Background and Objectives: Transient receptor potential melastatin 7 (TRPM7) is a unique channel protein, and functionally responsible for transportation of calcium and magnesium. Physiologically, the TRPM7 channel is involved in homeostasis of calcium and magnesium, and cell survival. TRPM7 expression is up-regulated in many cancers as malignant behaviors of cancer cells, and its deficiency suppresses their growth. Materials and Methods: In this study, we aimed to analyze clinical and prognostic characteristics of TRPM7 expression in colorectal cancers (CRC) using The Cancer Genome Atlas. Results: High expression of TRPM7 was observed in younger patients with rectal cancer (p = 0.0002). By quantitative correlation analysis, TRPM7 was negatively correlated with age (R = −0.239, p = 0.003) and p53 (R = −0.240, p = 0.002). Furthermore, it was positively correlated with APC expression (R = 0.534, p < 0.001) and KRAS expression (R = 0.319, p < 0.001). In colon cancer, there were no variables that showed a significant correlation with TRPM7. Survival analysis found that TRPM7 expression did not have any prognostic value in colon and rectal cancers. Conclusions: Our study highlights that TRPM7 expression in CRC, particularly in rectal cancer, may be a potential marker. Future studies are needed to provide deeper insights into the role of TRPM7 in rectal cancer.

Background: Pancreatic cancer, while relatively uncommon, is extrapolated to become the second leading cause of cancer-related deaths worldwide. Despite identifying well-known markers like the KRAS gene, the exact regulation of pancreatic cancer progression remains elusive. Methods: Clinical value of PRC1 was analyzed using bioinformatics database. The role of PRC1 was further evaluated through cell-based assays, including viability, wound healing, and sensitivity with the drug. Results: We demonstrate that PRC1 was significantly overexpressed in pancreatic cancer compared to pancreases without cancer, as revealed through human databases and cell lines analysis. Furthermore, high PRC1 expression had a negative correlation with CD4+ T cells, which are crucial for the immune response against cancers. Additionally, PRC1 showed a positive correlation with established pancreatic cancer markers. Silencing PRC1 expression using siRNA significantly inhibited cancer cell proliferation and viability and increased chemotherapeutic drug sensitivity. Conclusions: These findings suggest that targeting PRC1 in pancreatic cancer may enhance immune cell infiltration and inhibit cancer cell proliferation, offering a promising avenue for developing anticancer therapies.