CAPG interference induces apoptosis and ferroptosis in colorectal cancer cells through the P53 pathway

Yingying Zhao1, Rui Ma1, Chuyue Wang1

  • 1Guangdong Institute of Gastroenterology, Guangzhou, China; Guangdong Provincial Key Laboratory of Colorectal and Pelvic Floor Disease, The Sixth Affiliated Hospital, Sun Yat-sen University, Guangzhou, China.

PubMed
Abstract

Insights

Capping Actin Protein (CAPG) is overexpressed in colorectal cancer (CRC), promoting tumor growth. Inhibiting CAPG halts CRC cell proliferation and triggers cell death, suggesting CAPG as a promising therapeutic target for CRC.

Area of Science:

  • Oncology
  • Molecular Biology
  • Biochemistry

Background:

  • Colorectal cancer (CRC) presents high incidence and mortality rates.
  • Existing treatments for CRC are inadequate for many patients.
  • Capping Actin Protein (CAPG) plays a role in actin dynamics.

Purpose of the Study:

  • Investigate Capping Actin Protein (CAPG) as a novel therapeutic target for colorectal cancer (CRC).
  • Determine the role of CAPG in CRC progression and patient prognosis.

Main Methods:

  • Utilized bioinformatic analysis (UALCAN) for gene expression profiling.
  • Assessed cell proliferation, cell cycle, apoptosis, and ferroptosis via CCK-8 assay and flow cytometry.
  • Evaluated tumorigenesis in vivo using mouse models and identified differentially expressed genes/pathways through RNA sequencing.

Main Results:

  • CAPG was significantly overexpressed in CRC tissues, correlating with poor overall survival.
  • CAPG knockdown inhibited CRC cell proliferation both in vitro and in vivo.
  • CAPG interference blocked the cell cycle at G1 phase and induced apoptosis and ferroptosis via the P53 pathway.

Conclusions:

  • Elevated CAPG levels in CRC patients indicate a poorer prognosis.
  • CAPG promotes CRC proliferation by suppressing the P53 pathway, while inhibiting apoptosis and ferroptosis.
  • CAPG represents a potential therapeutic target for improving CRC prognosis and treatment outcomes.

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