GSE184867
Next Generation Sequencing Facilitates Quantitative Analysis of KMT2C Knockdown/Control VCaP Cell Line Transcriptomes
Prostate cancer (PCa) is a leading cause of male morbidity and mortality. Epigenetic modifier abnormalities are becoming a driving event in prostate cancer (PCa). The specific role of KMT2C, a histone methyltransferase that is frequently aberrant in various tumors, is poorly understood in PCa. This study aimed to reveal the potential carcinogenic role of KMT2C in PCa. Herein we confirmed the KMT2C overexpression in PCa, at transcript and protein level. Knockdown KMT2C in VCaP and LNCaP cells attenuated malignant phenotype, suppressing cell viability, clony, and migration. Consistently, stable KMT2C depletion effectively decreases tumor growth by about 70% in vivo. Mechanically, the results suggest that CLDN8 and ITGAV are two key downstream genes of KMT2C. Overall design: Retinal mRNA profiles of KMT2C knockdown and control VCaP cells were generated by deep sequencing, using Illumina NovaSeq 6000.