il6 inhibitor lmt 28  (MedChemExpress)

Journal: Cancer Medicine

Article Title: MCPIP1 Controls Hybrid EMT and Tumor Stemness via the IL6 / JAK2 / STAT3 Axis in Pancreatic Cancer

doi: 10.1002/cam4.71179

Figure Lengend Snippet: MCPIP1 is involved in the IL6/JAK/STAT3 signaling pathway in pancreatic cancer. (A) MCPIP1 protein interaction graph obtained from the STRING database. (B) After silencing MCPIP1 expression in pancreatic tumor cells, protein expression of IL6, P‐JAK2, P‐STAT3 in the above two cell lines were measured and analyzed by western blotting, and their statistical analysis is shown. (C) After overexpression of MCPIP1 in pancreatic tumor cells, protein expression of IL6, phosphorylation (P)‐JAK2, and P‐STAT3 was measured by immunoblotting; the statistical analysis is shown in graphs. (D) Detection of the levels of IL6, P‐JAK, and P‐STAT3 in the subcutaneous tumors of nude mice by immunoblotting; the statistical analysis is shown in graphs. (E) Immunohistochemical staining was used to examine IL6 and P‐STAT3 expression in subcutaneous tumors of nude mice (magnification ×200; scale bar 50 μm). NC, negative control group, shMCPIP1; short hairpin RNA targeting MCPIP1; vector, empty vector lentivirus, oe‐MCPIP1, overexpression of MCPIP1. The mean ± SD of the three experimental groups. Statistical significance of comparisons is indicated by * p < 0.05, ** p < 0.01, *** p < 0.001 and **** p < 0.0001.

Article Snippet: The IL6 inhibitor LMT‐28 (HY‐102084, Med‐ChemExpress, USA) was dissolved in Dimethyl Sulfoxide (DMSO) (Sigma‐Aldrich, USA).

Techniques: Expressing, Western Blot, Over Expression, Phospho-proteomics, Immunohistochemical staining, Staining, Negative Control, shRNA, Plasmid Preparation

Journal: Cancer Medicine

Article Title: MCPIP1 Controls Hybrid EMT and Tumor Stemness via the IL6 / JAK2 / STAT3 Axis in Pancreatic Cancer

doi: 10.1002/cam4.71179

Figure Lengend Snippet: MCPIP1 inhibits mixed EMT and tumor stemness through IL6/JAK2/STAT3 signaling. (A) shMCPIP1 pancreatic tumor cell lines were exposed with 10 μM LMT‐28 for 6 h. Protein levels of IL6, phosphorylated (P)‐JAK2, and P‐STAT3 was examined by immunoblotting. (B) Western blot showing changes in EMT‐related proteins in pancreatic cancer knockdown cell lines exposed to LMT‐28. (C) Western blotting indicated changes in CD44 and CD133 proteins in pancreatic cancer knockdown cell lines exposed to LMT‐28. (D) Changes in tumor sphere formation after the addition of the IL6 inhibitor were detected (magnification ×100; scale bar 100 μm). (E) Cell Count Kit‐8 was used to identify alterations in the cell growth capacity of shMCPIP1 pancreatic tumor cells exposed to 10 μM LMT‐28. (F) Wound healing of pancreatic cancer cells from the shMCPIP1 control group was detected by a cell scratch assay in the presence of 10 μM LMT‐28 (scale, 100 μm). (G) Number of invasive cells and pancreatic cancer cell migrating cells in the control group shMCPIP1 detected by the Transwell assay in the presence of 10 μM LMT‐28 (magnification ×100; scale bar 100 μm). NC, negative control group; shMCPIP1, short hairpin RNA targeting MCPIP1; shMCPIP1 + DMSO, shMCPIP1 group treated with DMSO; and shMCPIP1 + LMT‐28, shMCPIP1 group treated with LMT‐28. The mean ± SD of the three experimental groups. Statistical significance of comparisons is indicated by * p < 0.05, ** p < 0.01, *** p < 0.001 and **** p < 0.0001.

Article Snippet: The IL6 inhibitor LMT‐28 (HY‐102084, Med‐ChemExpress, USA) was dissolved in Dimethyl Sulfoxide (DMSO) (Sigma‐Aldrich, USA).

Techniques: Western Blot, Knockdown, Cell Counting, Control, Wound Healing Assay, Transwell Assay, Negative Control, shRNA