LncRNA BX357664 inhibits the proliferation and invasion of non-small cell lung cancer cells.

OBJECTIVE

To explore the level of long non-coding RNA (lncRNA) BX357664 in non-small cell lung cancer (NSCLC) and its role in the development of NSCLC. Meanwhile, the potential regulatory mechanism of BX357664 was also what we were interested in.

PATIENTS AND METHODS

Real-time quantitative polymerase chain reaction (RT-qPCR) was performed to examine the level of BX357664 in 82 pairs of cancer tissues and adjacent normal tissues collected from patients with NSCLC, and the relationship between BX357664 level and pathological parameters or prognosis of NSCLC patients was analyzed. Further verification by RT-qPCR was to examine BX357664 expression in NSCLC cell lines, and BX357664 overexpression model was constructed using lentivirus in NSCLC cell lines including SPCA1 and H1299. In addition, cell counting kit-8 (CCK-8), cell clone formation assay, and transwell assay were performed to analyze the influence of BX357664 on the biological function of NSCLC cells. Western Blot was conducted to explore its underlying mechanisms.

RESULTS

RT-qPCR results indicated that BX357664 in NSCLC was remarkably lower than that in normal tissues. Compared with patients with highly-expressed BX357664, patients with lowly-expressed had worse tumor stage, higher incidence of lymph node metastasis or distant metastasis and lower overall survival rate. In addition, compared with NC group, the proliferation, invasion and migration ability of cells in BX357664 overexpression group was attenuated significantly, and the key proteins in TGF-β1/Smad pathway including transforming growth factor-β1 (TGF-β1), p-Smad2, p-Smad3, N-cad, Vimentin and MMP-9 were also remarkably reduced.

CONCLUSIONS

BX357664 level was significantly reduced in tumor tissues of NSCLC patients, resulting in advanced tumor staging, lymph node metastasis, distant metastasis, and poor prognosis. Additionally, BX357664 may inhibit the proliferation as well as invasion and migration of NSCLC cells by regulating TGF-β1/Smad pathway.