A growing body of evidence indicates that long non-coding RNAs (lncRNAs) play crucial roles in the chemoresistance of human cancers. However, the molecular mechanisms underlying the functions of certain lncRNAs in the chemotherapeutic resistance of hepatocellular carcinoma (HCC) remain unclear. The aim of the present study was to investigate the function and potential mechanism of action of lncRNA LINC00173 in HCC cisplatin (DDP) resistance. Reverse transcription-quantitative PCR analysis indicated that LINC00173 was highly expressed in DDP-resistant HCC tissues and cell lines, and high expression levels of LINC00173 were found to be associated with poor prognosis in patients with HCC. Moreover, LINC00173-knockdown improved the DDP sensitivity of DDP-resistant HCC cells. A luciferase reporter assay also demonstrated that microRNA (miR)-641 was a direct target of LINC00173. miR-641 inhibition restored the promoting effect of LINC00173 knockdown on DDP sensitivity in HCC cells. Furthermore, RAB14 was identified as a target of miR-641, and RAB14 overexpression restrained the inducing effect of LINC00173 knockdown on HCC cell DDP sensitivity. The findings of the present study demonstrated that LINC00173 increased DDP resistance in HCC via the miR-641/RAB14 axis, which may represent a promising therapeutic strategy for HCC.

Mothers against decapentaplegic homolog 7 (SMAD7) rs12953717 polymorphism has been implicated to alter the risk of colorectal cancer (CRC), but the results are controversial. The objective of this study was to quantitatively evaluate the association between SMAD7 rs12953717 polymorphism and CRC susceptibility. A comprehensive search was conducted to identify all eligible studies of SMAD7 rs12953717 polymorphism and CRC risk. Pooled odds ratio and 95% confidence interval were calculated using a fixed or random effects model. Statistical analysis was performed with Review Manager 5.0 and Stata 11. A total of 11 case-control studies, including 12,058 cases and 11,444 controls, were identified. The combined results based on all studies suggested that rs12953717 was associated with CRC risk under all genetic models. When stratifying for race, the data showed that the rs12953717 was associated with a significantly increased CRC risk under all genetic models in Caucasians. Statistically significant association was found in all genetic models except in recessive model comparison in the subgroup of Asians. After stratifying the studies by study design, there was a significant association between rs12953717 polymorphism and CRC risk under all genetic models in the subgroup of population-based studies. Our study suggests that rs12953717 polymorphism is associated with an increased CRC risk.