LncRNA BCAR4 promotes proliferation, invasion and metastasis of non-small cell lung cancer cells by affecting epithelial-mesenchymal transition

N. Li, W.-J. Gao, N.-S. Liu

Department of Pathology, Nanjing Medical University, Nanjing, Jiangsu, China. xiashi474959@163.com

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• Oncology

OBJECTIVE: Long non-coding RNAs (lncRNAs) play an important role in various cellular biological processes. It is also involved in the occurrence and development of the tumor. BCAR4 is reported to be highly expressed in breast cancer and promotes cell proliferation. However, the biological effects of BCAR4 in non-small cell lung cancer (NSCLC) remains unclear.

PATIENTS AND METHODS: qRT-PCR was performed for detecting BCAR4 expression in 76 pairs of NSCLC tissues and corresponding cancer-adjacent tissues and 6 NSCLC cell lines. BCAR4 expression was knocked down, and its effects on NSCLC cell proliferation, cycle, apoptosis, invasion and metastasis were studied via MTT, clone formation, flow cytometry, TUNEL and Transwell assay. Metastatic tumor model of nude mice was established to investigate its effects on NSCLC cell metastasis. BCAR4 downstream target gene protein expression was detected using Western blotting and immunofluorescence assay.

RESULTS: BCAR4 was higher in NSCLC tissues than that in cancer-adjacent tissues and was positively correlated with tumor size, clinical stage, and distant metastasis, suggesting that BCAR4 can be used as an independent predictor of prognosis. Results also showed that BCAR4 knockdown could inhibit tumor cell invasion, metastasis, and proliferation, induce cell cycle arrest and increase cell apoptosis. BCAR4 knockdown inhibits the metastasis and invasion of tumor cells via regulating Vimentin, N-cadherin and E-cadherin in Epithelial-Mesenchymal Transition (EMT).

CONCLUSIONS: BCAR4 promotes the invasion and metastasis of NSCLC via regulating EMT and BCAR4/EMT interaction can be used as a new target for the diagnosis and therapeutics of NSCLC.

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