These data suggest that miR-592 may promote the progression and metastasis, in part, by targeting FoxO3A in CRC. miR-592 may be a novel target for CRC treatment and antagomir-592 may inhibit the proliferation and metastasis of CRC cells.

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Colorectal cancer (CRC) is one of the most common cancers worldwide. The development of resistance to anti-cancer treatment is one of the major challenges in the treatment of CRC, which limits the efficacy of both conventional and targeted therapies in clinical settings. Understanding the mechanisms underpinning resistances is therefore critical in developing novel agents to reverse drug resistance and for more specific targeted treatments. Accumulating studies have reported that microRNAs (miRNAs) are key players in the regulation of cancer cells with intrinsic/acquired drug resistance through varied mechanisms that endow cells with a drug-resistant phenotype. miRNAs have been evolved in the regulation of chemoresistance to various CRC treatments and the stemness of CRC stem cells (CRSCs), sequentially modulating the sensitivity of CRC cells to anti-cancer treatments. Targeting miRNAs may be a novel strategy for eradicating CRSCs, re-sensitizing drug-resistant cells to anti-cancer agents, improving drug efficiency and developing novel biological agents for CRC treatment. This paper highlights the role of miRNAs in the regulation of chemoresistance and CRSCs in CRC, with focus on the mechanisms underlying how miRNAs alter CRSCs fate, and the process of epithelial-to-mesenchymal transition, cell cycle and apoptosis in CRC cells.

Background. Growing studies have demonstrated that long noncoding RNAs (lncRNAs) play important roles in tumor progression. In this study, we aimed to explore the potential roles of lncRNA LINC00958 (LINC00958) and its biological functions in epithelial ovarian cancer (EOC). Methods. The expression of LINC00958 in 11 cases of EOC and adjacent nontumor specimens and five cell lines was detected by qRT-PCR. CCK-8, colony formation, and flow cytometry assays were conducted to study the cell viabilities of EOC cells. Wound scratch and transwell analyses were carried out for the examination of cell invasion and migration of EOC cells. The targeting associations between LINC00958 and STAT1 were demonstrated by ChIP analyses combined with luciferase reporter assays. The related proteins of Wnt/β-catenin signaling were determined using RT-PCR. Results. Higher levels of LINC00958 were observed in EOC tissues and cell lines. Our data also revealed that high LINC00958 expression was partly induced by STAT1. Functionally, knockdown of LINC00958 suppressed the proliferation, migration, and invasion of EOC cells. Mechanistic investigation showed that the inhibitory effect of LINC00958 knockdown on EOC cells was mediated by the Wnt/β-catenin signaling. Conclusion. Our findings suggested that STAT1-induced overexpression of LINC00958 promoted EOC progression by modulating Wnt/β-catenin signaling.