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stat3 inhibitor  (MedChemExpress)
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MedChemExpress stat3 inhibitor
The <t>STAT3/NF-κB/Notch1</t> signaling was critical for IL-17░A-induced migration and invasion in NSCLC cells. (A) The activation of STAT3, NF-κB and Notch1in A549 and H460 cells treated with rhIL-17░A was analyzed using western blotting. (B) The migration activities of A549 and H460 cells treated with or without rhIL-17░A and STAT3, or NF-κB, or Notch1 inhibitor were assessed by transwell assay. One representative analysis is shown. The data from A549 (C) and H460 (D) cells are presented as histogram. (E) The invasion activities of A549 and H460 cells treated with or without rhIL-17░A and these molecular inhibitors were assessed by transwell assay. One representative analysis is shown. The data from A549 (F) and H460 (G) cells are presented as a histogram. (H) The expression of N-cadherin in A549 and H460 cells treated with or without rhIL-17░A and STAT3, or NF-κB, or Notch1 inhibitor was analyzed using western blotting. * indicates P < 0.05. Scale bar represents 50 μm.
Stat3 Inhibitor, supplied by MedChemExpress, used in various techniques. Bioz Stars score: 94/100, based on 1 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
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The STAT3/NF-κB/Notch1 signaling was critical for IL-17░A-induced migration and invasion in NSCLC cells. (A) The activation of STAT3, NF-κB and Notch1in A549 and H460 cells treated with rhIL-17░A was analyzed using western blotting. (B) The migration activities of A549 and H460 cells treated with or without rhIL-17░A and STAT3, or NF-κB, or Notch1 inhibitor were assessed by transwell assay. One representative analysis is shown. The data from A549 (C) and H460 (D) cells are presented as histogram. (E) The invasion activities of A549 and H460 cells treated with or without rhIL-17░A and these molecular inhibitors were assessed by transwell assay. One representative analysis is shown. The data from A549 (F) and H460 (G) cells are presented as a histogram. (H) The expression of N-cadherin in A549 and H460 cells treated with or without rhIL-17░A and STAT3, or NF-κB, or Notch1 inhibitor was analyzed using western blotting. * indicates P < 0.05. Scale bar represents 50 μm.

Journal: Oncoimmunology

Article Title: Th17 cell-derived IL-17A promoted tumor progression via STAT3/NF-κB/Notch1 signaling in non-small cell lung cancer

doi: 10.1080/2162402X.2018.1461303

Figure Lengend Snippet: The STAT3/NF-κB/Notch1 signaling was critical for IL-17░A-induced migration and invasion in NSCLC cells. (A) The activation of STAT3, NF-κB and Notch1in A549 and H460 cells treated with rhIL-17░A was analyzed using western blotting. (B) The migration activities of A549 and H460 cells treated with or without rhIL-17░A and STAT3, or NF-κB, or Notch1 inhibitor were assessed by transwell assay. One representative analysis is shown. The data from A549 (C) and H460 (D) cells are presented as histogram. (E) The invasion activities of A549 and H460 cells treated with or without rhIL-17░A and these molecular inhibitors were assessed by transwell assay. One representative analysis is shown. The data from A549 (F) and H460 (G) cells are presented as a histogram. (H) The expression of N-cadherin in A549 and H460 cells treated with or without rhIL-17░A and STAT3, or NF-κB, or Notch1 inhibitor was analyzed using western blotting. * indicates P < 0.05. Scale bar represents 50 μm.

Article Snippet: For blocking STAT3/NF-κB/Notch1 pathway with inhibitors, STAT3 inhibitor (Niclosamide, Sigma, #N3510), NF-κB inhibitor (PDTC, MCE, # HY-18738) and Notch1 inhibitor ( {"type":"entrez-nucleotide","attrs":{"text":"LY411575","term_id":"1257853995","term_text":"LY411575"}} LY411575 , MCE, # HY-50752) were added respectively in the bottom 30 minutes before rhIL-17░A was added.

Techniques: Migration, Activation Assay, Western Blot, Transwell Assay, Expressing

Blockade of STAT3/NF-κB/Notch1 signaling inhibited NSCLC stemness promoted by IL-17░A. (A) After the treatment with STAT3░or NF-κB or Notch1 inhibitor, the sphere forming of A549 and H460 cells induce by rhIL-17░A was blocked. One representative photomicrograph is shown. The results from A549 (B) and H460 (C) cells were shown as histogram. (D) The expression of Oct4 in A549 and H460 cells treated with or without rhIL-17░A and these molecular inhibitors were assessed by western blotting. The apoptosis of A549 (E) and H460 (F) cells treated with or without rhIL-17░A and these molecular inhibitors were assessed by transwell assay. * indicates P < 0.05. Scale bar represents 100 μm.

Journal: Oncoimmunology

Article Title: Th17 cell-derived IL-17A promoted tumor progression via STAT3/NF-κB/Notch1 signaling in non-small cell lung cancer

doi: 10.1080/2162402X.2018.1461303

Figure Lengend Snippet: Blockade of STAT3/NF-κB/Notch1 signaling inhibited NSCLC stemness promoted by IL-17░A. (A) After the treatment with STAT3░or NF-κB or Notch1 inhibitor, the sphere forming of A549 and H460 cells induce by rhIL-17░A was blocked. One representative photomicrograph is shown. The results from A549 (B) and H460 (C) cells were shown as histogram. (D) The expression of Oct4 in A549 and H460 cells treated with or without rhIL-17░A and these molecular inhibitors were assessed by western blotting. The apoptosis of A549 (E) and H460 (F) cells treated with or without rhIL-17░A and these molecular inhibitors were assessed by transwell assay. * indicates P < 0.05. Scale bar represents 100 μm.

Article Snippet: For blocking STAT3/NF-κB/Notch1 pathway with inhibitors, STAT3 inhibitor (Niclosamide, Sigma, #N3510), NF-κB inhibitor (PDTC, MCE, # HY-18738) and Notch1 inhibitor ( {"type":"entrez-nucleotide","attrs":{"text":"LY411575","term_id":"1257853995","term_text":"LY411575"}} LY411575 , MCE, # HY-50752) were added respectively in the bottom 30 minutes before rhIL-17░A was added.

Techniques: Expressing, Western Blot, Transwell Assay