PRKD3 promotes proliferation of liver cancer cells: a downstream proteomics profiling study

Ye Tian1,2, Bei Xie2, Shuaiyang Wang1

  • 1Department of Clinical Laboratory Center, Lanzhou University Second Hospital Lanzhou 730030, Gansu, China.

Abstract

Insights

Protein kinase D 3 (PRKD3) inhibits hepatocellular carcinoma (HCC) cell proliferation by inducing cell cycle arrest. This study reveals PRKD3

Area of Science:

  • Oncology
  • Molecular Biology
  • Proteomics

Background:

  • Protein kinase D 3 (PRKD3) is a serine/threonine kinase implicated in various cancers.
  • Its specific role and regulatory mechanisms in hepatocellular carcinoma (HCC) proliferation are not well understood.

Purpose of the Study:

  • To investigate the function and mechanism of PRKD3 in regulating HCC cell proliferation.
  • To identify proteomic alterations associated with PRKD3 activity in liver cancer.

Main Methods:

  • Constructed a PRKD3 knockdown cell line for HCC.
  • Assessed proliferation using CCK-8, EdU, and clonogenic assays.
  • Analyzed proteomic changes via 4D-label-free technology and identified key protein interactions.

Main Results:

  • PRKD3 expression is abnormal in HCC, correlating with poorer prognosis.
  • PRKD3 knockdown significantly reduced HCC cell proliferation and induced G2/M cell cycle arrest.
  • Proteomic analysis identified 330 differentially expressed proteins and highlighted CDK4, SERPINE1, SQSTM1, RAB8A, and NRBF2 as key regulatory nodes.

Conclusions:

  • PRKD3 knockdown inhibits HCC proliferation, revealing its regulatory role.
  • Key proteins like CDK4, SERPINE1, SQSTM1, RAB8A, and NRBF2 are implicated in PRKD3-mediated pathways in HCC.