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STEAP1 facilitates metastasis and epithelial–mesenchymal transition of lung adenocarcinoma via the JAK2/STAT3 signaling pathway
Author(s) -
Shufen Huo,
Wenli Shang,
Min Yu,
Xiaoping Ren,
Hongxia Wen,
Chunyan Chai,
Li Sun,
Ke Hui,
Ling-Hua Liu,
Shenghong Wei,
Xiaoxiao Wang,
Yi Wang,
Yingxuan Tian
Publication year - 2020
Publication title -
bioscience reports
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 0.938
H-Index - 77
eISSN - 1573-4935
pISSN - 0144-8463
DOI - 10.1042/bsr20193169
Subject(s) - epithelial–mesenchymal transition , metastasis , cancer research , adenocarcinoma , lung , signal transduction , stat3 , transition (genetics) , biology , chemistry , microbiology and biotechnology , medicine , cancer , gene , biochemistry , genetics
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.

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