Glutathione S‑transferase ω 1 promotes the proliferation, migration and invasion, and inhibits the apoptosis of non‑small cell lung cancer cells, via the JAK/STAT3 signaling pathway
- Kai Wang
- Fu-Lian Zhang
- Wei Jia
Affiliations: Department of Respiratory and Critical Care Medicine, Tianjin Chest Hospital, Tianjin 300222, P.R. China, Integrated TCM and Western Medicine Department, Tianjin Medical University Chu Hsien‑I Memorial Hospital, Tianjin 300134, P.R. China
- Published online on: November 20, 2020 https://doi.org/10.3892/mmr.2020.11709
Copyright: © Wang
et al. This is an open access article distributed under the
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Glutathione S‑transferase ω 1 (GSTO1) expression levels have been discovered to be upregulated in various types of cancer. However, to the best of our knowledge, the role of GSTO1 in non‑small cell lung cancer (NSCLC) has not been investigated. The present study aimed to investigate the role of GSTO1 in NSCLC and to determine the potential molecular mechanism. GSTO1 expression levels in A549 cells were knocked down using short hairpin RNA and GSTO1 overexpression in H2122 cells was achieved using cDNA constructs. Reverse transcription‑quantitative PCR was used to analyze the mRNA expression levels of GSTO1. Cell proliferation was determined using a Cell Counting Kit‑8 assay, whereas cell migration and invasion were analyzed using Transwell assays. Flow cytometric analysis was performed to determine the levels of cell apoptosis. The expression levels of GSTO1, Bax, caspase 3, JAK and STAT3 were analyzed using western blotting. The results revealed that GSTO1 overexpression significantly promoted the proliferation, migration and invasion, and inhibited the apoptosis of H2122 cells, whereas the opposite trend was achieved in A549 cells with GSTO1 knockdown. GSTO1 overexpression also significantly increased the phosphorylation levels of JAK and STAT3, whereas the knockdown of GSTO1 promoted the opposite effects. In conclusion, the findings of the present study indicated that GSTO1 may serve as an oncogene in NSCLC. The results suggested that GSTO1 may have an important role in NSCLC by regulating the JAK/STAT3 signaling pathway. Therefore, inhibiting the expression levels of GSTO1 may represent a potential novel therapeutic strategy for NSCLC.