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Updated: Jan 14, 2026

Establishment of a Co-culture System of Patient-Derived Colorectal Tumor Organoids and Tumor-Infiltrating Lymphocytes (TILs)
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Establishment of a Co-culture System of Patient-Derived Colorectal Tumor Organoids and Tumor-Infiltrating Lymphocytes (TILs)

Published on: June 27, 2025

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HNRNPA2B1 Orchestrates Immune Evasion in Colorectal Cancer by Rewiring Tumor-Immune Cell Interactions and Suppressing

Chuwei Liu1,2, Heng Liang2, Peipei Wang3

  • 1Department of Gastrointestinal Surgery, The First Affiliated Hospital, Sun Yat-Sen University, Guangzhou, China.

Cancer Immunology Research
|October 20, 2025
PubMed

Insights

HNRNPA2B1 protein promotes immune evasion in colorectal cancer by suppressing anti-tumor immunity. Its inhibition sensitizes tumors to immune checkpoint blockade (ICB), offering a new therapeutic strategy.

Area of Science:

  • Oncology
  • Immunology
  • Molecular Biology

Background:

  • Immune checkpoint blockade (ICB) shows promise in colorectal cancer (CRC) therapy.
  • Most microsatellite-stable CRC (MSS-CRC) are resistant to ICB due to poor tumor-immune cell interactions.
  • Identifying regulators of the tumor immune microenvironment (TIME) is vital for improving ICB efficacy.

Purpose of the Study:

  • To identify molecular regulators of immune evasion in MSS-CRC.
  • To investigate the role of HNRNPA2B1 in modulating the TIME and ICB response.

Main Methods:

  • Utilized bioinformatics and molecular biology techniques to identify HNRNPA2B1.
  • Assessed HNRNPA2B1's impact on immune signaling pathways (Cxcl9/Cxcl10-Cxcr3), CD8+ T-cell infiltration, and MHC class I presentation.
  • Generated HNRNPA2B1 knockout models to evaluate its role in tumor clearance and ICB sensitivity.
  • Developed and validated a computational A2B1 score.

Main Results:

  • HNRNPA2B1 is upregulated in CRC and drives immune evasion by suppressing key immune signaling pathways.
  • HNRNPA2B1 deletion enhanced CD8+ T-cell infiltration and sensitized MSS-CRC to ICB.
  • The A2B1 score correlated with immune infiltration, epithelial-mesenchymal transition (EMT) status, and patient prognosis.

Conclusions:

  • HNRNPA2B1 is a critical driver of immune evasion in MSS-CRC.
  • Targeting HNRNPA2B1 can reprogram the TIME and enhance anti-tumor immunity.
  • The A2B1 score may serve as a predictive biomarker for ICB response in CRC patients.

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