ANP32B inhibition suppresses the growth of prostate cancer cells by regulating c-Myc signaling.

ABSTRACT

ANP32B is a histone chaperone that interacts with various transcription factors that regulate cancer cell proliferation, immigration, and apoptosis. c-Myc, a well-known oncogenic protein, is a principal player in the initiation and progression of prostate cancer (PC). The means by which ANP32B and c-Myc act remain unknown. We downloaded clinical data from the GEO, TCGA, and other databases to explore ANP32B expression and its effects on the survival of PC and normal tissues. ANP32B-knockdown cell lines were used to evaluate how ANP32B affected cell proliferation in vitro and in vivo. Gene set enrichment analysis and RNAseq were employed to define how ANP32B regulated PC pathways. Immunohistochemical measures were used to detect the expression levels of relevant proteins in xenografts and PC tissues. ANP32B expression increased in PC tissues; ANP32B knockdown inhibited cell growth but this was rescued by c-Myc signaling. ANP32B is thus a PC oncogene and may serve as a valuable therapeutic target when seeking to treat PC.