Gu Z, et al. - Researchers investigated if chloride channel-3 (CLC-3) has prognostic value for gastric cancer (GC) patients, as well as the molecular mechanisms by which CLC-3 is regulated in GC. They used immunohistochemistry to analyze the expression of CLC-3 and X-ray repair cross-complementing 5 (XRCC5) in human specimens. According to findings, XRCC5 regulated the overexpression of CLC-3. Data also suggested that CLC-3 is a poor prognostic biomarker for gastric cancer. A promising therapeutic potential for GC treatment could be offered by double targeting CLC-3 and XRCC5. In the mechanistic study, they found that the binding of XRCC5 to the CLC-3 promoter and subsequent promoter activity was suppressed by knockdown of XRCC5, therefore, regulating CLC-3 expression at the transcriptional level by interacting with poly (ADP-ribose) polymerase 1 (PARP1).