CDC5L binds to ELAVL1 to inhibit pyroptosis in hepatocellular carcinoma through the Caspase 3/GSDME signaling pathway

  • 0Department of Bile and Pancreatic Surgery, Xiangya Hospital, Central South University, Changsha, Hunan 410008, P.R. China.

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Summary

This summary is machine-generated.

High cell division cycle 5 like (CDC5L) levels indicate poor prognosis in hepatocellular carcinoma (HCC). Silencing CDC5L promotes pyroptosis and inhibits HCC tumor growth by regulating the Caspase 3/GSDME pathway.

Area Of Science

  • Oncology
  • Molecular Biology
  • Cell Death Mechanisms

Background

  • Hepatocellular carcinoma (HCC) presents a significant global health challenge due to high morbidity and mortality.
  • Elevated cell division cycle 5 like (CDC5L) expression is a known biomarker for poor prognosis in HCC patients.

Purpose Of The Study

  • To investigate the role of CDC5L in the development and progression of HCC.
  • To elucidate the underlying molecular mechanisms by which CDC5L influences pyroptosis in HCC.

Main Methods

  • Bioinformatics analysis and clinical sample validation to assess CDC5L expression.
  • In vitro and in vivo experiments involving CDC5L knockdown and overexpression.
  • Investigation of pyroptosis pathways by manipulating CDC5L and ELAV like RNA binding protein 1 (ELAVL1) expression.
  • Validation of the CDC5L/ELAVL1/Caspase 3/gasdermin E (GSDME) axis in HCC pyroptosis.

Main Results

  • CDC5L expression is upregulated in HCC and correlates with adverse patient outcomes.
  • Suppression of CDC5L reduces HCC cell viability, proliferation, migration, and invasion while enhancing pyroptosis.
  • CDC5L knockdown inhibits tumor growth in vivo, whereas CDC5L overexpression promotes it.
  • CDC5L interacts with ELAVL1, inhibiting ELAVL1 binding to Caspase 3 mRNA and suppressing pyroptosis.

Conclusions

  • CDC5L promotes HCC progression by inhibiting pyroptosis via the Caspase 3/GSDME pathway through interaction with ELAVL1.
  • Targeting the CDC5L/ELAVL1 axis offers a potential therapeutic strategy for improving HCC treatment and patient prognosis.

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