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Long non-coding RNA BX357664 inhibits cell proliferation and metastasis in human lung cancer.

ABSTRACT: Long non-coding RNAs (lncRNAs) have been investigated in human carcinogenesis. The lncRNA BX357664 has emerged as a novel lncRNA that was initially recognized by a microarray analysis. The present study aimed to identify the expression and functional roles of lncRNA BX357664 in lung cancer. The transcription level of BX357664 was initially revealed to be downregulated in clinical lung cancer tissues and in a series of lung cancer cell lines. Clinical data demonstrated that the high expression of BX357664 was associated with tumor size, distant metastasis and Tumor-Node-Metastasis stage. Following the overexpression of BX357664 in A549 and 95D cells, the potential of cells to form colonies, as well as the proliferation and motility abilities, were revealed to be decreased. Furthermore, the cell cycle was arrested in the G0/G1 phase by BX357664 modulation. Transwell analysis and a wound-healing assay also demonstrated that overexpression of BX357664 in A549 and 95D cells significantly inhibited cell migration and invasion. These data suggested that BX357664 inhibits cell proliferation and metastasis in lung cancer. The results of the present study provided evidence that BX357664 is a novel lncRNA that may aid in the diagnosis and treatment of lung cancer.

SUBMITTER: Xiao SH

PROVIDER: S-EPMC6365958 | biostudies-literature |

REPOSITORIES: biostudies-literature

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Project description:Long non-coding RNA (lncRNA) ADAM metallopeptidase with thrombospondin type 1 motif 9 antisense RNA 2 (ADAMTS9-AS2) is involved in various types of cancer, such as ovarian cancer, lung cancer and clear cell renal cell carcinoma. However, the roles of ADAMTS9-AS2 in liver cancer are not completely understood. The present study aimed to determine the functional role of ADAMTS9-AS2 in human liver cancer and investigate the potential underlying molecular mechanisms. The expression levels of ADAMTS9-AS2 and ADAMTS9 were determined following ADAMTS9-AS2 overexpression and knockdown. The results indicated that ADAMTS9-AS2 overexpression and knockdown increased and decreased ADAMTS9 mRNA and protein expression levels, respectively, indicating that alterations in ADAMTS9 expression corresponded with ADAMTS9-AS2 expression. Subsequently, the effects of ADAMTS9-AS2 on liver cancer cell proliferation, migration and invasion were analyzed by performing Cell Counting Kit-8, wound healing and Transwell assays, respectively. The results demonstrated that ADAMTS9-AS2 inhibited liver cancer cell proliferation, migration and invasion. Finally, the effect of ADAMTS9 on PI3K/AKT/mTOR signaling pathway-associated proteins [AKT, phosphorylated-AKT, phosphatidylinositol-4, 5-bisphosphate 3-kinase catalytic subunit β (PIK3CB), mTOR and phosphorylated-mTOR], several key autophagy-related proteins [light chain 3-I/II (LC3-I/II), beclin 1 (BECN1) and sequestosome 1 (SQSTM1)] and apoptosis-related proteins (Bax and Bcl-2) was detected via western blotting. The results suggested that ADAMTS9-AS2 downregulated the phosphorylation of AKT and mTOR, the protein expression level of PIK3CB, as well as the expression levels of autophagy protein SQSTM1 and antiapoptotic protein Bcl-2. By contrast, ADAMTS9-AS2 upregulated the expression levels of autophagy proteins LC3-II and BECN1, and the proapoptotic protein Bax. Collectively, ADAMTS9-AS2 inhibited liver cancer cell proliferation, migration and invasion via inhibiting the PI3K/AKT/mTOR signaling pathway. The present study provided a novel insight into the role of ADAMTS9-AS2 in liver cancer.

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Long non-coding RNA BX357664 inhibits cell proliferation and metastasis in human lung cancer.

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