LncRNA BC200 regulates the cell proliferation and cisplatin resistance in non-small cell lung cancer via PI3K/AKT pathway

Abstract

Objective: Long non-coding RNA (lncRNA) exerts tissue specificity and regulates the occurrence and progression of tumors. Previous bioinformatics showed that lncRNA BC200 is served as an oncogene. However, the specific role of BC200 in lung cancer (LC) is rarely reported. The aim of this study is to elucidate the regulatory effects of BC200 on tumor development and cisplatin resistance in non-small cell lung cancer (NSCLC).

Patients and methods: The expression level of BC200 in 76 pairs of NSCLC tissues and adjacent normal tissues was detected by quantitative Real Time-Polymerase Chain Reaction (qRT-PCR). Correlation analyses were conducted to investigate the relation between BC200 expression and prognosis of NSCLC patients. Subsequently, BC200 expression in LC cell lines was detected. After construction of si-BC200 and si-NC, the cellular functions of LC cells were detected through colony formation, flow cytometry and transwell assay, respectively. Western blot was performed to detect the protein expressions of key genes in the PI3K/AKT pathway in LC cells. Finally, cell counting kit-8 (CCK-8) assay was carried out to explore the effect of BC200 on cisplatin resistance of LC cells via calculating IC50.

Results: Higher expression of BC200 was found in NSCLC tissues than that of adjacent normal tissues. BC200 expression was positively correlated with tumor stage, lymph node metastasis and distant metastasis of NSCLC patients, whereas not correlated to age and sex. Knockdown of BC200 inhibited proliferation, invasion and migration of LC cells. Western blot results showed that protein expressions of PI3K, AKT and STAT3 were downregulated after BC200 knockdown in LC cells. Additionally, the IC50 in H1299/DDP cells transfected with si-BC200 was lower than in those transfected with si-NC. The apoptotic rate in H1299 cells transfected with si-BC200 was remarkably lower than those transfected with si-NC.

Conclusions: BC200 is highly expressed in NSCLC, which is positively correlated with tumor stage and metastasis of NSCLC patients. BC200 promotes the malignant progression of NSCLC via regulating cisplatin-induced apoptosis of H1299/DDP cells.