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Related Experiment Video

Updated: Apr 28, 2026

SorLA and CLC:CLF-1-dependent Downregulation of CNTFRα as Demonstrated by Western Blotting, Inhibition of Lysosomal Enzymes, and Immunocytochemistry
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Protein Expression Analysis and Functional Characterization of Sorcin in Gallbladder Cancer.

Vaishali Jain1,2, Neeraj Saklani1,2, Srishti Kawatra1,2

  • 1ICMR-Centre for Cancer Pathology (Formerly a Part of ICMR-National Institute of Pathology), Safdarjung Hospital Campus, New Delhi 110029, India.

Cells
|April 27, 2026
PubMed
Summary

Sorcin (SRI) is significantly upregulated in gallbladder cancer (GBC) and promotes tumor growth and spread. Targeting SRI may offer a new therapeutic strategy for GBC patients.

Keywords:
Sorcinepithelial–mesenchymal transitiongallbladder cancerimmunohistochemistrytherapeutic target

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Area of Science:

  • Oncology
  • Molecular Biology
  • Biochemistry

Background:

  • Gallbladder cancer (GBC) is an aggressive malignancy with poor outcomes.
  • Novel molecular targets are crucial for developing effective GBC therapies.
  • Sorcin (SRI), a calcium-binding protein, has a known role in tumor progression but its role in GBC is understudied.

Purpose of the Study:

  • To investigate the expression of Sorcin (SRI) in GBC tissues.
  • To determine the functional role of SRI in GBC cell proliferation, migration, invasion, and epithelial-mesenchymal transition (EMT).

Main Methods:

  • Immunohistochemistry (IHC) was used to analyze SRI expression in 85 GBC tissues and 85 gallstone disease (GSD) controls.
  • siRNA-mediated SRI knockdown was performed in the NOZ GBC cell line.
  • Functional assays included cell proliferation, wound healing, transwell invasion, and Western blot analysis of EMT markers.

Main Results:

  • SRI was significantly upregulated in 67% of GBC cases compared to negative staining in all GSD controls (p < 0.001).
  • SRI knockdown reduced GBC cell proliferation, migration, and invasion.
  • SRI knockdown suppressed vimentin expression, indicating inhibition of EMT.

Conclusions:

  • SRI is significantly overexpressed in GBC and promotes key oncogenic behaviors.
  • SRI is a potential therapeutic target for GBC.
  • Further studies in animal models are warranted for clinical translation.