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Regulation and signaling of SNX10, a tumor suppressor in hepatocellular carcinoma

Lidia C Diaz-Fernandez1, Carolina Piña-Vázquez1, Hury V Hernandez-Galdamez1

  • 1Center for Research and Advanced Studies of the National Polytechnic Institute, Department of Cell Biology. Mexico City, Mexico.

Biochimie
|July 5, 2025
PubMed

Insights

Sorting Nexin 10 (SNX10) acts as a tumor suppressor in hepatocellular carcinoma (HCC). Lower SNX10 expression correlates with HCC progression and reduced patient survival, inhibiting cancer growth and spread.

Area of Science:

  • Oncology
  • Molecular Biology
  • Cell Biology

Background:

  • Sorting Nexin 10 (SNX10), a PX domain-containing protein, is implicated in endosomal regulation.
  • SNX10's role in cancer is debated, with evidence suggesting both tumor-suppressive and oncogenic functions.
  • Hepatocellular carcinoma (HCC) is a leading cause of cancer mortality globally, necessitating research into its underlying mechanisms.

Purpose of the Study:

  • To investigate the role of SNX10 in hepatocellular carcinoma (HCC) pathogenesis.
  • To determine the relationship between SNX10 expression levels and HCC progression.
  • To elucidate the molecular mechanisms by which SNX10 influences HCC development.

Main Methods:

  • Analysis of SNX10 expression in HCC patient tissues and animal models.
  • Comparison of SNX10 expression in HCC cell lines with varying mesenchymal and epithelial traits.
  • Investigation of SNX10's regulatory effects on chaperone-mediated autophagy (CMA) components (LAMP2A) and target proteins (p21, IκBα).
  • Assessment of SNX10's impact on the transcription of key HCC-associated genes (AFP, BCL-2, DKK1).
  • Examination of the regulatory relationship between miR-30d and SNX10 in HCC cells.

Main Results:

  • SNX10 expression was significantly lower in HCC tumors compared to healthy tissues and correlated with disease progression.
  • Reduced SNX10 expression was observed in HCC cell lines with mesenchymal characteristics.
  • SNX10 negatively regulated LAMP2A and CMA, while positively affecting p21 and IκBα levels.
  • SNX10 downregulated the transcription of AFP, BCL-2, and DKK1.
  • An inverse relationship between miR-30d and SNX10 was identified, with miR-30d acting as a negative regulator of SNX10.

Conclusions:

  • SNX10 functions as a tumor suppressor in HCC by inhibiting proliferation, migration, invasion, and tumorigenesis.
  • Decreased SNX10 expression is associated with HCC progression and potentially poorer outcomes.
  • The miR-30d/SNX10 axis represents a novel regulatory pathway in HCC development.
Keywords:
Chaperone-mediated autophagyHCCLAMP2ALiver cancerSNX10miR-30d

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