HJURP promotes proliferation in prostate cancer cells through increasing CDKN1A degradation via the GSK3β/JNK signaling pathway.
Wenjie LaiWeian ZhuChutian XiaoXiaojuan LiYu WangYuefu HanJiayu ZhengYingqiu LiMingqiang LiXingqiao WenPublished in: Cell death & disease (2021)
Genes with cross-cancer aberrations are most likely to be functional genes or potential therapeutic targets. Here, we found a total of 137 genes were ectopically expressed in eight cancer types, of which Holliday junction recognition protein (HJURP) was significantly upregulated in prostate cancer (PCa). Moreover, patients with higher HJURP mRNA and protein levels had poorer outcomes, and the protein levels served as an independent prognosis factor for the overall survival of PCa patients. Functionally, ectopic HJURP expression promoted PCa cells proliferation in vitro and in vivo. Mechanistically, HJURP increased the ubiquitination of cyclin-dependent kinase inhibitor 1 (CDKN1A) via the GSK3β/JNK signaling pathway and decreased its stability. This study investigated the role of HJURP in PCa proliferation and may provide a novel prognostic and therapeutic target for PCa.
Keyphrases
- signaling pathway
- induced apoptosis
- pi k akt
- cell cycle arrest
- prostate cancer
- epithelial mesenchymal transition
- papillary thyroid
- binding protein
- genome wide
- ejection fraction
- squamous cell
- protein protein
- end stage renal disease
- amino acid
- newly diagnosed
- poor prognosis
- radical prostatectomy
- type diabetes
- gene expression
- risk assessment
- lymph node metastasis
- young adults
- prognostic factors
- cell cycle
- endoplasmic reticulum stress
- dna methylation
- transcription factor
- childhood cancer
- free survival
- oxidative stress
- weight loss
- patient reported
- human health