PAQR3 inhibits proliferation via suppressing PI3K/AKT signaling pathway in non-small cell lung cancer
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Submission date: 2017-10-10
Final revision date: 2017-10-25
Acceptance date: 2017-10-29
Online publication date: 2017-12-13
Publication date: 2018-10-31
Arch Med Sci 2018;14(6):1289-1297
Lung cancer is the leading cause of cancer-related death worldwide and non-small cell lung cancer (NSCLC) accounts for approximately 85% of all lung cancer cases. PAQR (progestin and adipoQ receptor family) 3, a Golgi-anchored membrane protein, has been demonstrated to act as a tumor suppressor in multiple cancers. However, the expression and role of PAQR3 have never been explored in NSCLC. The purpose of this study was to investigate the expression and role of PAQR3 in NSCLC.

Material and methods:
Expression of PAQR3 at mRNA and protein levels was determined by qRT-PCR and western blot, respectively. Cell proliferation was analyzed by MTT assay. Apoptosis and cell cycle distribution were evaluated by flow cytometry.

The expression of PAQR3 was downregulated in NSCLC tissue samples and cell lines at both mRNA and protein levels (p < 0.05). Overexpression of PAQR3 significantly inhibited cell proliferation, induced apoptosis and promoted cell cycle arrest at G0/G1 phase in NSCLC cell lines (p < 0.05). In contrast, knockdown of PAQR3 showed a reverse effect on NSCLC cells (p < 0.05). Moreover, PAQR3 may exert its tumor suppressive roles via suppressing the PI3K/AKT signaling pathway in NSCLC.

Our findings suggest that PAQR3 is a tumor suppressor in the development of NSCLC and may serve as a novel therapeutic target in the treatment of patients with NSCLC.

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