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STAC3 as a poor prognostic biomarker in renal clear cell carcinoma: relationship with immune infiltration

  • 0The Fourth Affiliated Hospital of Harbin Medical University Harbin 150001, Heilongjiang, China.
American Journal of Cancer Research +

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August 8, 2024

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August 8, 2024

View abstract on PubMed

Summary

This summary is machine-generated.

Elevated STAC3 gene expression in Kidney Renal Clear Cell Carcinoma (KIRC) promotes tumor growth and immune evasion. Targeting STAC3 offers a promising strategy to improve KIRC patient prognosis and therapeutic outcomes.

Area Of Science

  • Oncology
  • Molecular Biology
  • Immunology

Background

  • Calcium ions (Ca2+) play a critical role in cancer development, and their dysregulation is linked to poor prognosis in Kidney Renal Clear Cell Carcinoma (KIRC).
  • The specific impact of calcium ion-regulating genes on KIRC patient survival and their interplay with the tumor immune microenvironment remain incompletely understood.

Purpose Of The Study

  • To identify differentially expressed calcium ion-regulating genes in KIRC.
  • To investigate the prognostic value of these genes and their association with tumor immunity.
  • To elucidate the role of STAC3 in KIRC progression and immune infiltration.

Main Methods

  • Analysis of The Cancer Genome Atlas (TCGA)-KIRC dataset for gene expression differences.
  • Development of prognostic risk models using univariate and LASSO-Cox regression.
  • In vivo and in vitro experiments, including gene silencing, single-cell, and pseudotime analyses.

Main Results

  • STAC3 was significantly overexpressed in KIRC tumors and correlated with higher malignancy and poorer patient prognosis.
  • Increased STAC3 expression was associated with enhanced immune cell infiltration in KIRC.
  • STAC3 knockdown inhibited KIRC cell proliferation, migration, invasion, stemness, and reduced tumor growth in mouse models.

Conclusions

  • STAC3 is a key driver of KIRC progression, linked to aggressive tumor behavior and immune infiltration.
  • Targeting STAC3 represents a potential therapeutic strategy to improve KIRC treatment efficacy and patient survival.

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