Drug resistance limits the efficacy of chemotherapy in human cancers. Previous studies reported that long noncoding RNA colon cancer-associated transcript 1 (CCAT1) regulated progression of prostate cancer (PCa). However, the potential role of CCAT1 in the sensitivity of paclitaxel (PTX) in PCa and its mechanism remain largely unknown. The PTX-resistant PCa cells were established in PC3 and DU145 cells by increasing concentrations of PTX. The expressions of CCAT1, microRNA-24-3p (miR-24-3p) and fascin1 (FSCN1) were measured by quantitative real-time polymerase chain reaction. The viability and apoptosis were detected by 3-(4,5-dimethyl-2-thiazolyl)-2,5-diphenyl-2-H-tetrazolium bromide assay, flow cytometry and western blot, respectively. The interaction among CCAT1, miR-24-3p and FSCN1 was explored by luciferase activity, RNA immunoprecipitation, RNA pull-down and western blot, respectively. Results showed that the expressions of CCAT1 were up-regulated and miR-24-3p was down-regulated in PCa and PTX-resistant PCa cells (PC3-TXR and DU145-TXR). Knockdown of CCAT1 or overexpression of miR-24-3p inhibited survival rate, half maximal inhibitory concentration (IC50) of PTX but increased apoptosis in PC3-TXR and DU145-TXR cells after treatment of PTX. miR-24-3p was bound to CCAT1 and its abrogation reversed knockdown of CCAT1-mediated increase of PTX sensitivity in PC3-TXR and DU145-TXR cells. Moreover, FSCN1 restoration attenuated miR-24-3p-mediated inhibition of PTX resistance. Besides, FSCN1 level was enhanced in PCa and PTX-resistant PCa cells and regulated by CCAT1 and miR-24-3p. Our data suggested interference of CCAT1 contributed to PTX sensitivity in PCa by regulating miR-24-3p and FSCN1, indicating a novel avenue for treatment of PCa through regulating chemoresistance.

A polysaccharide from the traditional Chinese medicinal herb, Bletilla striata (Thunb.) Reichb. f., was isolated, purified and characterized. It induced the proliferation of human umbilical vascular endothelial cells and the expression of vascular endothelial growth factor up to 156% and 147% of control after 72 h, respectively.

The purpose of this study was to analyze the existing studies and to investigate the relationship between the risk of colorectal cancer (CRC) and intakes of four individual dietary elements calcium (Ca), iron (Fe), magnesium (Mg), and potassium (K). All relevant articles in both Chinese and English were searched and collected from PubMed, Web of Science, and Chinese National Knowledge Infrastructure databases up to December 17, 2017. There were 29 eligible literatures selected for further meta-analysis, including 14 cohort studies and 15 case-control studies. The meta-analysis of cohort studies indicated that the high intakes of dietary Ca and Mg were negatively associated with the risk of CRC, as the hazard ratios (HR) were 0.76 (95% confidence interval (CI) 0.72, 0.80) and 0.80 (95% CI 0.73, 0.87), respectively. Nevertheless, high intake of dietary heme Fe was positively correlated to the incidence of colon cancer (HR = 1.01, 95% CI 0.82, 1.19) and rectal cancer (HR = 1.04, 95% CI 0.67, 1.42). A meta-analysis of case-control studies indicated that high intakes of dietary Ca, Mg, and K were negatively related with the occurrence of CRC, because the odds ratios (OR) were 0.36 (95% CI 0.32, 0.40), 0.80 (95% CI 0.63, 0.98) and 0.97 (95% CI 0.74, 1.21), respectively. However, high Fe intake from diet was positively correlated with the rising increasing of CRC (OR = 1.04, 95% CI 0.91, 1.18). More research is needed to indicate the risk relationship between element intake and CRC.

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