Therapeutic Implications of PTEN in Non-Small Cell Lung Cancer

Abstract

Lung cancer remains one of the major human malignancies affecting both men and women worldwide, with non-small cell lung cancer (NSCLC) being the most prevalent type. Multiple mechanisms have been identified that favor tumor growth as well as impede the efficacy of therapeutic regimens in lung cancer patients. Among tumor suppressor genes that play critical roles in regulating cancer growth, the phosphatase and tensin homolog (PTEN) constitutes one of the important family members implicated in controlling various functional activities of tumor cells, including cell proliferation, apoptosis, angiogenesis, and metastasis. Notably, clinical studies have also documented that lung tumors having an impaired, mutated, or loss of PTEN are associated with low survival or high tumor recurrence rates. To that end, PTEN has been explored as a promising target for anti-cancer agents. Importantly, the ability of PTEN to crosstalk with several signaling pathways provides new approaches to devise effective treatment options for lung cancer treatment. The current review highlights the significance of PTEN and its implications in therapeutic approaches against NSCLC.

Plk3 Enhances Cisplatin Sensitivity of Nonsmall-Cell Lung Cancer Cells through Inhibition of the PI3K/AKT Pathway via Stabilizing PTEN

“…Previous in vitro and in vivo studies showed that impaired, mutated, or loss of PTEN is associated with high tumor recurrence, low survival rates, or chemoresistance in lung cancers. , Recent studies have found that Plk3 has the capacity to phosphorylate and stabilize PTEN phosphatase. Xu et al reported that Plk3 null murine embryonic fibroblasts contain a reduced expression level of PTEN.…”

Dichotomous Effects of Glypican-4 on Cancer Progression and Its Crosstalk with Oncogenes

“…Additionally, we observed enrichment in genes that take part in the signaling pathway of phosphatase and tensin homologue (PTEN), known to suppress tumor growth and metastasis via inhibition of PI3K/Akt/mTOR [37]. Notably, aberrant PTEN signaling has been implicated as one of the key mechanisms in both lung cancer, lung metastasis, and in glioblastoma [37,38]. Other enriched terms include signaling pathways in embryonic and brain development, whose deregulation is often implicated in cancer development [39].…”