As an essential nutrient, copper’s redox properties are both beneficial and toxic to cells. Therefore, leveraging the characteristics of copper-dependent diseases or using copper toxicity to treat copper-sensitive diseases may offer new strategies for specific disease treatments. In particular, copper concentration is typically higher in cancer cells, making copper a critical limiting nutrient for cancer cell growth and proliferation. Hence, intervening in copper metabolism specific to cancer cells may become a potential tumor treatment strategy, directly impacting tumor growth and metastasis. In this review, we discuss the metabolism of copper in the body and summarize research progress on the role of copper in promoting tumor cell growth or inducing programmed cell death in tumor cells. Additionally, we elucidate the role of copper-related drugs in cancer treatment, intending to provide new perspectives for cancer treatment.

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Purpose Colorectal cancer (CRC) is one of the most common malignancies in the world. The prognosis of advanced CRC is still poor. The purpose of this study was to identify a gene expression profile associated with CRC that may contribute to the early diagnosis of CRC and improve patient prognosis. Patients and Methods Five pairs of CRC tissues and paracancerous tissues were used to identify causative genes using microarray assays. The prognostic value of Cytochrome C Oxidase Assembly Factor 1 Homolog (COA1) in CRC was assessed in 90 CRC patients. Loss-of-function assays, cell proliferation assays using Celigo and MTT, colony formation assays, a subcutaneous xenograft mouse model, and apoptosis assays were used to define the effects of downregulation of COA1 in CRC cells in vitro and in vivo. The underlying molecular mechanisms of COA1 in CRC were also investigated. Results The causative gene COA1 was identified through microarray analysis. COA1 expression in CRC was notably associated with pathologic differentiation, tumor size, and tumor depth. COA1 expression may act as an independent prognostic factor for overall survival of CRC. Knockdown of COA1 inhibited the proliferation of CRC cells in vitro and the tumorigenicity of CRC cells in vivo. Decreased COA1 expression induced apoptosis of CRC cells. Based on the microarray assay results comparing HCT116 cells transfected with lentivirus encoding anti-COA1 shRNA or negative control shRNA, ingenuity pathway analysis (IPA) revealed that the PI3K/AKT signaling pathway was significantly enriched. Moreover, CCND1, mTOR, AKT1, and MDM2 were identified as the downstream genes of COA1. Conclusion These findings demonstrate that COA1 promotes CRC cell proliferation and inhibits apoptosis by regulating the PI3K/AKT signaling pathway. Our results implicate COA1 as a potential oncogene involved in tumor growth and progression of CRC.

n-methyl d-aspartate receptors (nMdars) are closely associated with the development, growth and metastasis of cancer. Glutamate receptor, ionotropic, n-methyl d-aspartate-associated protein 1 (Grina) is a member of the of the nMdar family, and its aberrant expression is associated with gastric cancer. However, the role of Grina in colorectal cancer (crc) is not completely understood. in the present study, expression profiles of GRINA in several crc databases were obtained and further verified using clinical crc samples. The effects of Grina overexpression on crc progression both in vivo and in vitro were assessed. Briefly, cell proliferation was detected using MTT assay, and cell migration and invasion ability were evaluated by wound healing and Transwell assay. in addition, the molecular mechanism underlying the upregulated expression of Grina in crc was investigated. The regulatory association between Grina and mir-296-3p was detected by luciferase assay, reverse transcription-quantitative Pcr and western blotting. The results demonstrated that Grina expression levels were significantly increased in tumor samples compared with those in healthy samples, and upregulated expression of Grina was associated with a less favorable prognostic outcome in patients with crc. Grina overexpression significantly increased crc cell proliferation, invasion and migration. additionally, it was determined that Grina was post-transcriptionally regulated by microrna (mir)-296-3p. Together, the results of the present study suggested the potential importance of the mir-296-3p/Grina axis and highlighted potential novel targets for the management of crc.