PRMT5 disruption drives antitumor immunity in cervical cancer by reprogramming T cell-mediated response and regulating PD-L1 expression
Yongshuai Jiang, Yuanyang Yuan, Ming Chen, Shengzhe Li, Jun Bai, Yuanteng Zhang, Ying Sun, Guojue Wang, Haiyan Xu, Ziyu Wang, Yingxia Zheng, Hong Nie
Abstract
: Our results clarify a new mechanism which PRMT5 knockdown in cervical cancer cells drives an antitumor function via reprogramming T cell-mediated response and regulating PD-L1 expression. Thus, our study highlights that PRMT5 may be a potential target for cervical cancer therapy.
Topics & Concepts
Protein arginine methyltransferase 5Cancer researchTumor microenvironmentChromatin immunoprecipitationOncogeneBiologyGene knockdownTumor progressionCell cultureCancerMethyltransferaseCell cycleGene expressionMethylationBiochemistryTumor cellsPromoterGeneGeneticsCancer-related gene regulationEpigenetics and DNA Methylation