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Multi-omics analysis reveals that knockdown of IMPA2 induces apoptosis in cervical cancer cells through ROS/MYC/CDK1

Xinyi Wu1, Bingqi Wang1, Lei Liu2

  • 1Department of Laboratory Medicine, The Second Xiangya Hospital of Central South University, Changsha, 410011, Hunan, China.

Clinical & Translational Oncology : Official Publication of the Federation of Spanish Oncology Societies and of the National Cancer Institute of Mexico
|December 23, 2025
PubMed
Abstract

Insights

In cervical cancer (CC), IMPA2 knockdown induces apoptosis and G2/M phase arrest by downregulating the MYC/CDK1 pathway in a ROS-dependent manner, offering new therapeutic targets.

Area of Science:

  • Oncology
  • Molecular Biology
  • Cell Biology

Background:

  • Cervical cancer (CC) presents a significant health challenge for women.
  • IMPA2 has been identified as an oncogene in CC and linked to apoptosis, but its regulatory mechanism remains unclear.

Purpose of the Study:

  • To elucidate the precise role and mechanism of IMPA2 in regulating apoptosis and cell cycle progression in cervical cancer.
  • To investigate the molecular pathways involved in IMPA2-mediated apoptosis.

Main Methods:

  • Electron microscopy for cellular morphology, DCFH-DA probes for reactive oxygen species (ROS) measurement, and western blotting for apoptosis-related proteins.
  • Multi-omics analysis of protein and phosphoprotein profiles to understand the apoptotic mechanism.
  • Validation through apoptosis and cell cycle assays, RT-PCR, and western blotting.

Main Results:

  • IMPA2 knockdown promotes apoptosis by increasing cleaved caspase-3, Bax, and Bak, decreasing Bcl-2, altering mitochondrial morphology, releasing cytochrome c, and accumulating ROS.
  • Multi-omics data suggest IMPA2 regulates the cell cycle via CDK1/CDK2. IMPA2 knockdown induced G2/M arrest, reduced P-CDK1, CDK1, and MYC, which was reversed by MYC overexpression.
  • ROS scavenger NAC reversed MYC downregulation and prevented apoptosis.

Conclusions:

  • IMPA2 regulates cervical cancer cell cycle and apoptosis through the MYC/CDK1 pathway.
  • IMPA2 knockdown downregulates MYC/CDK1 in a ROS-dependent manner, leading to G2/M arrest and apoptosis.
  • This pathway presents a potential therapeutic target for cervical cancer treatment.
Keywords:
ApoptosisCDK1Cell cycleCervical cancerIMPA2Multi-omics technologies

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