Journal: Chemistry & Biodiversity

Article Title: CA IX Inhibition by a Sulfonamide Compound: A Therapeutic Approach Against Breast Cancer

doi: 10.1002/cbdv.202501618

Figure Lengend Snippet: Protein and gene expression levels of CA IX, Caspase‐3 (CAS‐3), Vimentin (VIM), and E‐Cadherin (E‐CAD) across groups. The data were presented as mean ± SD ( n = 10). * p < 0.05 and ** p < 0.01 represent significance for comparisons between tumor (T) and normal breast (N) tissues.

Article Snippet: Protein levels of CA IX (Catalog No: E‐EL‐M0227, Elabscience), Vimentin (Catalog No: E2669Mo, BT Lab), E‐Cadherin (Catalog No: E‐EL‐M0211), and Caspase‐3 (Catalog No: E‐EL‐M0238) were determined using ELISA kits, following the manufacturer's protocols.

Techniques: Gene Expression

Journal: Cancer Medicine

Article Title: Role of Ca 2+ ‐Dependent Epithelial‐Mesenchymal Transition in Malignant Progression of Colorectal Cancer: Special Focus on REG Iα/ EDNRB

doi: 10.1002/cam4.71754

Figure Lengend Snippet: REG Iα promotes cell migration, invasion, and EMT via EDNRB. (A) Cell migration was assessed by Transwell assay. (B) Matrigel‐coated Transwell assay assessed cell invasion. (C) Western blot analysis of EMT‐related markers, including the epithelial marker E‐Cadherin and mesenchymal markers N‐Cadherin and Vimentin. β‐actin was used as the loading control. Data are presented as mean ± SD. * p < 0.05, ** p < 0.01, *** p < 0.001, **** p < 0.0001.

Article Snippet: CHOP (Abcam, ab317378), Cleaved‐Caspase 3 (Abcam, ab32042), Cleaved‐PARP (Cell Signaling Technology, 9541), E‐Cadherin (BOSTER, PB9561), N‐Cadherin (BOSTER, A01577‐3), and Vimentin (BOSTER, BM4029).

Techniques: Migration, Transwell Assay, Western Blot, Marker, Control

Journal: Cancer Medicine

Article Title: Role of Ca 2+ ‐Dependent Epithelial‐Mesenchymal Transition in Malignant Progression of Colorectal Cancer: Special Focus on REG Iα/ EDNRB

doi: 10.1002/cam4.71754

Figure Lengend Snippet: The REG Iα‐EDNRB axis promotes cell migration, invasion, and EMT via the Ca 2+ signaling pathway. (A) Transwell assay assessed cell migration. (B) Cell invasion was assessed by Matrigel‐coated Transwell assay. (C) EMT‐related protein levels (E‐Cadherin, N‐Cadherin, Vimentin) were detected by Western blot. β‐actin served as the loading control. Data are presented as mean ± SD. * p < 0.05, ** p < 0.01, *** p < 0.001, **** p < 0.0001.

Article Snippet: CHOP (Abcam, ab317378), Cleaved‐Caspase 3 (Abcam, ab32042), Cleaved‐PARP (Cell Signaling Technology, 9541), E‐Cadherin (BOSTER, PB9561), N‐Cadherin (BOSTER, A01577‐3), and Vimentin (BOSTER, BM4029).

Techniques: Migration, Transwell Assay, Western Blot, Control

Journal: Cancer Medicine

Article Title: Role of Ca 2+ ‐Dependent Epithelial‐Mesenchymal Transition in Malignant Progression of Colorectal Cancer: Special Focus on REG Iα/ EDNRB

doi: 10.1002/cam4.71754

Figure Lengend Snippet: The REG Iα‐EDNRB‐Ca 2+ axis promotes tumor growth and EMT in vivo. (A) Representative images of the xenograft tumors and excised tumor tissues from the indicated groups. (B) Statistical analysis of the final tumor weights. (C) Tumor growth curves measuring tumor volume over time. (D) H&E staining showed pathological changes in tumor tissues. (E) TUNEL assay detected cell apoptosis in tumor tissues. (F) Cell proliferation in tumor tissues was shown by Ki67 IHC staining. (G) Expression of REG Iα (Immunofluorescence, upper row) and EDNRB (IHC, lower row) in tumor tissues. (H) Western blot analysis of REG Iα, EDNRB, and p‐CaMKII protein levels in tumor tissues. β‐actin was used as the loading control. (I) Western blot analysis of EMT‐related proteins (E‐Cadherin, N‐Cadherin, Vimentin) in tumor tissues. β‐actin was used as the loading control. Data are presented as mean ± SD. * p < 0.05, ** p < 0.01, *** p < 0.001, **** p < 0.0001.

Article Snippet: CHOP (Abcam, ab317378), Cleaved‐Caspase 3 (Abcam, ab32042), Cleaved‐PARP (Cell Signaling Technology, 9541), E‐Cadherin (BOSTER, PB9561), N‐Cadherin (BOSTER, A01577‐3), and Vimentin (BOSTER, BM4029).

Techniques: In Vivo, Staining, TUNEL Assay, Immunohistochemistry, Expressing, Immunofluorescence, Western Blot, Control

Journal: Heliyon

Article Title: LncBIRC3-OT promotes the malignant progression of glioma by interacting with RELA to upregulate stanniocalcin-1 expression

doi: 10.1016/j.heliyon.2023.e21777

Figure Lengend Snippet: LncBIRC3-OT is required for malignant behaviours of glioma cells. (A) LncBIRC3-OT was silenced in U87 and U251 cells by shRNAs. (B) Cell viability was detected in lncBIRC3-OT-depleted cells by CCK-8 assay. (C) LncBIRC3-OT depletion causes a diminished colony-forming capacity in U87 and U251 cells. (D) Cell migration was detected in lncBIRC3-OT-depleted cells by wound-healing assays. (E) Cell invasion was analyzed in lncBIRC3-OT-silenced U87 and U251 cells by Transwell invasion assay. (F) N-cadherin, Vimentin, and E-cadherin were analyzed in lncBIRC3-OT-depleted cells by Western blot analysis. Uncropped images of blots are shown in Supplementary material. Data were shown as mean ± SD from three independent experiments. **P < 0.01, ***P < 0.001 vs. the NC groups.

Article Snippet: The primary antibodies used in this study are listed as follows: E-cadherin (1:5000, #60335-1-lg), N-cadherin (1:2000, #66219-1-lg), Vimentin (1:2000, #60330-1-lg), RELA (1:1000, #66535-1-lg), STC1 (1:1000, #20621-1-AP) and GAPDH (1:10000, #60004-1-lg) were obtained from Proteintech (Wuhan, China).

Techniques: CCK-8 Assay, Migration, Transwell Invasion Assay, Western Blot