<p>miRNA-101-5p inhibits the growth and aggressiveness of NSCLC cells through targeting CXCL6</p>

Abstract

BackgroundThe purpose of this study is to explore the potential biological roles of miR-101-5p in the progression of non-small-cell lung carcinoma (NSCLC).MethodsThe levels of miR-101-5p and chemokine (C-X-C motif) ligand 6 (CXCL6) in NSCLC tissues and cells were detected using the quantitative real-time PCR (qRT-PCR) assay. Proliferation, colony formation, migration and invasion assays were conducted using miR-101-5p-transfected NSCLC cells in vitro. The expression of CXCL6 was measured using immunofluorescence assay. Xenograft model and lung metastasis model were constructed to further reveal the precise roles of miR-101-5p in the lung metastasis and growth of NSCLC cells in vivo.ResultsmiR-101-5p was underregulated in NSCLC tissues when compared with that in the normal controls. The levels of miR-101-5p were lower in NSCLC cells (H1975, A549, HCC827 and H1650) than in non-tumorigenic human bronchial epithelial cells (BEAS-2B). Overregulation of miR-101-5p restrained the aggressiveness phenotypes of NSCLC cells in vitro. Furthermore, overregulation of miR-101-5p reduced the tumor growth and pulmonary metastasis of NSCLC cells in vivo. CXCL6 was the target gene of miR-101-5p in NSCLC. The mRNA levels of CXCL6 were negatively associated with the levels of miR-101-5p in NSCLC tissues. Finally, the rescue experiments suggested that the inhibitory role of miR-101-5p was mediated by regulating the expression of CXCL6 in NSCLC.ConclusionThese findings indicated that overregulation of miR-101-5p restrained the progression of NSCLC cells by targeting CXCL6 and might function as a potential therapeutic target for NSCLC.

Circular RNA hsa_circ_0007364 increases cervical cancer progression through activating methionine adenosyltransferase II alpha (MAT2A) expression by restraining microRNA-101-5p

“…Interaction between hsa_circ_0007364 and miR-101-5p was confirmed using a dual-luciferase reporter and RIP assay. MiR-101-5p delays tumor growth in various cancers, including liver cancer, lung cancer and clear cell renal cell carcinoma [11][12][13]. In agreement with these reports, we showed that miR-101-5p expression is suppressed in CC tissues, and that miR-101-5p suppression abated the suppression of the proliferative and invasion ability of CC cells caused by hsa_-circ_0007364 silencing.…”

“…For example, Yamada et al [ 11 ] showed that miR‐101‐5p acted as an antitumor miRNA in clear cell renal cell carcinoma cells. Chen et al [ 12 ] revealed that miRNA-101-5p suppressed lung cancer cell growth and aggressiveness via targeting CXCL6. Furthermore, Shen et al [ 13 ] found that miRNA-101-5p reduced CC cells’ proliferation and invasion through suppressing CXCL6.…”

Replisome genes regulation by antitumor miR‐101‐5p in clear cell renal cell carcinoma

“…In a few reports, miR‐101‐5p expression was found to be downregulated. miR‐101‐5p was shown to inhibit cell aggressiveness through targeting of C‐X‐C motif chemokine ligand 6 ( CXCL6 ) in cervical cancer and nonsmall‐cell lung carcinoma . To our knowledge, the present study is the first report to show the antitumor functions of miR‐101‐5p in ccRCC.…”

RNA‐sequence‐based microRNA expression signature in breast cancer: tumor‐suppressive miR‐101‐5p regulates molecular pathogenesis

“…Compared with reports of miR-101-3p, few studies have reported the tumor-suppressive functions of miR-101-5p and its target molecules in cancer cells. More recently, downregulation of miR-101-5p was reported in non-small cell lung carcinoma tissues compared with that in normal tissues (Chen et al, 2019). Overexpression of miR-101-5p was shown to suppress the aggressive phenotypes of cancer cells (in vitro) and pulmonary metastasis (in vivo) by regulating CXCL6 (Chen et al, 2019).…”