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High expression of ARPC1B promotes the proliferation and apoptosis of clear cell renal cell carcinoma cells, leading

Hongbo Wang1, Zhendong Liu2, Yuelin Du3

  • 1Department of Urology Surgery, Lanzhou University Second Hospital, Lanzhou, 730030, China; Department of Microbiome Laboratory, Henan Provincial People's Hospital, People's Hospital of Zhengzhou University, Zhengzhou University, Zhengzhou, 450003, China.

Molecular and Cellular Probes
|January 16, 2025
PubMed
Summary
This summary is machine-generated.

High ARPC1B expression in clear cell renal cell carcinoma (ccRCC) correlates with poor prognosis and promotes tumor growth. This suggests ARPC1B is a potential biomarker and therapeutic target for ccRCC.

Keywords:
Actin-related protein 2/3 complexCell proliferationImmune microenvironmentPrognostic biomarkersRenal cell carcinoma

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Area of Science:

  • Oncology
  • Molecular Biology
  • Genetics

Background:

  • Actin-related protein 2/3 complex subunit 1B (ARPC1B) is implicated in tumor malignancy.
  • Its role in clear cell renal cell carcinoma (ccRCC) is not well-defined.
  • This study investigates ARPC1B's impact on ccRCC prognosis and progression.

Purpose of the Study:

  • To evaluate the prognostic significance of ARPC1B in ccRCC.
  • To explore the association of ARPC1B with clinical features, immune microenvironment, and drug sensitivity.
  • To elucidate the functional role and molecular mechanisms of ARPC1B in ccRCC pathogenesis.

Main Methods:

  • Analysis of multi-omics data and clinical information from public databases.
  • Co-expression, gene set enrichment, and functional assays (RT-qPCR, CCK8, colony formation, immunofluorescence, IHC).
  • In vivo xenograft models, flow cytometry, and Western blotting to assess ARPC1B's effects on proliferation, apoptosis, and molecular pathways.

Main Results:

  • ARPC1B was significantly upregulated in ccRCC, correlating with poor prognosis and serving as an independent risk factor.
  • ARPC1B expression linked to altered immune microenvironment and drug sensitivity.
  • ARPC1B knockdown inhibited ccRCC cell proliferation and induced apoptosis via the BAX-Bcl-2/c-caspase3/c-PARP pathway, confirmed in vitro and in vivo.

Conclusions:

  • ARPC1B overexpression is linked to adverse prognosis, immune dysregulation, and altered drug sensitivity in ccRCC.
  • ARPC1B promotes ccRCC malignant behavior.
  • ARPC1B presents a promising prognostic biomarker and therapeutic target for ccRCC.