TL;DR
RMI2 may promote OC development by activating the ATR/CHK1 pathway to sustain genomic stability, highlighting its potential as a prognostic biomarker and therapeutic target in OC.
Checkpoint kinase 2 (CHK2) participates in the DNA damage response (DDR) by regulating the cell cycle or inducing apoptosis, and its abnormal activity can lead to cancer development. CHK2 loss-of-function mutations correlate with the onset of many types of tumors and with therapy resistance. As the exact molecula...
Genome instability (GI) is a hallmark of cancer. GI is associated with accumulative DNA damage and tumor-specific defects in DNA repair. Multiple antitumor drugs have been developed to promote persistent GI and to drive DNA damage beyond a threshold that tumor cells can survive. However, regulatory roles of circular RN...
Cisplatin resistance in hepatoblastoma (HB) is a major therapeutic barrier. Emerging evidence suggests that cancer cells can activate DNA double-strand break repair pathways to evade chemotherapy-induced apoptosis and sustain stemness; however, the mechanisms underlying cisplatin resistance in HB remain poorly understo...
Resistance to PARP inhibitors (PARPi) remains a major clinical challenge in ovarian cancer (OC), emphasizing the need for novel strategies to enhance therapeutic efficiency. Our previous work revealed that the antimalarial drug quinacrine (QC) can be repurposed to induce cell death in OC by promoting lysosomal release...
Cisplatin resistance remains a major limitation in the treatment of cervical cancer, with enhanced DNA damage repair contributing to reduced therapeutic sensitivity. The role of STAT5A in coordinating DNA double-strand break repair under therapeutic stress remains unclear. Here, we investigated the role of STAT5A in ci...
Findings reveal a dual oncogenic role for SETX, which represents a promising therapeutic target, as its inhibition simultaneously suppresses tumor growth and overcomes chemotherapy resistance in ovarian cancer.
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