PTEN inhibits non‑small cell lung cancer cell growth by promoting G0/G1 arrest and cell apoptosis

Abstract

Non-small cell lung cancer (NSCLC) is a major type of human lung cancer and the primary cause of cancer-associated cases of mortality worldwide. Phosphatase and tensin homolog (PTEN) is a potent tumor suppressor gene in various human cancer types. The aim of the current study was to explore the role of PTEN and its associated regulatory mechanisms in NSCLC. Firstly, the expression of PTEN was detected using western blotting in a variety of NSCLC cell lines. The results revealed that compared with normal control cells, PTEN levels were significantly decreased in NSCLC cell lines (P<0.01). Short hairpin (sh)RNAs specific to PTEN were also used to knockdown endogenous PTEN in NSCLC cells. The results indicated that cell viability was significantly increased in PTEN-knockdown cells compared with those transfected with negative control shRNA (P<0.01). Conversely, overexpression of PTEN in A549 and SK-MES-1 cells significantly decreased the optical density of NSCLC cells (P<0.01). Flow cytometry was used to investigate the cell cycle; the results revealed that PTEN knockdown significantly increased the percentage of cells at G 0 /G 1 phase (P<0.01) and decreased the number of cells at S phase (P<0.01). The molecular mechanism was further explored using western blotting and the results demonstrated that PTEN overexpression increased the levels of cleaved caspase-3 (P<0.01). These results suggest that PTEN may be a potential target gene for gene therapy in patients with NSCLCs.

lncRNA F11-AS1 Suppresses Glioma by Regulation miRNA-3146/PTEN

“…PTEN is intervened by gene or small-molecule inhibitor. Some good laboratory results on the inhibition of the proliferation of tumor cells by P13K/AKT pathway have been obtained [18][19][20][21][22][23]. The results of this study proved that the overexpression of F11-AS1 causes the decrease of the expression of miRNA-3146, so as to inhibit the PI3K/AKT signaling pathway after the activation of PTEN and inhibit the bioactivity of glioma cells.…”

LncRNA SOX2‐OT regulates AKT/ERK and SOX2/GLI‐1 expression, hinders therapy, and worsens clinical prognosis in malignant lung diseases

“…Therefore, our results support the hypothesis that LncRNAs are functional participants in therapy resistance/sensitivity to cancer drugs, and target‐gene therapies ‘EGFR/AKT/ERK/mTOR’ [47]. It has been previously reported that SOX2‐OT participates in the activation of the AKT‐member of cellular signaling pathways in cholangiocarcinoma [14], as well as being involved in the magnitude of resistance mechanism to EGFR‐TKIs‐based treatment related to the functionality of phosphatase PTEN, reducing AKT phosphorylation in NSCLC [54]. In this sense, PTEN has been previously considered as a tumor suppressor gene, associated with cisplatin resistance mechanisms in gastric cancer [55].…”

Molecular Mechanisms of Chemoresistance Induced by Cisplatin in NSCLC Cancer Therapy

“…MiRNA-15b targeting PEBP4 induces cisplatin resistance and is linked to overall poor prognosis [80]. One of the most important tumour suppressors in lung cancer is phosphatase and tensin homolog deleted in chromosome 10 (PTEN), which inhibits NSCLC cell growth by promoting G0/G1 arrest and cell apoptosis [81,82]. In many types of cancer (including NSCLC) aggressive phenotype correlates with downregulation of PTEN [83,84].…”