ArticleClinical & translational oncology : official publication of the Federation of Spanish Oncology Societies and of the National Cancer Institute of Mexico2026
Multi-omics analysis reveals that knockdown of IMPA2 induces apoptosis in cervical cancer cells through ROS/MYC/CDK1 signaling.
Article in Clinical & translational oncology : official publication of the Federation of Spanish Oncology Societies and of the National Cancer Institute of Mexico, 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 1 paper.
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Who cites it
1 citing paper in PubMed.
- IMPA2 ameliorates high-fat diet-induced obesity by enhancing adaptive thermogenesis in a Ca²⁺-activated mitochondrial biogenesis pathway.Journal of translational medicine · 2026Article
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5 authors.
Funding
Abstract
backgroundCervical cancer (CC) poses a significant health risk for women. Our previous studies have found that IMPA2 is an oncogene in CC and is associated with apoptosis; however, the exact regulatory mechanism is not clear.
methodsTo further investigate the role of IMPA2 in apoptosis, cellular morphology was examined using electron microscopy, ROS levels were measured with DCFH-DA probes, and apoptosis-related proteins were analyzed by western blot to characterize the apoptosis induced by IMPA2 knockdown. To gain a deeper understanding of the apoptotic mechanism of IMPA2 knockdown in CC cells, multi-omics analysis was performed on protein and phosphoprotein profiles. Apoptosis assay, cell cycle assay, RT-PCR, and western blotting were subsequently used for validation.
resultsCytological experiments confirmed that IMPA2 knockdown enhances the expression of cleaved caspase-3, Bax, and Bak, downregulates Bcl-2, induces mitochondrial morphological alterations, facilitates cytochrome c release from mitochondria, and promotes apoptosis through ROS accumulation. Multi-omics analysis showed IMPA2 may regulate cell cycle and DNA replication via CDK1/CDK2, with IMPA2 knockdown in CC cells inducing G2/M phase arrest, reducing P-CDK1, CDK1, and MYC expression, effects reversed by MYC overexpression. Meanwhile, the ROS scavenger NAC rescues MYC downregulation and its downstream effects to prevent apoptosis.
conclusionThis study demonstrates that IMPA2 regulates CC cell cycle and apoptosis via the MYC/CDK1 pathway, with IMPA2 knockdown downregulating MYC/CDK1 in a ROS-dependent manner to induce G2/M arrest and apoptosis.
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