LncRNA LINC01278 accelerates colorectal cancer progression via miR-134-5p/KDM2A axis.

OBJECTIVE: Long non-coding RNAs (lncRNAs) play vital roles in the pathogenesis and development of multiple cancers, including colorectal cancer (CRC). Nevertheless, the regulatory mechanisms of LINC01278 in CRC remain unknown. Our research aims to identify the regulatory mechanisms of LINC01278 in CRC. PATIENTS AND METHODS: The expression of LINC01278 was examined by quantitative real-time polymerase chain reaction (RT-qPCR). StarBase and TargetScan websites were used to predict the interaction between miR-134 and LINC01278 or KDM2A, which was further confirmed by Dual-Luciferase reporter assay and RNA immunoprecipitation (RIP) assay. Cell viability, migration, and invasion were detected by Cell Counting Kit-8 (CCK-8) and transwell assays. RESULTS: LINC01278 was upregulated in CRC tissues and cell lines, and knockdown of LINC01278 suppressed CRC cell progression. In addition, LINC01278 inhibited miR-134 expression by direct interaction, and the inhibition of miR-134 abolished the suppressive effects of LINC01278 knockdown on viability, migration, and invasion of CRC cells. Furthermore, KDM2A was confirmed to be a target gene of miR-134. Overexpression of KDM2A facilitated the tumorigenesis of CRC, while this effect was reversed by the upregulation of miR-143. Finally, it was demonstrated that miR-134 inhibitor reversed the shLINC01278­mediated inhibitory effect on KDM2A expression. CONCLUSIONS: Our study demonstrated that LINC01278 upregulated KDM2A to promote CRC progression by interacting with miR-143, suggesting that LINC01278 might be a new therapeutic target of CRC.

Long noncoding RNA TPTE2P1 promotes the migration and invasion of hepatocellular carcinoma.

OBJECTIVE: Hepatocellular carcinoma (HCC) is a common malignant tumor that poses a serious threat to human health and life. Metastasis is one of the reasons for high rate of relapse. Due to the lack of effective treatment, the prognosis of HCC patients is far from satisfactory. The aim of this study was to investigate the role of long non-coding RNA (lncRNA)-TPTE2P1 in HCC development. Moreover, we aimed to search for new biomarkers which could predict the metastasis and provide novel therapeutic strategies for HCC. PATIENTS AND METHODS: Quantitative real-time polymerase chain reaction (qRT-PCR) was used to evaluate the expression level of lncRNA-TPTE2P1 in both HCC tissues and cell lines. Wound-healing assay and transwell assay were applied to determine the ability of cell migration. Meanwhile, transwell matrigel assay was applied to detect the invasion of HCC cells. The protein expressions of E-cadherin, Vimentin and N-cadherin in chosen cell lines were detected by Western blotting. RESULTS: Results found that lncRNA-TPTE2P1 was overexpressed in both HCC tissues and cell lines. Further analysis revealed that overexpression of lncRNA-TPTE2P1 was correlated with tumor size, distant metastasis, differentiation degree, as well as tumor node metastasis (TNM) stage of HCC patients. Subsequent wound-healing assay, transwell assay and Matrigel assay confirmed that down-regulated lncRNA-TPTE2P1 could significantly suppress the invasion and migration of cells. However, up-regulation of lncRNA-TPTE2P1 showed the opposite results. Moreover, lowly expressed lncRNA-TPTE2P1 significantly decreased the protein levels of E-cadherin, Vimentin and N-cadherin. These results indicated that lncRNA-TPTE2P1 might stimulate the migration and invasion of HCC cells by promoting epithelial-mesenchymal transition (EMT). CONCLUSIONS: In summary, our results suggested that lncRNA-TPTE2P1 functioned as an oncogene in HCC. Meanwhile, lncRNA-TPTE2P1 stimulated HCC cell migration and invasion by promoting EMT. LncRNA-TPTE2P1 might play a vital role in the development and progression of HCC. Our findings demonstrated that lncRNA-TPTE2P1 could serve as an early biomarker of metastasis and therapeutic target for HCC.