Interference with CHD1L inhibits the malignant progression and enhances cisplatin sensitivity of ovarian cancer cells by binding PLK1

• Published in: Journal of ovarian research Vol. 18; no. 1; pp. 38 - 15
• Main Authors: Qiao, Kun, Guan, Yuanxiazi, Xing, Wenjing
• Format: Journal Article
• Language: English
• Published: England BioMed Central Ltd 24.02.2025; BioMed Central; BMC
• Subjects: Animals; Antineoplastic Agents - pharmacology; Apoptosis; Apoptosis - drug effects; Cancer; Cell cycle arrest; Cell Cycle Proteins - genetics; Cell Cycle Proteins - metabolism; Cell Line, Tumor; Cell Movement - drug effects; Cell Proliferation - drug effects; CHD1L; Cisplatin; Cisplatin - pharmacology; Cisplatin - therapeutic use; Development and progression; Disease Progression; DNA Helicases - genetics; DNA Helicases - metabolism; DNA-Binding Proteins - genetics; DNA-Binding Proteins - metabolism; Dosage and administration; Drug Resistance, Neoplasm - genetics; Drug therapy; Female; Genetic aspects; Health aspects; Humans; Mice; Mice, Nude; Oncogenes; Oncology, Experimental; Ovarian cancer; Ovarian Neoplasms - drug therapy; Ovarian Neoplasms - genetics; Ovarian Neoplasms - metabolism; Ovarian Neoplasms - pathology; Physiological aspects; PLK1; Polo-Like Kinase 1; Proliferation; Protein kinases; Protein Serine-Threonine Kinases - genetics; Protein Serine-Threonine Kinases - metabolism; Proto-Oncogene Proteins - genetics; Proto-Oncogene Proteins - metabolism; Xenograft Model Antitumor Assays; China; PLK1; Cell cycle arrest; CHD1L; Proliferation; Cisplatin sensitivity; Apoptosis; Ovarian cancer

Chromodomain helicase/ATPase DNA-binding protein 1-like gene (CHDIL) is an oncogene with abnormal expression in ovarian cancer (OC), but its regulatory role in the malignant biological properties of OC cells and its mechanisms have not been reported. In this study, CHD1L and polo-like Kinase 1 (PLK1...