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STEAP1 facilitates metastasis and epithelial–mesenchymal transition of lung adenocarcinoma via the JAK2/STAT3 signaling pathway
Six-transmembrane epithelial antigen of prostate-1 (STEAP1) is a relatively newly identified gene target from prostate cancer, breast cancer, and gastric cancer. However, functions of STEAP1 in lung adenocarcinoma (LUAD) are still unknown. In the present study, we explored the molecular and cellular...
Autores principales: | , , , , , , , , , , , , |
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Formato: | Online Artículo Texto |
Lenguaje: | English |
Publicado: |
Portland Press Ltd.
2020
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Materias: | |
Acceso en línea: | https://www.ncbi.nlm.nih.gov/pmc/articles/PMC7300283/ https://www.ncbi.nlm.nih.gov/pubmed/32515474 http://dx.doi.org/10.1042/BSR20193169 |
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author | Huo, Shu-fen Shang, Wen-li Yu, Min Ren, Xiao-ping Wen, Hong-xia Chai, Chun-yan Sun, Li Hui, Ke Liu, Ling-hua Wei, Sheng-hong Wang, Xiao-xiao Wang, Yi Tian, Ying-xuan |
author_facet | Huo, Shu-fen Shang, Wen-li Yu, Min Ren, Xiao-ping Wen, Hong-xia Chai, Chun-yan Sun, Li Hui, Ke Liu, Ling-hua Wei, Sheng-hong Wang, Xiao-xiao Wang, Yi Tian, Ying-xuan |
author_sort | Huo, Shu-fen |
collection | PubMed |
description | Six-transmembrane epithelial antigen of prostate-1 (STEAP1) is a relatively newly identified gene target from prostate cancer, breast cancer, and gastric cancer. However, functions of STEAP1 in lung adenocarcinoma (LUAD) are still unknown. In the present study, we explored the molecular and cellular mechanisms of STEAP1 in LUAD. Western blot and Q-PCR were conducted to detect the protein and mRNA expressions respectively. The cell proliferation was tested by CCK8 assay. The effects of STEAP1 on the metastasis and epithelial–mesenchymal transition (EMT) of LUAD were evaluated by EdU assay, wound healing assay, and transwell migratory assay. H1650, H358, HCC827, H1299, H23, A549, H1693 were selected as human LUAD cell lines in the study. Results have shown that STEAP1 expression was up-regulated in LUAD cells compared with normal lung epithelial cells. Knockdowning of STEAP1 suppressed the proliferation, migration, and invasion of LUAD epithelial cells. Importantly, after comparing the proliferation, migration, and invasion of LUAD to the corresponding control groups treated in STAT3 inhibitor ADZ1480, we found that STEAP1 regulates EMT via Janus kinase 2/signal transducer and activator of transcription 3 (JAK2/STAT3) signaling pathway. In conclusion, STEAP1 can serve as a therapeutic target, and it may have important clinical implications for LUAD treatment. |
format | Online Article Text |
id | pubmed-7300283 |
institution | National Center for Biotechnology Information |
language | English |
publishDate | 2020 |
publisher | Portland Press Ltd. |
record_format | MEDLINE/PubMed |
spelling | pubmed-73002832020-06-19 STEAP1 facilitates metastasis and epithelial–mesenchymal transition of lung adenocarcinoma via the JAK2/STAT3 signaling pathway Huo, Shu-fen Shang, Wen-li Yu, Min Ren, Xiao-ping Wen, Hong-xia Chai, Chun-yan Sun, Li Hui, Ke Liu, Ling-hua Wei, Sheng-hong Wang, Xiao-xiao Wang, Yi Tian, Ying-xuan Biosci Rep Cancer Six-transmembrane epithelial antigen of prostate-1 (STEAP1) is a relatively newly identified gene target from prostate cancer, breast cancer, and gastric cancer. However, functions of STEAP1 in lung adenocarcinoma (LUAD) are still unknown. In the present study, we explored the molecular and cellular mechanisms of STEAP1 in LUAD. Western blot and Q-PCR were conducted to detect the protein and mRNA expressions respectively. The cell proliferation was tested by CCK8 assay. The effects of STEAP1 on the metastasis and epithelial–mesenchymal transition (EMT) of LUAD were evaluated by EdU assay, wound healing assay, and transwell migratory assay. H1650, H358, HCC827, H1299, H23, A549, H1693 were selected as human LUAD cell lines in the study. Results have shown that STEAP1 expression was up-regulated in LUAD cells compared with normal lung epithelial cells. Knockdowning of STEAP1 suppressed the proliferation, migration, and invasion of LUAD epithelial cells. Importantly, after comparing the proliferation, migration, and invasion of LUAD to the corresponding control groups treated in STAT3 inhibitor ADZ1480, we found that STEAP1 regulates EMT via Janus kinase 2/signal transducer and activator of transcription 3 (JAK2/STAT3) signaling pathway. In conclusion, STEAP1 can serve as a therapeutic target, and it may have important clinical implications for LUAD treatment. Portland Press Ltd. 2020-06-17 /pmc/articles/PMC7300283/ /pubmed/32515474 http://dx.doi.org/10.1042/BSR20193169 Text en © 2020 The Author(s). https://creativecommons.org/licenses/by/4.0/ This is an open access article published by Portland Press Limited on behalf of the Biochemical Society and distributed under the Creative Commons Attribution License 4.0 (CC BY). |
spellingShingle | Cancer Huo, Shu-fen Shang, Wen-li Yu, Min Ren, Xiao-ping Wen, Hong-xia Chai, Chun-yan Sun, Li Hui, Ke Liu, Ling-hua Wei, Sheng-hong Wang, Xiao-xiao Wang, Yi Tian, Ying-xuan STEAP1 facilitates metastasis and epithelial–mesenchymal transition of lung adenocarcinoma via the JAK2/STAT3 signaling pathway |
title | STEAP1 facilitates metastasis and epithelial–mesenchymal transition of lung adenocarcinoma via the JAK2/STAT3 signaling pathway |
title_full | STEAP1 facilitates metastasis and epithelial–mesenchymal transition of lung adenocarcinoma via the JAK2/STAT3 signaling pathway |
title_fullStr | STEAP1 facilitates metastasis and epithelial–mesenchymal transition of lung adenocarcinoma via the JAK2/STAT3 signaling pathway |
title_full_unstemmed | STEAP1 facilitates metastasis and epithelial–mesenchymal transition of lung adenocarcinoma via the JAK2/STAT3 signaling pathway |
title_short | STEAP1 facilitates metastasis and epithelial–mesenchymal transition of lung adenocarcinoma via the JAK2/STAT3 signaling pathway |
title_sort | steap1 facilitates metastasis and epithelial–mesenchymal transition of lung adenocarcinoma via the jak2/stat3 signaling pathway |
topic | Cancer |
url | https://www.ncbi.nlm.nih.gov/pmc/articles/PMC7300283/ https://www.ncbi.nlm.nih.gov/pubmed/32515474 http://dx.doi.org/10.1042/BSR20193169 |
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