Long non-coding RNA FAM201A promotes lung squamous cell carcinoma progression through interaction with miR-101.

Objective This study aimed to investigate the mechanism of LncRNA FAM201A mediating lung squamous cell carcinoma progression through interaction with miR-101. Patients and methods NCI-H520 cells and SK-MES-1 cells were transfected with miRNA-101-mimics and miRNA-101-inhibitor, the quantitative Real Time-Polymerase Chain Reaction (qRT-PCR) was used to detect FAM201A and miR-101 expression. CCK-8, Wound healing assay and transwell assay were utilized to detect the influence of FAM201A on the malignancy of NCI-H520NCI-H520 and SK-MES-1SK-MES-1 cells. Cell apoptosis was determined by flow cytometry. The underlying pathways of FAM201A were measured using Western blot. Xenograft tumor experiments were conducted to detect tumor growth and metastasis in vivo.NCI-H520SK-MES-1 Kaplan-Meier method calculated patient survival. Results (1) Silencing of FAM201A inhibited the proliferation, migration and invasion of NCI-H520 and SK-MES-1cells and stimulated cell apoptosis significantly. Furthermore, FAM201A elimination hindered tumor growth and metastasis in vivo. (2) Compared with the si-control group, the protein expression of Ki67, Vimentin, Cleaved-caspase-3 and N-cadherin were decreased in the si-FAM201A group. (3) After transfection of miR-101-mimics, the expression level of Vimentin protein was significantly increased, while the expression level of Vimentin protein was significantly decreased after miR-101-inhibitor transfection. (4) MiR-101 mimics could alleviate FAM201A silencing-induced inhibitive effects on cell proliferation, migration, invasion and promotive effects on cell apoptosis. Conclusions FAM201A could target miR-101 and upregulate Vimentin to inhibit lung cancer progression. FAM201A was expected to be a potential biomarker and therapeutic target for lung cancer.