech, used in various techniques. Bioz Stars score: 86/100, based on 1 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
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Proteintech anti caspase 1
Anti Caspase 1, supplied by Proteintech, used in various techniques. Bioz Stars score: 92/100, based on 1 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
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Proteintech caspase 10
The combination of C49 and DOX inhibited P-gp expression, apoptotic signaling pathway and the PI3K/Akt signaling pathway. (A) The P-gp expression in MCF-7 cells and MCF-7/DOX cells. (B–F) WB and quantitative analysis of P-gp, PI3K, p-PI3K, Akt, p-Akt, Caspase-3, <t>Caspase-10,</t> Caspase-9, p53, p-p53, Bcl-2, and Bcl-xL proteins expression compared with β-actin. * p < 0.05, ** p < 0.01 vs. MCF-7/DOX cells.
Caspase 10, supplied by Proteintech, used in various techniques. Bioz Stars score: 92/100, based on 1 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
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1) Product Images from "A New Chalcone Derivative C49 Reverses Doxorubicin Resistance in MCF-7/DOX Cells by Inhibiting P-Glycoprotein Expression"

Article Title: A New Chalcone Derivative C49 Reverses Doxorubicin Resistance in MCF-7/DOX Cells by Inhibiting P-Glycoprotein Expression

Journal: Frontiers in Pharmacology

doi: 10.3389/fphar.2021.653306

The combination of C49 and DOX inhibited P-gp expression, apoptotic signaling pathway and the PI3K/Akt signaling pathway. (A) The P-gp expression in MCF-7 cells and MCF-7/DOX cells. (B–F) WB and quantitative analysis of P-gp, PI3K, p-PI3K, Akt, p-Akt, Caspase-3, Caspase-10, Caspase-9, p53, p-p53, Bcl-2, and Bcl-xL proteins expression compared with β-actin. * p < 0.05, ** p < 0.01 vs. MCF-7/DOX cells.
Figure Legend Snippet: The combination of C49 and DOX inhibited P-gp expression, apoptotic signaling pathway and the PI3K/Akt signaling pathway. (A) The P-gp expression in MCF-7 cells and MCF-7/DOX cells. (B–F) WB and quantitative analysis of P-gp, PI3K, p-PI3K, Akt, p-Akt, Caspase-3, Caspase-10, Caspase-9, p53, p-p53, Bcl-2, and Bcl-xL proteins expression compared with β-actin. * p < 0.05, ** p < 0.01 vs. MCF-7/DOX cells.

Techniques Used: Expressing


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Proteintech p23
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    Proteintech p23
    AIL inhibits DNA damage repair of GC cells. (A) Transcriptome sequencing and pathway enrichment were performed on PDX tumor tissues from DMSO- and AIL-treated mice. (B) Differential gene expression analysis of the transcriptome sequencing. (C) AGS, SNU719 and SGC7901 cells were treated with AIL (0.5 µM) for 0, 12, and 24 hours, the cells were then lysed, and the expression levels of <t>P23</t> and XRCC1 were detected by western blotting. (D) Western blotting was performed to analyze the expression of HSP90, XRCC1, AKT and P23 in GC cell lines (AGS, SNU719 and SGC7901) after treatment with the specified concentrations of AIL for 24 hours. (E) AGS, SNU719 and SGC7901 cells were treated with 17-AAG (HSP90 inhibitor, 5 µM), CEL (P23 inhibitor, 2 µM) and AIL (1 µM) for 24 hours, and the expression of XRCC1 was detected by western blotting. (F) Representative images of P23, HSP90, and XRCC1 in PDX tumor tissue as detected via immunohistochemistry (100X). Scale bars, 200 µm. (G) Data were derived from experiments conducted in triplicate in (F). The PDX tumor tissues were compared with the control group, *P<0.05, **P<0.01, ***P<0.001.
    P23, supplied by Proteintech, used in various techniques. Bioz Stars score: 93/100, based on 1 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
    https://www.bioz.com/result/p23/product/Proteintech
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    Proteintech anti caspase 1
    AIL inhibits DNA damage repair of GC cells. (A) Transcriptome sequencing and pathway enrichment were performed on PDX tumor tissues from DMSO- and AIL-treated mice. (B) Differential gene expression analysis of the transcriptome sequencing. (C) AGS, SNU719 and SGC7901 cells were treated with AIL (0.5 µM) for 0, 12, and 24 hours, the cells were then lysed, and the expression levels of <t>P23</t> and XRCC1 were detected by western blotting. (D) Western blotting was performed to analyze the expression of HSP90, XRCC1, AKT and P23 in GC cell lines (AGS, SNU719 and SGC7901) after treatment with the specified concentrations of AIL for 24 hours. (E) AGS, SNU719 and SGC7901 cells were treated with 17-AAG (HSP90 inhibitor, 5 µM), CEL (P23 inhibitor, 2 µM) and AIL (1 µM) for 24 hours, and the expression of XRCC1 was detected by western blotting. (F) Representative images of P23, HSP90, and XRCC1 in PDX tumor tissue as detected via immunohistochemistry (100X). Scale bars, 200 µm. (G) Data were derived from experiments conducted in triplicate in (F). The PDX tumor tissues were compared with the control group, *P<0.05, **P<0.01, ***P<0.001.
    Anti Caspase 1, supplied by Proteintech, used in various techniques. Bioz Stars score: 92/100, based on 1 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
    https://www.bioz.com/result/anti caspase 1/product/Proteintech
    Average 92 stars, based on 1 article reviews
    Price from $9.99 to $1999.99
    anti caspase 1 - by Bioz Stars, 2024-04
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    Proteintech caspase 10
    AIL inhibits DNA damage repair of GC cells. (A) Transcriptome sequencing and pathway enrichment were performed on PDX tumor tissues from DMSO- and AIL-treated mice. (B) Differential gene expression analysis of the transcriptome sequencing. (C) AGS, SNU719 and SGC7901 cells were treated with AIL (0.5 µM) for 0, 12, and 24 hours, the cells were then lysed, and the expression levels of <t>P23</t> and XRCC1 were detected by western blotting. (D) Western blotting was performed to analyze the expression of HSP90, XRCC1, AKT and P23 in GC cell lines (AGS, SNU719 and SGC7901) after treatment with the specified concentrations of AIL for 24 hours. (E) AGS, SNU719 and SGC7901 cells were treated with 17-AAG (HSP90 inhibitor, 5 µM), CEL (P23 inhibitor, 2 µM) and AIL (1 µM) for 24 hours, and the expression of XRCC1 was detected by western blotting. (F) Representative images of P23, HSP90, and XRCC1 in PDX tumor tissue as detected via immunohistochemistry (100X). Scale bars, 200 µm. (G) Data were derived from experiments conducted in triplicate in (F). The PDX tumor tissues were compared with the control group, *P<0.05, **P<0.01, ***P<0.001.
    Caspase 10, supplied by Proteintech, used in various techniques. Bioz Stars score: 92/100, based on 1 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
    https://www.bioz.com/result/caspase 10/product/Proteintech
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    caspase 10 - by Bioz Stars, 2024-04
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    AIL inhibits DNA damage repair of GC cells. (A) Transcriptome sequencing and pathway enrichment were performed on PDX tumor tissues from DMSO- and AIL-treated mice. (B) Differential gene expression analysis of the transcriptome sequencing. (C) AGS, SNU719 and SGC7901 cells were treated with AIL (0.5 µM) for 0, 12, and 24 hours, the cells were then lysed, and the expression levels of P23 and XRCC1 were detected by western blotting. (D) Western blotting was performed to analyze the expression of HSP90, XRCC1, AKT and P23 in GC cell lines (AGS, SNU719 and SGC7901) after treatment with the specified concentrations of AIL for 24 hours. (E) AGS, SNU719 and SGC7901 cells were treated with 17-AAG (HSP90 inhibitor, 5 µM), CEL (P23 inhibitor, 2 µM) and AIL (1 µM) for 24 hours, and the expression of XRCC1 was detected by western blotting. (F) Representative images of P23, HSP90, and XRCC1 in PDX tumor tissue as detected via immunohistochemistry (100X). Scale bars, 200 µm. (G) Data were derived from experiments conducted in triplicate in (F). The PDX tumor tissues were compared with the control group, *P<0.05, **P<0.01, ***P<0.001.

    Journal: International Journal of Biological Sciences

    Article Title: Ailanthus Altissima-derived Ailanthone enhances Gastric Cancer Cell Apoptosis by Inducing the Repression of Base Excision Repair by Downregulating p23 Expression

    doi: 10.7150/ijbs.60674

    Figure Lengend Snippet: AIL inhibits DNA damage repair of GC cells. (A) Transcriptome sequencing and pathway enrichment were performed on PDX tumor tissues from DMSO- and AIL-treated mice. (B) Differential gene expression analysis of the transcriptome sequencing. (C) AGS, SNU719 and SGC7901 cells were treated with AIL (0.5 µM) for 0, 12, and 24 hours, the cells were then lysed, and the expression levels of P23 and XRCC1 were detected by western blotting. (D) Western blotting was performed to analyze the expression of HSP90, XRCC1, AKT and P23 in GC cell lines (AGS, SNU719 and SGC7901) after treatment with the specified concentrations of AIL for 24 hours. (E) AGS, SNU719 and SGC7901 cells were treated with 17-AAG (HSP90 inhibitor, 5 µM), CEL (P23 inhibitor, 2 µM) and AIL (1 µM) for 24 hours, and the expression of XRCC1 was detected by western blotting. (F) Representative images of P23, HSP90, and XRCC1 in PDX tumor tissue as detected via immunohistochemistry (100X). Scale bars, 200 µm. (G) Data were derived from experiments conducted in triplicate in (F). The PDX tumor tissues were compared with the control group, *P<0.05, **P<0.01, ***P<0.001.

    Article Snippet: Antibodies used were: XRCC1 (1: 100, Abcam, ab44830), P23 (1: 200, Proteintech, 10824-1-AP), HSP90 (1: 400, Proteintech, 60318-1-Ig), Lamin B1 (1: 20000, Proteintech, 66095-1-Ig), GAPDH (1: 20000, Proteintech, 60004-1-Ig).

    Techniques: Sequencing, Expressing, Western Blot, Immunohistochemistry, Derivative Assay

    AIL regulates XRCC1 through P23 to inhibit DNA damage repair. (A) Western blotting was performed to detect the expression of P23, HSP90 and XRCC1 in AGS, SNU719 and SGC7901 cells after treatment with different concentrations of CEL (P23 inhibitor) for 24 hours. (B) GC1, GC2, and GC3 organoids were flow-sorted to separate P23(-) and P23(+) organoid strains. (C) qPCR was performed to detect P23 mRNA levels in P23(-) and P23(+) organoid strains. (D) qPCR analysis of XRCC1 expression in P23(-) and P23(+) organoid strains. (E) Western blot analysis of the expression of HSP90 and XRCC1 in AGS, SNU719 and SGC7901 cells treated with the specified concentrations of 17-AAG (HSP90 inhibitor) for 24 hours. (F) Representative images of GC organoids treated with DMSO (control group), 17-AAG (10 µM), CEL (2 µM), and AIL (1 µM) for 14 days. The number of cell clusters (G) and size of clusters (H) were counted. Data were derived from experiments conducted in triplicate. The treated organoids were compared with the control group, *P<0.05, **P<0.01, ***P<0.001.

    Journal: International Journal of Biological Sciences

    Article Title: Ailanthus Altissima-derived Ailanthone enhances Gastric Cancer Cell Apoptosis by Inducing the Repression of Base Excision Repair by Downregulating p23 Expression

    doi: 10.7150/ijbs.60674

    Figure Lengend Snippet: AIL regulates XRCC1 through P23 to inhibit DNA damage repair. (A) Western blotting was performed to detect the expression of P23, HSP90 and XRCC1 in AGS, SNU719 and SGC7901 cells after treatment with different concentrations of CEL (P23 inhibitor) for 24 hours. (B) GC1, GC2, and GC3 organoids were flow-sorted to separate P23(-) and P23(+) organoid strains. (C) qPCR was performed to detect P23 mRNA levels in P23(-) and P23(+) organoid strains. (D) qPCR analysis of XRCC1 expression in P23(-) and P23(+) organoid strains. (E) Western blot analysis of the expression of HSP90 and XRCC1 in AGS, SNU719 and SGC7901 cells treated with the specified concentrations of 17-AAG (HSP90 inhibitor) for 24 hours. (F) Representative images of GC organoids treated with DMSO (control group), 17-AAG (10 µM), CEL (2 µM), and AIL (1 µM) for 14 days. The number of cell clusters (G) and size of clusters (H) were counted. Data were derived from experiments conducted in triplicate. The treated organoids were compared with the control group, *P<0.05, **P<0.01, ***P<0.001.

    Article Snippet: Antibodies used were: XRCC1 (1: 100, Abcam, ab44830), P23 (1: 200, Proteintech, 10824-1-AP), HSP90 (1: 400, Proteintech, 60318-1-Ig), Lamin B1 (1: 20000, Proteintech, 66095-1-Ig), GAPDH (1: 20000, Proteintech, 60004-1-Ig).

    Techniques: Western Blot, Expressing, Derivative Assay

    AIL inhibits the binding of P23 and XRCC1 to HSP90 in GC cells. (A) The colocalization of HSP90 with P23 and XRCC1 was demonstrated with immunofluorescence in GC organoids treated with AIL (1 µM) for 24 hours. Scale bars, 100 µm. (B) Data were derived from experiments conducted in triplicate in (A). (C) Pull-down of selected proteins with HSP90 in the nucleus and cytoplasm of GC cells treated with AIL for 24 hours, and then the IP fractions were immunoblotted with HSP90, XRCC1, P23, Lamin B1 and GAPDH. (D) Graphical illustration of the functions of AIL in inhibiting tumor growth. The treated cells were compared with the control group, *P<0.05, **P<0.01, ***P<0.001.

    Journal: International Journal of Biological Sciences

    Article Title: Ailanthus Altissima-derived Ailanthone enhances Gastric Cancer Cell Apoptosis by Inducing the Repression of Base Excision Repair by Downregulating p23 Expression

    doi: 10.7150/ijbs.60674

    Figure Lengend Snippet: AIL inhibits the binding of P23 and XRCC1 to HSP90 in GC cells. (A) The colocalization of HSP90 with P23 and XRCC1 was demonstrated with immunofluorescence in GC organoids treated with AIL (1 µM) for 24 hours. Scale bars, 100 µm. (B) Data were derived from experiments conducted in triplicate in (A). (C) Pull-down of selected proteins with HSP90 in the nucleus and cytoplasm of GC cells treated with AIL for 24 hours, and then the IP fractions were immunoblotted with HSP90, XRCC1, P23, Lamin B1 and GAPDH. (D) Graphical illustration of the functions of AIL in inhibiting tumor growth. The treated cells were compared with the control group, *P<0.05, **P<0.01, ***P<0.001.

    Article Snippet: Antibodies used were: XRCC1 (1: 100, Abcam, ab44830), P23 (1: 200, Proteintech, 10824-1-AP), HSP90 (1: 400, Proteintech, 60318-1-Ig), Lamin B1 (1: 20000, Proteintech, 66095-1-Ig), GAPDH (1: 20000, Proteintech, 60004-1-Ig).

    Techniques: Binding Assay, Immunofluorescence, Derivative Assay

    Highly expressed P23 is associated with GC recurrence. (A) Representative images of high and low expression levels of P23 detected via IHC (100X) in recurrent GC tissues. Scale bars, 200 µm. (B) Recurrence time curves of 93 patients with GC recurrence, including 42 patients with high P23 expression and 51 patients with low P23 expression. *P<0.05, **P<0.01, ***P<0.001.

    Journal: International Journal of Biological Sciences

    Article Title: Ailanthus Altissima-derived Ailanthone enhances Gastric Cancer Cell Apoptosis by Inducing the Repression of Base Excision Repair by Downregulating p23 Expression

    doi: 10.7150/ijbs.60674

    Figure Lengend Snippet: Highly expressed P23 is associated with GC recurrence. (A) Representative images of high and low expression levels of P23 detected via IHC (100X) in recurrent GC tissues. Scale bars, 200 µm. (B) Recurrence time curves of 93 patients with GC recurrence, including 42 patients with high P23 expression and 51 patients with low P23 expression. *P<0.05, **P<0.01, ***P<0.001.

    Article Snippet: Antibodies used were: XRCC1 (1: 100, Abcam, ab44830), P23 (1: 200, Proteintech, 10824-1-AP), HSP90 (1: 400, Proteintech, 60318-1-Ig), Lamin B1 (1: 20000, Proteintech, 66095-1-Ig), GAPDH (1: 20000, Proteintech, 60004-1-Ig).

    Techniques: Expressing