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Abstract. The WW domain-containing oxidoreductase (WWOX) gene which encompasses the common human fragile site FRA16D has been proposed as a putative tumor suppressor gene, and loss of WWOX expression has been found in several types of solid cancer. As the role of WWOX in human leukemia has not yet been fully elucidated, the present study examined the expression of WWOX in patients with different types of leukemia as well as in leukemia-derived cell lines. Based on the data, WWOX mRNA (WWOX) and protein (Wwox) were significantly reduced or absent in the leukemia patients as well as in the cell lines. In addition, a recombinant expression vector, pGC-FU-WWOX, was constructed and transfected WWOX cDNA into Jurkat cells (acute T-lymphoblastic leukemia) and K562 cells (chronic myeloid leukemia in erythroid crisis) which all lack endogenous Wwox. In vitro experiments indicated that restoration of Wwox in Jurkat and K562 cells significantly suppressed proliferation and colony formation. Of note, apoptosis was also induced by Wwox restoration. Furthermore, we traced the mechanisms underlying this process and found that Wwox restoration could trigger the mitochondrial pathway in leukemia. Our data provide evidence that WWOX exerts a role as a tumor suppressor gene in leukemia, possibly by inhibiting proliferation and promoting apoptosis via the mitochondrial pathway.

The cancer/testis antigen (CTA) lactate dehydrogenase C (LDHC) is a unique LDH isoenzyme associated with glucose and adenosine triphosphate production in mammalian germ cells. However, the role of LDHC in cancer has thus far largely remained elusive. The present study described the expression status of LDHC in human MDA‑MB‑231 breast cancer cells as well as its role in tumor invasion and migration. Immunohistochemical analysis revealed endogenous LDHC expression in the cytoplasm and nuclei of MDA‑MB‑231 cells yielded. In addition, in vitro cell invasion and migration assays revealed that when LDHC expression was blocked by its specific inhibitor, cell invasion and migration were compromised in MDA‑MB‑231 cells. Of note, inhibition of LDHC was unable to induce apoptosis in MDA‑MB‑231 cells. The present study provided evidence that the LDHC enzyme acts as a CTA in breast carcinoma and exerts an essential role in tumor invasion and migration.

Abstract. The methylation status of septin-9 gene in plasma has been developed as a promising biomarker to aid in the diagnosis of colorectal cancer (CRC). In this study, we aimed to evaluate the overall diagnostic ability of septin-9 methylation for detection of CRC. Studies on the diagnostic performance of plasma septin-9 in CRC were searched from the online databases up to January 31st, 2017. Risk of bias among the studies was estimated according to the Quality Assessment of Studies of Diagnostic Accuracy included in the Systematic Reviews (QUADAS) II checklist. The aggregation of the effect sizes was enabled by utilizing a bivariate analysis model. A meta-regression test and influence analysis were conducted to determine the underlying sources of heterogeneity. According to the predefined criteria, 1,462 patients with CRC from 14 eligible trials were included. The quantitative meta-analyses showed that methylated septin-9 in plasma sustained a pooled sensitivity of 0.67 (95% CI, 0.61-0.73) and specificity of 0.89 (95% CI, 0.86-0.92) in discriminating CRC patients from cancer-free individuals, along with an area under the curve of 0.87. Moreover, the stratified analyses grouped by ethnicity demonstrated that methylayted septin-9 testing achieved a better sensitivity of 0.72 (95% CI, 0.68-0.76) in the European-based population group and a higher specificity of 0.90 (95% CI, 0.88-0.92) in the Asian-based population group. Plasmic methylated septin-9 suggests a promising diagnostic efficacy in confirming CRC. However, more studies are required to confirm our findings.