2. Academic Validation
  3. Lysine demethylase 5A promotes prostate adenocarcinoma progression by suppressing microRNA-330-3p expression and activating the COPB2/PI3K/AKT axis in an ETS1-dependent manner

Lysine demethylase 5A promotes prostate adenocarcinoma progression by suppressing microRNA-330-3p expression and activating the COPB2/PI3K/AKT axis in an ETS1-dependent manner

  • J Cell Commun Signal. 2022 May 18. doi: 10.1007/s12079-022-00671-5.
Yuanyuan Mi  # 1,  Lifeng Zhang  # 2,  Chuanyu Sun 3,  Yanyan Feng 1,  Jian Sun 1,  Jun Wang 1,  Dongjie Yang 4,  Xiaowei Qi 4,  Hongyuan Wan 1,  Guowei Xia 3,  Sheng Wu 5,  Lijie Zhu 6
Affiliations

Affiliations

  • 1 Department of Urology, Affiliated Hospital of Jiangnan University, No. 1000 Hefeng Road, Wuxi, 214122, Jiangsu, China.
  • 2 Department of Urology, Affiliated Changzhou No. 2 People's Hospital of Nanjing Medical University, Changzhou, 213003, Jiangsu, China.
  • 3 Department of Urology, Huashan Hospital, Fudan University, Shanghai, 200040, China.
  • 4 Department of Pathology, Affiliated Hospital of Jiangnan University, Wuxi, 214122, Jiangsu, China.
  • 5 Department of Urology, Affiliated Hospital of Jiangnan University, No. 1000 Hefeng Road, Wuxi, 214122, Jiangsu, China. shengW_7@163.com.
  • 6 Department of Urology, Affiliated Hospital of Jiangnan University, No. 1000 Hefeng Road, Wuxi, 214122, Jiangsu, China. zhulijie_09@163.com.
  • # Contributed equally.
PMID: 35581421 DOI: 10.1007/s12079-022-00671-5
Abstract

Lysine demethylase 5A (KDM5A) is a Histone Demethylase frequently involved in Cancer progression. This research aimed to explore the function of KDM5A in prostate adenocarcinoma (PRAD) and the molecular mechanism. KDM5A was highly expressed in collected PRAD tissues and acquired PRAD cells. High KDM5A expression was correlated with reduced survival and poor prognosis of patients with PRAD. Knockdown of KDM5A suppressed the proliferation, colony formation, migration, and invasiveness of PRAD cells and reduced angiogenesis ability of endothelial cells. Downstream molecules implicated in KDM5A mediation were predicted using integrated bioinformatic analyses. KDM5A enhanced ETS proto-oncogene 1 (ETS1) expression through demethylation of H3K4me2 at its promoter. ETS1 suppressed the transcription activity of miR-330-3p, and either further ETS1 overexpression or miR-330-3p inhibition blocked the functions of KDM5A knockdown in PRAD. miR-330-3p targeted coatomer protein complex subunit β2 (COPB2) mRNA. Downregulation of miR-330-3p restored the expression of COPB2 and activated the PI3K/Akt pathway in PRAD. The results in vitro were reproduced in vivo where KDM5A downregulation suppressed the growth and metastasis of xenograft tumors in nude mice. In conclusion, this study demonstrated that KDM5A promoted PRAD by suppressing miR-330-3p and activating the COPB2/PI3K/Akt axis in an ETS1-dependent manner.

Keywords

ETS proto-oncogene 1; Lysine demethylase 5A; PI3K/AKT signaling pathway; miR-330-3p, COPB2.

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