annexin green apoptosis cell detection reagent kit  (Cell Signaling Technology Inc)


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    Cell Signaling Technology Inc annexin green apoptosis cell detection reagent kit
    Schematic model of IRE 1‐ XBP 1‐induced radioresistance via interleukin‐6 ( IL ‐6) upregulation. Exposure to X‐ray irradiation causes endoplasmic reticulum stress (ERS) , and increased levels of IRE 1 promote the splicing of XBP 1 mRNA . The activated transcription factor XBP 1s translocates to the nucleus and induces the expression of IL ‐6. Concurrently, the formation of DNA double‐strand breaks (DSB) is inhibited and helps decrease <t>apoptosis,</t> which is related to radioresistance
    Annexin Green Apoptosis Cell Detection Reagent Kit, supplied by Cell Signaling Technology Inc, 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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    Average 92 stars, based on 1 article reviews
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    1) Product Images from "Interleukin‐6 production mediated by the IRE 1‐ XBP 1 pathway confers radioresistance in human papillomavirus‐negative oropharyngeal carcinoma"

    Article Title: Interleukin‐6 production mediated by the IRE 1‐ XBP 1 pathway confers radioresistance in human papillomavirus‐negative oropharyngeal carcinoma

    Journal: Cancer Science

    doi: 10.1111/cas.14094

    Schematic model of IRE 1‐ XBP 1‐induced radioresistance via interleukin‐6 ( IL ‐6) upregulation. Exposure to X‐ray irradiation causes endoplasmic reticulum stress (ERS) , and increased levels of IRE 1 promote the splicing of XBP 1 mRNA . The activated transcription factor XBP 1s translocates to the nucleus and induces the expression of IL ‐6. Concurrently, the formation of DNA double‐strand breaks (DSB) is inhibited and helps decrease apoptosis, which is related to radioresistance
    Figure Legend Snippet: Schematic model of IRE 1‐ XBP 1‐induced radioresistance via interleukin‐6 ( IL ‐6) upregulation. Exposure to X‐ray irradiation causes endoplasmic reticulum stress (ERS) , and increased levels of IRE 1 promote the splicing of XBP 1 mRNA . The activated transcription factor XBP 1s translocates to the nucleus and induces the expression of IL ‐6. Concurrently, the formation of DNA double‐strand breaks (DSB) is inhibited and helps decrease apoptosis, which is related to radioresistance

    Techniques Used: Irradiation, Expressing

    annexin green apoptosis cell detection reagent kit  (Cell Signaling Technology Inc)


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    Cell Signaling Technology Inc annexin green apoptosis cell detection reagent kit
    Schematic model of IRE 1‐ XBP 1‐induced radioresistance via interleukin‐6 ( IL ‐6) upregulation. Exposure to X‐ray irradiation causes endoplasmic reticulum stress (ERS) , and increased levels of IRE 1 promote the splicing of XBP 1 mRNA . The activated transcription factor XBP 1s translocates to the nucleus and induces the expression of IL ‐6. Concurrently, the formation of DNA double‐strand breaks (DSB) is inhibited and helps decrease <t>apoptosis,</t> which is related to radioresistance
    Annexin Green Apoptosis Cell Detection Reagent Kit, supplied by Cell Signaling Technology Inc, 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/annexin green apoptosis cell detection reagent kit/product/Cell Signaling Technology Inc
    Average 92 stars, based on 1 article reviews
    Price from $9.99 to $1999.99
    annexin green apoptosis cell detection reagent kit - by Bioz Stars, 2023-03
    92/100 stars

    Images

    1) Product Images from "Interleukin‐6 production mediated by the IRE 1‐ XBP 1 pathway confers radioresistance in human papillomavirus‐negative oropharyngeal carcinoma"

    Article Title: Interleukin‐6 production mediated by the IRE 1‐ XBP 1 pathway confers radioresistance in human papillomavirus‐negative oropharyngeal carcinoma

    Journal: Cancer Science

    doi: 10.1111/cas.14094

    Schematic model of IRE 1‐ XBP 1‐induced radioresistance via interleukin‐6 ( IL ‐6) upregulation. Exposure to X‐ray irradiation causes endoplasmic reticulum stress (ERS) , and increased levels of IRE 1 promote the splicing of XBP 1 mRNA . The activated transcription factor XBP 1s translocates to the nucleus and induces the expression of IL ‐6. Concurrently, the formation of DNA double‐strand breaks (DSB) is inhibited and helps decrease apoptosis, which is related to radioresistance
    Figure Legend Snippet: Schematic model of IRE 1‐ XBP 1‐induced radioresistance via interleukin‐6 ( IL ‐6) upregulation. Exposure to X‐ray irradiation causes endoplasmic reticulum stress (ERS) , and increased levels of IRE 1 promote the splicing of XBP 1 mRNA . The activated transcription factor XBP 1s translocates to the nucleus and induces the expression of IL ‐6. Concurrently, the formation of DNA double‐strand breaks (DSB) is inhibited and helps decrease apoptosis, which is related to radioresistance

    Techniques Used: Irradiation, Expressing

    annexin green apoptosis cell detection reagent kit  (Cell Signaling Technology Inc)


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    Cell Signaling Technology Inc annexin green apoptosis cell detection reagent kit
    EGFR regulates the radiosensitivity of OSCC cells via ERS and is associated with <t>apoptosis,</t> DSB repair, and autophagy. A, γ‐H2AX foci formation and B, LC3 immunopositive dots in control and EGFR siRNA transfected FaDuR, Detroit562R, FaDuP, and Detroit562P cells followed by irradiation (5 Gy, 2 h). C, DNA‐PKcs, LC3B (LC3B‐II/β‐actin), Atg3, and cleaved caspase 3 levels in control and EGFR siRNA transfected OSCC cells pre‐treated with or without 100 µg/L cetuximab, 10 µmol/L salubrinal, or 1.0 µg/mL tunicamycin for 12 h followed by 5 Gy of irradiation. D, Also shown, cleaved caspase 3 and cleaved PARP in FaDuR, Detroit562R, FaDuP, and Detroit562P cells pre‐treated with or without 20 µmol/L Ly294002 and 5 mmol/L 3‐MA followed by 5 Gy irradiation. E, FACS analysis by AnnexinV/PI double staining of control and EGFR siRNA transfected FaDuR, Detroit562R, FaDuP, and Detroit562P cells, pre‐treated with or without 20 µmol/L Ly294002 and 5 mmol/L 3‐MA followed by 5 Gy irradiation. Note: * denotes P < 0.05 compared to the control group
    Annexin Green Apoptosis Cell Detection Reagent Kit, supplied by Cell Signaling Technology Inc, 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/annexin green apoptosis cell detection reagent kit/product/Cell Signaling Technology Inc
    Average 92 stars, based on 1 article reviews
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    annexin green apoptosis cell detection reagent kit - by Bioz Stars, 2023-03
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    1) Product Images from "EGFR confers radioresistance in human oropharyngeal carcinoma by activating endoplasmic reticulum stress signaling PERK‐eIF2α‐GRP94 and IRE1α‐XBP1‐GRP78"

    Article Title: EGFR confers radioresistance in human oropharyngeal carcinoma by activating endoplasmic reticulum stress signaling PERK‐eIF2α‐GRP94 and IRE1α‐XBP1‐GRP78

    Journal: Cancer Medicine

    doi: 10.1002/cam4.1862

    EGFR regulates the radiosensitivity of OSCC cells via ERS and is associated with apoptosis, DSB repair, and autophagy. A, γ‐H2AX foci formation and B, LC3 immunopositive dots in control and EGFR siRNA transfected FaDuR, Detroit562R, FaDuP, and Detroit562P cells followed by irradiation (5 Gy, 2 h). C, DNA‐PKcs, LC3B (LC3B‐II/β‐actin), Atg3, and cleaved caspase 3 levels in control and EGFR siRNA transfected OSCC cells pre‐treated with or without 100 µg/L cetuximab, 10 µmol/L salubrinal, or 1.0 µg/mL tunicamycin for 12 h followed by 5 Gy of irradiation. D, Also shown, cleaved caspase 3 and cleaved PARP in FaDuR, Detroit562R, FaDuP, and Detroit562P cells pre‐treated with or without 20 µmol/L Ly294002 and 5 mmol/L 3‐MA followed by 5 Gy irradiation. E, FACS analysis by AnnexinV/PI double staining of control and EGFR siRNA transfected FaDuR, Detroit562R, FaDuP, and Detroit562P cells, pre‐treated with or without 20 µmol/L Ly294002 and 5 mmol/L 3‐MA followed by 5 Gy irradiation. Note: * denotes P < 0.05 compared to the control group
    Figure Legend Snippet: EGFR regulates the radiosensitivity of OSCC cells via ERS and is associated with apoptosis, DSB repair, and autophagy. A, γ‐H2AX foci formation and B, LC3 immunopositive dots in control and EGFR siRNA transfected FaDuR, Detroit562R, FaDuP, and Detroit562P cells followed by irradiation (5 Gy, 2 h). C, DNA‐PKcs, LC3B (LC3B‐II/β‐actin), Atg3, and cleaved caspase 3 levels in control and EGFR siRNA transfected OSCC cells pre‐treated with or without 100 µg/L cetuximab, 10 µmol/L salubrinal, or 1.0 µg/mL tunicamycin for 12 h followed by 5 Gy of irradiation. D, Also shown, cleaved caspase 3 and cleaved PARP in FaDuR, Detroit562R, FaDuP, and Detroit562P cells pre‐treated with or without 20 µmol/L Ly294002 and 5 mmol/L 3‐MA followed by 5 Gy irradiation. E, FACS analysis by AnnexinV/PI double staining of control and EGFR siRNA transfected FaDuR, Detroit562R, FaDuP, and Detroit562P cells, pre‐treated with or without 20 µmol/L Ly294002 and 5 mmol/L 3‐MA followed by 5 Gy irradiation. Note: * denotes P < 0.05 compared to the control group

    Techniques Used: Transfection, Irradiation, Double Staining

    annexin green apoptosis cell detection reagent kit  (Cell Signaling Technology Inc)


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    Cell Signaling Technology Inc annexin green apoptosis cell detection reagent kit
    (A) Silencing GRP78 inhibited the radiation-induced (5 Gy, 12 h) expression of the DNA double-strand break repair protein DNA-PK and increased the phosphorylation level of ATM. Silencing GRP78 also inhibited the radiation-induced expression of the autophagy-related proteins LC3B (LC3B-II/β-actin) and Atg16L1 and increased the expression of the <t>apoptosis</t> marker protein cleaved caspase-3 and cleaved PARP. (B) Immunofluorescence studies showed that after oropharyngeal carcinoma cells received 5 Gy radiation for 1 h, the γ-H2AX foci in nucleus increased (the blue background indicates the cell nucleus, and light red dots indicate γ-H2AX foci). In addition, the effect of radiation after GRP78 silencing was more evident than that of simple radiation. (C) Immunofluorescence studies by LC3B staining also showed autophagy regions in the nucleus after 5 Gy radiation for 1 h (the blue background indicates the cell nucleus, and light green dots indicate LC3B foci), which was reversed after GRP78 silencing. The oropharyngeal carcinoma cells were pretreated with 20 μmol/L Ly294002 or 5 mmol/L 3-MA for 12 h. The cells were then treated with 5 Gy of radiation. Compared with the IR group, *P < 0.05. For (A), bands were quantified using ImageJ software and were normalized to a loading control. Fold changes are shown compared with the negative control lane without radiation. N/A = not applicable.
    Annexin Green Apoptosis Cell Detection Reagent Kit, supplied by Cell Signaling Technology Inc, 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/annexin green apoptosis cell detection reagent kit/product/Cell Signaling Technology Inc
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    annexin green apoptosis cell detection reagent kit - by Bioz Stars, 2023-03
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    1) Product Images from "Inhibition of GRP78 abrogates radioresistance in oropharyngeal carcinoma cells after EGFR inhibition by cetuximab"

    Article Title: Inhibition of GRP78 abrogates radioresistance in oropharyngeal carcinoma cells after EGFR inhibition by cetuximab

    Journal: PLoS ONE

    doi: 10.1371/journal.pone.0188932

    (A) Silencing GRP78 inhibited the radiation-induced (5 Gy, 12 h) expression of the DNA double-strand break repair protein DNA-PK and increased the phosphorylation level of ATM. Silencing GRP78 also inhibited the radiation-induced expression of the autophagy-related proteins LC3B (LC3B-II/β-actin) and Atg16L1 and increased the expression of the apoptosis marker protein cleaved caspase-3 and cleaved PARP. (B) Immunofluorescence studies showed that after oropharyngeal carcinoma cells received 5 Gy radiation for 1 h, the γ-H2AX foci in nucleus increased (the blue background indicates the cell nucleus, and light red dots indicate γ-H2AX foci). In addition, the effect of radiation after GRP78 silencing was more evident than that of simple radiation. (C) Immunofluorescence studies by LC3B staining also showed autophagy regions in the nucleus after 5 Gy radiation for 1 h (the blue background indicates the cell nucleus, and light green dots indicate LC3B foci), which was reversed after GRP78 silencing. The oropharyngeal carcinoma cells were pretreated with 20 μmol/L Ly294002 or 5 mmol/L 3-MA for 12 h. The cells were then treated with 5 Gy of radiation. Compared with the IR group, *P < 0.05. For (A), bands were quantified using ImageJ software and were normalized to a loading control. Fold changes are shown compared with the negative control lane without radiation. N/A = not applicable.
    Figure Legend Snippet: (A) Silencing GRP78 inhibited the radiation-induced (5 Gy, 12 h) expression of the DNA double-strand break repair protein DNA-PK and increased the phosphorylation level of ATM. Silencing GRP78 also inhibited the radiation-induced expression of the autophagy-related proteins LC3B (LC3B-II/β-actin) and Atg16L1 and increased the expression of the apoptosis marker protein cleaved caspase-3 and cleaved PARP. (B) Immunofluorescence studies showed that after oropharyngeal carcinoma cells received 5 Gy radiation for 1 h, the γ-H2AX foci in nucleus increased (the blue background indicates the cell nucleus, and light red dots indicate γ-H2AX foci). In addition, the effect of radiation after GRP78 silencing was more evident than that of simple radiation. (C) Immunofluorescence studies by LC3B staining also showed autophagy regions in the nucleus after 5 Gy radiation for 1 h (the blue background indicates the cell nucleus, and light green dots indicate LC3B foci), which was reversed after GRP78 silencing. The oropharyngeal carcinoma cells were pretreated with 20 μmol/L Ly294002 or 5 mmol/L 3-MA for 12 h. The cells were then treated with 5 Gy of radiation. Compared with the IR group, *P < 0.05. For (A), bands were quantified using ImageJ software and were normalized to a loading control. Fold changes are shown compared with the negative control lane without radiation. N/A = not applicable.

    Techniques Used: Expressing, Marker, Immunofluorescence, Staining, Software, Negative Control

    Oropharyngeal carcinoma cells were pretreated with 20 μmol/L Ly294002 or 5 mmol/L 3-MA for 12 h. The cells were then treated with different doses of radiation. (A) The results of cloning showed that Ly294002 and 3-MA could increase the radiosensitivity of oropharyngeal carcinoma cells. Additionally, radiation parameters were fitted to a classic multitarget single hit model as shown in the table. (B) Western blot analysis showed that Ly294002 and 3-MA increased the radiation-induced protein expression of cleaved PARP and inhibited the radiation-induced expression of the anti-apoptotic protein Bcl-2 and the cell proliferation regulatory protein EGR1. (C) At 48 h after irradiation, CCK-8 analysis showed that Ly294002 and 3-MA further reduced the proliferation of cells inhibited by radiation alone. (D) At 48 h after irradiation, apoptosis was detected by flow cytometry after Annexin V/PI staining. The results showed that Ly294002 and 3-MA increased radiation-induced apoptosis. For (C) and (D), compared with the IR group, *P < 0.05. For (B), bands were quantified using ImageJ software and were normalized to a loading control. Fold changes are shown compared with the negative control lane without radiation. N/A = not applicable.
    Figure Legend Snippet: Oropharyngeal carcinoma cells were pretreated with 20 μmol/L Ly294002 or 5 mmol/L 3-MA for 12 h. The cells were then treated with different doses of radiation. (A) The results of cloning showed that Ly294002 and 3-MA could increase the radiosensitivity of oropharyngeal carcinoma cells. Additionally, radiation parameters were fitted to a classic multitarget single hit model as shown in the table. (B) Western blot analysis showed that Ly294002 and 3-MA increased the radiation-induced protein expression of cleaved PARP and inhibited the radiation-induced expression of the anti-apoptotic protein Bcl-2 and the cell proliferation regulatory protein EGR1. (C) At 48 h after irradiation, CCK-8 analysis showed that Ly294002 and 3-MA further reduced the proliferation of cells inhibited by radiation alone. (D) At 48 h after irradiation, apoptosis was detected by flow cytometry after Annexin V/PI staining. The results showed that Ly294002 and 3-MA increased radiation-induced apoptosis. For (C) and (D), compared with the IR group, *P < 0.05. For (B), bands were quantified using ImageJ software and were normalized to a loading control. Fold changes are shown compared with the negative control lane without radiation. N/A = not applicable.

    Techniques Used: Clone Assay, Western Blot, Expressing, Irradiation, CCK-8 Assay, Flow Cytometry, Staining, Software, Negative Control

    Oropharyngeal carcinoma cells transfected with siRNA to silence GRP78 or negative siRNA were treated with 50 μg/mL cetuximab for 12 h and then irradiated. (A) Colony formation experiments showed that cetuximab inhibited the colony formation of FaDu cells, which was further enhanced by silencing GRP78. In contrast, cetuximab alone did not affect the colony formation of Detroit562 cells, which was reversed by the silencing of GRP78. (B) Cetuximab weakened the radiation-mediated inhibition of FaDu cell proliferation, which was further enhanced by the silencing of GRP78. In addition, cetuximab had no significant effects on the radiation-mediated inhibition of Detroit562 cell proliferation, which was reversed by the silencing of GRP78. (C) Cetuximab increased the radiation-induced apoptosis of FaDu cells, which was further enhanced by the silencing of GRP78. The effect of cetuximab on the apoptosis of Detroit562 cells was not obvious, and this changed after GRP78 was silenced. Note: CTX = cetuximab, Neg = negative. *P < 0.05 Compared with Negative siRNA + IR; ΔP < 0.01 Compared with Negative siRNA + IR + CTX; ФP = 0.05 Compared with Negative siRNA + IR + CTX.
    Figure Legend Snippet: Oropharyngeal carcinoma cells transfected with siRNA to silence GRP78 or negative siRNA were treated with 50 μg/mL cetuximab for 12 h and then irradiated. (A) Colony formation experiments showed that cetuximab inhibited the colony formation of FaDu cells, which was further enhanced by silencing GRP78. In contrast, cetuximab alone did not affect the colony formation of Detroit562 cells, which was reversed by the silencing of GRP78. (B) Cetuximab weakened the radiation-mediated inhibition of FaDu cell proliferation, which was further enhanced by the silencing of GRP78. In addition, cetuximab had no significant effects on the radiation-mediated inhibition of Detroit562 cell proliferation, which was reversed by the silencing of GRP78. (C) Cetuximab increased the radiation-induced apoptosis of FaDu cells, which was further enhanced by the silencing of GRP78. The effect of cetuximab on the apoptosis of Detroit562 cells was not obvious, and this changed after GRP78 was silenced. Note: CTX = cetuximab, Neg = negative. *P < 0.05 Compared with Negative siRNA + IR; ΔP < 0.01 Compared with Negative siRNA + IR + CTX; ФP = 0.05 Compared with Negative siRNA + IR + CTX.

    Techniques Used: Transfection, Irradiation, Inhibition

    annexin green apoptosis cell detection reagent kit  (Cell Signaling Technology Inc)


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    Cell Signaling Technology Inc annexin green apoptosis cell detection reagent kit
    eIF 2α regulated radioresistance in oropharyngeal carcinoma cells by activating the NF ‐κB pathway. Cells were transfected with si RNA to silence eIF 2α and irradiated with 5 Gy X‐ray. (a) Cells were collected after 24 h to detect <t>apoptosis</t> using <t>Annexin</t> V/ PI staining followed by flow cytometry analysis. (b) Cells were collected after 48 h to identify the cell cycle using PI staining followed by flow cytometry. The results are expressed as the mean ± SD of three independent experiments. Compared with the IR group, * P < 0.05, # P < 0.01. (c) Cells were transfected with si RNA to silence eIF 2α and irradiated with 5 Gy for 12 h. Nuclear and cytoplasm proteins were extracted to detect the expression of phospho‐p65 and its downstream protein HIF ‐1α. Total protein was extracted to evaluate the expression of Rad50, Mre11, Nbs1 and phospho‐ ATM proteins. Western blot results showed that eIF 2α silencing inhibited radiation‐induced nuclear phospho‐p65 protein expression. Conversely, radiation inhibited cytoplasmic p65 protein phosphorylation, whereas eIF 2α silencing reversed this function. These results indicated that eIF 2α silencing inhibited radiation‐induced p65 nuclear translocation. In addition, eIF 2α silencing inhibited the radiation‐induced HIF ‐1α, Rad50 and Nbs1 expression, increased radiation‐induced phospho‐ ATM expression, and did not affect Mre11 protein expression. (d) After eIF 2α was silenced by si RNA transfection, the cells were irradiated (5 Gy, 1 h). The real‐time quantitative PCR results showed that eIF 2α silencing decreased the radiation‐induced expression of p65 mRNA expression. Compared to the irradiated group, * P < 0.05 and # P < 0.01. (e) Immunofluorescence studies showed that after oropharyngeal carcinoma cells received 5 Gy radiation for 1 h, the γ‐H2 AX foci in nucleus increased (the blue background indicates the cell nucleus, and light red dots indicate γ‐H2 AX foci). In addition, the effect of radiation after eIF 2α silencing was more evident than that of simple radiation. (f) The western blot results showed that eIF 2α silencing inhibited radiation (5 Gy, 12 h)‐induced phospho‐cdc2, Cyclin B, Bcl‐2 and Bcl‐ xL protein expression and increased radiation‐induced cleaved‐Caspase 3 and cleaved‐ PARP protein expression. The above functions were inhibited by pretreatment of the oropharyngeal carcinoma cells with the NF ‐κB activator TNF α (10 ng/mL) and the ATM inhibitor Ku55933 (10 μmol/L) for 12 h. Bands were quantified using ImageJ software and normalized to a loading control. Fold changes are shown compared with the negative control lane without radiation. NA, not applicable.
    Annexin Green Apoptosis Cell Detection Reagent Kit, supplied by Cell Signaling Technology Inc, 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/annexin green apoptosis cell detection reagent kit/product/Cell Signaling Technology Inc
    Average 92 stars, based on 1 article reviews
    Price from $9.99 to $1999.99
    annexin green apoptosis cell detection reagent kit - by Bioz Stars, 2023-03
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    1) Product Images from "Endoplasmic reticulum stress pathway PERK ‐ eIF 2α confers radioresistance in oropharyngeal carcinoma by activating NF ‐κB"

    Article Title: Endoplasmic reticulum stress pathway PERK ‐ eIF 2α confers radioresistance in oropharyngeal carcinoma by activating NF ‐κB

    Journal: Cancer Science

    doi: 10.1111/cas.13260

    eIF 2α regulated radioresistance in oropharyngeal carcinoma cells by activating the NF ‐κB pathway. Cells were transfected with si RNA to silence eIF 2α and irradiated with 5 Gy X‐ray. (a) Cells were collected after 24 h to detect apoptosis using Annexin V/ PI staining followed by flow cytometry analysis. (b) Cells were collected after 48 h to identify the cell cycle using PI staining followed by flow cytometry. The results are expressed as the mean ± SD of three independent experiments. Compared with the IR group, * P < 0.05, # P < 0.01. (c) Cells were transfected with si RNA to silence eIF 2α and irradiated with 5 Gy for 12 h. Nuclear and cytoplasm proteins were extracted to detect the expression of phospho‐p65 and its downstream protein HIF ‐1α. Total protein was extracted to evaluate the expression of Rad50, Mre11, Nbs1 and phospho‐ ATM proteins. Western blot results showed that eIF 2α silencing inhibited radiation‐induced nuclear phospho‐p65 protein expression. Conversely, radiation inhibited cytoplasmic p65 protein phosphorylation, whereas eIF 2α silencing reversed this function. These results indicated that eIF 2α silencing inhibited radiation‐induced p65 nuclear translocation. In addition, eIF 2α silencing inhibited the radiation‐induced HIF ‐1α, Rad50 and Nbs1 expression, increased radiation‐induced phospho‐ ATM expression, and did not affect Mre11 protein expression. (d) After eIF 2α was silenced by si RNA transfection, the cells were irradiated (5 Gy, 1 h). The real‐time quantitative PCR results showed that eIF 2α silencing decreased the radiation‐induced expression of p65 mRNA expression. Compared to the irradiated group, * P < 0.05 and # P < 0.01. (e) Immunofluorescence studies showed that after oropharyngeal carcinoma cells received 5 Gy radiation for 1 h, the γ‐H2 AX foci in nucleus increased (the blue background indicates the cell nucleus, and light red dots indicate γ‐H2 AX foci). In addition, the effect of radiation after eIF 2α silencing was more evident than that of simple radiation. (f) The western blot results showed that eIF 2α silencing inhibited radiation (5 Gy, 12 h)‐induced phospho‐cdc2, Cyclin B, Bcl‐2 and Bcl‐ xL protein expression and increased radiation‐induced cleaved‐Caspase 3 and cleaved‐ PARP protein expression. The above functions were inhibited by pretreatment of the oropharyngeal carcinoma cells with the NF ‐κB activator TNF α (10 ng/mL) and the ATM inhibitor Ku55933 (10 μmol/L) for 12 h. Bands were quantified using ImageJ software and normalized to a loading control. Fold changes are shown compared with the negative control lane without radiation. NA, not applicable.
    Figure Legend Snippet: eIF 2α regulated radioresistance in oropharyngeal carcinoma cells by activating the NF ‐κB pathway. Cells were transfected with si RNA to silence eIF 2α and irradiated with 5 Gy X‐ray. (a) Cells were collected after 24 h to detect apoptosis using Annexin V/ PI staining followed by flow cytometry analysis. (b) Cells were collected after 48 h to identify the cell cycle using PI staining followed by flow cytometry. The results are expressed as the mean ± SD of three independent experiments. Compared with the IR group, * P < 0.05, # P < 0.01. (c) Cells were transfected with si RNA to silence eIF 2α and irradiated with 5 Gy for 12 h. Nuclear and cytoplasm proteins were extracted to detect the expression of phospho‐p65 and its downstream protein HIF ‐1α. Total protein was extracted to evaluate the expression of Rad50, Mre11, Nbs1 and phospho‐ ATM proteins. Western blot results showed that eIF 2α silencing inhibited radiation‐induced nuclear phospho‐p65 protein expression. Conversely, radiation inhibited cytoplasmic p65 protein phosphorylation, whereas eIF 2α silencing reversed this function. These results indicated that eIF 2α silencing inhibited radiation‐induced p65 nuclear translocation. In addition, eIF 2α silencing inhibited the radiation‐induced HIF ‐1α, Rad50 and Nbs1 expression, increased radiation‐induced phospho‐ ATM expression, and did not affect Mre11 protein expression. (d) After eIF 2α was silenced by si RNA transfection, the cells were irradiated (5 Gy, 1 h). The real‐time quantitative PCR results showed that eIF 2α silencing decreased the radiation‐induced expression of p65 mRNA expression. Compared to the irradiated group, * P < 0.05 and # P < 0.01. (e) Immunofluorescence studies showed that after oropharyngeal carcinoma cells received 5 Gy radiation for 1 h, the γ‐H2 AX foci in nucleus increased (the blue background indicates the cell nucleus, and light red dots indicate γ‐H2 AX foci). In addition, the effect of radiation after eIF 2α silencing was more evident than that of simple radiation. (f) The western blot results showed that eIF 2α silencing inhibited radiation (5 Gy, 12 h)‐induced phospho‐cdc2, Cyclin B, Bcl‐2 and Bcl‐ xL protein expression and increased radiation‐induced cleaved‐Caspase 3 and cleaved‐ PARP protein expression. The above functions were inhibited by pretreatment of the oropharyngeal carcinoma cells with the NF ‐κB activator TNF α (10 ng/mL) and the ATM inhibitor Ku55933 (10 μmol/L) for 12 h. Bands were quantified using ImageJ software and normalized to a loading control. Fold changes are shown compared with the negative control lane without radiation. NA, not applicable.

    Techniques Used: Transfection, Irradiation, Staining, Flow Cytometry, Expressing, Western Blot, Translocation Assay, Real-time Polymerase Chain Reaction, Immunofluorescence, Software, Negative Control

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    Cell Signaling Technology Inc annexin green apoptosis cell detection reagent kit
    Schematic model of IRE 1‐ XBP 1‐induced radioresistance via interleukin‐6 ( IL ‐6) upregulation. Exposure to X‐ray irradiation causes endoplasmic reticulum stress (ERS) , and increased levels of IRE 1 promote the splicing of XBP 1 mRNA . The activated transcription factor XBP 1s translocates to the nucleus and induces the expression of IL ‐6. Concurrently, the formation of DNA double‐strand breaks (DSB) is inhibited and helps decrease <t>apoptosis,</t> which is related to radioresistance
    Annexin Green Apoptosis Cell Detection Reagent Kit, supplied by Cell Signaling Technology Inc, 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/annexin green apoptosis cell detection reagent kit/product/Cell Signaling Technology Inc
    Average 92 stars, based on 1 article reviews
    Price from $9.99 to $1999.99
    annexin green apoptosis cell detection reagent kit - by Bioz Stars, 2023-03
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    Schematic model of IRE 1‐ XBP 1‐induced radioresistance via interleukin‐6 ( IL ‐6) upregulation. Exposure to X‐ray irradiation causes endoplasmic reticulum stress (ERS) , and increased levels of IRE 1 promote the splicing of XBP 1 mRNA . The activated transcription factor XBP 1s translocates to the nucleus and induces the expression of IL ‐6. Concurrently, the formation of DNA double‐strand breaks (DSB) is inhibited and helps decrease apoptosis, which is related to radioresistance

    Journal: Cancer Science

    Article Title: Interleukin‐6 production mediated by the IRE 1‐ XBP 1 pathway confers radioresistance in human papillomavirus‐negative oropharyngeal carcinoma

    doi: 10.1111/cas.14094

    Figure Lengend Snippet: Schematic model of IRE 1‐ XBP 1‐induced radioresistance via interleukin‐6 ( IL ‐6) upregulation. Exposure to X‐ray irradiation causes endoplasmic reticulum stress (ERS) , and increased levels of IRE 1 promote the splicing of XBP 1 mRNA . The activated transcription factor XBP 1s translocates to the nucleus and induces the expression of IL ‐6. Concurrently, the formation of DNA double‐strand breaks (DSB) is inhibited and helps decrease apoptosis, which is related to radioresistance

    Article Snippet: Experiments were performed according to the protocol supplied with the Annexin‐Green Apoptosis cell detection reagent kit (Cell Signaling Technology).

    Techniques: Irradiation, Expressing