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Serine/threonine kinase 33 (STK33) is a novel protein that has been the focus of an increasing number of studies in recent years; however, the role of STK33 in tumorigenesis remains controversial. Previous studies have demonstrated that STK33 is overexpressed in several human cancers and exerts a pro-tumorigenic effect through the promotion of cell proliferation. However, the role of STK33 in colorectal cancer (CRC), which is one of the most aggressive human malignancies, remains unclear. The aim of the current study was to investigate the methylation status of STK33 in CRC and to determine its clinical significance. The results demonstrated that STK33 was hypermethylated in CRC cell lines and promoted the proliferation of CRC cells. In addition, the methylation status and expression of STK33 in 94 pairs of cancer and noncancerous tissues obtained from patients with CRC was investigated. STK33 methylation was significantly increased in cancer tissues when compared with adjacent noncancerous tissues (P<0.001). STK33 methylation was associated with lymph node metastasis (P<0.05), tumor invasion (P<0.05), distant metastases (P<0.01) and tumor stage (P<0.01). Reduced STK33 mRNA and protein expression in CRC was associated with STK33 hypermethylation (P<0.001). In addition, patients with hypermethylated STK33 exhibited shorter overall survival rates when compared with those with unmethylated STK33 (P<0.01). In conclusion, the results of the current study suggest that STK33 hypermethylation may be a promising novel biomarker for the diagnosis, prognosis and suitable treatment of CRC.

Background: Rectal cancer (RC) has been documented to be a highly invasive malignant neoplasm worldwide. Macrophage migration inhibitory factor (MIF) is a multifunctional cytokine involved in cell-mediated immunity, immunoregulation, inflammation. In vitro and in vivo studies have identified that MIF was involved in the carcinogenesis and progression of RC. Patients and Methods: This case-control study evaluated associations of genetic variants of the MIF gene and serum level of MIF with susceptibility of RC. Results: We found MIF level was associated with an increased risk of RC (OR for per unit: 1.38, 95% CI:1.32-1.44; P < 0.001). Both MIF rs2012133 (OR = 1.30; 95% CIs = 1.08-1.58; P = 0.007) and rs755622 (OR = 1.45; 95% CIs = 1.15-1.82; P = 0.002) were significantly associated with increased risk of RC. Besides, we also found MIF rs5844572 was significantly associated with increased susceptibility of RC, with OR for per CATT repeat of 1.28 (95% CIs: 1.16-1.41; P < 0.001). Further, we found all three variants of the MIF gene, rs5844572, rs2012133 and rs755622, could increase serum level of MIF. Conclusion: This study suggests that MIF plays an important role in the carcinogenesis of RC and could be used as a biomarker for early detection and prediction of RC.

This study explored miR-20a’s role in intestinal cancer cells. SW480 cell line was divided into control group, agonist group, inhibitor group, and negative control group, followed by analysis of cell proliferation, apoptosis, Met, Bad, and Bcl-2 protein expressions. Results showed that miR-20a expression in the agonist group was the highest, followed by blank group and negative control group, and inhibitor group was lowest. S-phase and G2/M cell number from inhibitor group was lowest, and cell apoptosis rate was highest. However, the agonist group showed contrary changes. There was no difference in G0/G1 phase cell number among the four groups (P > 0.05). Moreover, the expressions of Bad, Bcl-2, Met, Wnt, β-catenin, and p-Wnt in inhibitor group were all lower, while the expressions in agonist group were all high (P < 0.05). S-phase and G2/M cell number in inhibitor group was lowest, while cell apoptosis was highest. The agonist group was opposite, with G0/G1 phase cells in each group showing no difference (P > 0.05). Wnt, β-catenin, and p-Wnt expressions were lowest in the inhibitor group, while the agonist group was opposite. These results together showed that the miR-20a directly targeted and regulated Met protein. Finally, the miR-20a inhibited intestinal cancer cell proliferation mainly through inhibiting Wnt/β-catenin signaling activity.