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Background: The matrix metalloproteinases (MMPs) are a family of highly conserved, metal-dependent proteolytic enzymes that play an important role in tumor invasion and metastasis. Many studies have been carried out on the association between polymorphisms in the MMP1, MMP2, MMP3, MMP7, and MMP9 genes and urinary cancer risk. However, the data from these published studies are conflicting and have low statistical power. Methods: In this study, we performed a meta-analysis of 12 different publications from the PubMed and WanFang databases, published up to May 2015, to better assess the purported associations. Odds ratios (OR) and 95% confidence intervals (CI) were determined to reveal association strengths. Results: Some significant associations were found. For the MMP1 -1607 1G/2G polymorphism, a negative association was identified for the 2G allele in bladder cancer (2G2G+2G1G vs. 1G1G: OR = 0.57, 95% CI = 0.36–0.93, pheterogeneity = 0.001) and renal cell carcinoma (2G1G vs. 1G1G: OR = 0.57, 95% CI = 0.39–0.82, pheterogeneity = 0.567). For the MMP2 -1306 C/T polymorphism, there was a negative association with the T allele for bladder cancer in the Asian population (TT+TC vs. CC: OR = 0.41, 95% CI = 0.18–0.94, pheterogeneity = 0.195). For the MMP7 -181 A/G polymorphism, a decreased bladder cancer risk was found (G-allele vs. A-allele: OR = 0.81, 95% CI = 0.66–0.98, pheterogeneity = 0.325). Conclusion: In summary, our study showed evidence that genetic polymorphisms in MMP1 for all populations, but only in the Asian population for MMP2 and MMP7, may protect against bladder cancer risk. Future studies with larger sample sizes are warranted to further evaluate these associations in more detail.

Aims Delineates the role of TIS111D in bladder cancer. Materials and methods The expression of TIS111D in bladder cancer and adjacent tissues was assessed by immunohistochemistry, Western blot and real-time PCR. Western blot and real-time PCR were used to analyse the expression of TIS111D in HT1197, T24, 5637 and TCCSUP cells. After TIS111D was silenced in T24, 5637 and TCCSUP cells, MTT and Transwell assays were used to detect the effects of TIS111D on proliferation and migration. Western blot and real-time PCR were used to detect the regulatory effect of downregulation of TIS111D on N-cad and E-cad. In vivo experiments confirmed the role of TIS111D in the growth and migration of bladder cancer and determined whether the role of TIS111D in bladder cancer is related to its regulation of N-cad and E-cad. Key findings The expression of TIS11D was higher in tumour tissues and bladder cancer cells. Si-TIS111D could inhibit the growth and migration of bladder cancer cells, while TIS111D could regulate the expression of E-cad and N-cad to regulate epithelial-mesenchymal transition (EMT). We also demonstrated that TIS111D could promote the growth and migration of bladder cancer in vivo by regulating EMT. Significance TIS111D may participate in the regulation of bladder cancer progression by regulating EMT.

Paraquat is one of the most widely used herbicides worldwide. In green plants, paraquat targets the chloroplast by transferring electrons from photosystem I to molecular oxygen to generate toxic reactive oxygen species, which efficiently induce membrane damage and cell death. A number of paraquat-resistant biotypes of weeds and Arabidopsis (Arabidopsis thaliana) mutants have been identified. The herbicide resistance in Arabidopsis is partly attributed to a reduced uptake of paraquat through plasma membrane-localized transporters. However, the biochemical mechanism of paraquat resistance remains poorly understood. Here, we report the identification and characterization of an Arabidopsis paraquat resistant1 (par1) mutant that shows strong resistance to the herbicide without detectable developmental abnormalities. PAR1 encodes a putative l-type amino acid transporter protein localized to the Golgi apparatus. Compared with the wild-type plants, the par1 mutant plants show similar efficiency of paraquat uptake, suggesting that PAR1 is not directly responsible for the intercellular uptake of paraquat. However, the par1 mutation caused a reduction in the accumulation of paraquat in the chloroplast, suggesting that PAR1 is involved in the intracellular transport of paraquat into the chloroplast. We identified a PAR1-like gene, OsPAR1, in rice (Oryza sativa). Whereas the overexpression of OsPAR1 resulted in hypersensitivity to paraquat, the knockdown of its expression using RNA interference conferred paraquat resistance on the transgenic rice plants. These findings reveal a unique mechanism by which paraquat is actively transported into the chloroplast and also provide a practical approach for genetic manipulations of paraquat resistance in crops.