DHCR24 in Tumor Diagnosis and Treatment: A Comprehensive Review.

As an important nutrient in the human body, cholesterol can not only provide structural components for the body's cells, but also can be transformed into a variety of active substances to regulate cell signaling pathways. As an important cholesterol synthase, DHCR24 participates in important regulatory processes in the body. The application of DHCR24 in tumor clinical diagnosis and treatment also attracts much attention. This article reviews the structure and regulatory characteristics of DHCR24, and the research of DHCR24 on tumor progression. We summarize the possible mechanisms of DHCR24 promoting tumor progression through reactive oxygen species (ROS), p53, Ras and PI3K-AKT pathways. Through our review, we hope to provide more research ideas and reference value for the application of DHCR24 in tumor prevention and treatment.

CRABP2 affects chemotherapy resistance of ovarian cancer by regulating the expression of HIF1α.

Ovarian cancer is the most lethal malignancy among gynecologic cancers, and primary and secondary chemotherapy resistance is one of the important reasons for poor prognosis of ovarian cancer patients. However, the specifics of resistance to chemotherapy in ovarian cancer remain unclear. Herein, we find that the expression level of cellular retinoic acid binding protein 2 (CRABP2) is up-regulated in drug-resistant ovarian cancer tissues and cell lines, and the expression levels of CRABP2 in epithelial ovarian cancer tissues are closely related to tumor clinical stage and patients' prognosis, suggesting that CRABP2 plays an important role in the progression of ovarian cancer and the corresponding ability of tumor to chemotherapy. With the in-depth study, we demonstrates that CRABP2 is related to the high metabolic activity in drug-resistant cells, and all-trans retinoic acid exacerbates this activity. Further molecular mechanism exploration experiments show that CRABP2 not only up-regulates the expression level of HIF1α, but also increases the localization of HIF1α in the nucleus. In drug-resistant ovarian cancer cells, knocking down HIF1α can block the resistance of CRABP2 to chemotherapy drugs in ovarian cancer cells. Taken together, our findings suggest for the first time that CRABP2 affects chemotherapy resistance of ovarian cancer by regulating the expression of HIF1α. This study provides a possible molecular mechanism for drug resistance and a possible molecular target for clinical treatment of ovarian cancer.