Chuwei Liu
Current Organizations / Institutes
The organizations/institutes from the scholar's latest article
Research Subjects
Chuwei Liu has a total of 21 co-authors. Here are the top co-authors by number of shared publications:
- Guohui Wan
School of Pharmaceutical Sciences, Sun Yat-Sen University, Guangzhou 510006, China
31 shared publications - Shijia Yan
National-Local Joint Engineering Laboratory of Druggability and New Drug Evaluation, National Engineering Research Center for New Drug and Druggability (cultivation), Guangdong Province Key Laboratory of New Drug Design and Evaluation, School of Pharmaceutical Sciences, Sun Yat-Sen University, Guangzhou, China
31 shared publications - Weiling He
Department of Gastrointestinal Surgery, Xiang’an Hospital of Xiamen University, School of Medicine, Xiamen University, Xiamen, China
31 shared publications - Zhi Wang
Hospital of Stomatology, Guanghua School of Stomatology, Guangdong Provincial Key Laboratory of Stomatology, Sun Yat-Sen University, Guangzhou, China
31 shared publications - Arabella H. Wan
Department of pathology, The First Affiliated Hospital of Sun Yat-sen University, Guangzhou 510080, China
30 shared publications - Heng Liang
State Key Laboratory of Anti‐Infective Drug Discovery and Development, National‐Local Joint Engineering Laboratory of Druggability and New Drug Evaluation, Schools of Pharmaceutical Sciences & Materials Science and Engineering Sun Yat‐Sen University Guangzhou China
30 shared publications
Latest Publications
- Open Access
- 8 January 2026
- Published by American Association for Cancer Research (AACR)
Supplementary Table 13 from HNRNPA2B1 Orchestrates Immune Evasion in Colorectal Cancer by Rewiring Tumor–Immune Cell Interactions and Suppressing CD8+ T-cell Infiltration
Supplemental Table 13. Marker genes characterizing T-cell subclusters identified by scRNA-seq in subcutaneous CRC tumors.
- 8 January 2026
- Published by American Association for Cancer Research (AACR)
Open AccessSupplementary Table 13 from HNRNPA2B1 Orchestrates Immune Evasion in Colorectal Cancer by Rewiring Tumor–Immune Cell Interactions and Suppressing CD8+ T-cell Infiltration
Supplemental Table 13. Marker genes characterizing T-cell subclusters identified by scRNA-seq in subcutaneous CRC tumors.
- Open Access
- 8 January 2026
- Published by American Association for Cancer Research (AACR)
Supplementary Table 15 from HNRNPA2B1 Orchestrates Immune Evasion in Colorectal Cancer by Rewiring Tumor–Immune Cell Interactions and Suppressing CD8+ T-cell Infiltration
Supplemental Table 15. Gene signatures linked to epithelial–mesenchymal transition (EMT).
- 8 January 2026
- Published by American Association for Cancer Research (AACR)
Open AccessSupplementary Table 15 from HNRNPA2B1 Orchestrates Immune Evasion in Colorectal Cancer by Rewiring Tumor–Immune Cell Interactions and Suppressing CD8+ T-cell Infiltration
Supplemental Table 15. Gene signatures linked to epithelial–mesenchymal transition (EMT).
- Open Access
- 8 January 2026
- Published by American Association for Cancer Research (AACR)
Figure S5 from HNRNPA2B1 Orchestrates Immune Evasion in Colorectal Cancer by Rewiring Tumor–Immune Cell Interactions and Suppressing CD8+ T-cell Infiltration
Single-cell transcriptomic profiling of immune cell subsets in Hnrnpa2b1-deficient tumors.
- 8 January 2026
- Published by American Association for Cancer Research (AACR)
Open AccessFigure S5 from HNRNPA2B1 Orchestrates Immune Evasion in Colorectal Cancer by Rewiring Tumor–Immune Cell Interactions and Suppressing CD8+ T-cell Infiltration
Single-cell transcriptomic profiling of immune cell subsets in Hnrnpa2b1-deficient tumors.
- Open Access
- 8 January 2026
- Published by American Association for Cancer Research (AACR)
Supplementary Table 14 from HNRNPA2B1 Orchestrates Immune Evasion in Colorectal Cancer by Rewiring Tumor–Immune Cell Interactions and Suppressing CD8+ T-cell Infiltration
Supplemental Table 14. Mean expression values of marker genes for T-cell subclusters in subcutaneous tumor scRNA-seq data.
- 8 January 2026
- Published by American Association for Cancer Research (AACR)
Open AccessSupplementary Table 14 from HNRNPA2B1 Orchestrates Immune Evasion in Colorectal Cancer by Rewiring Tumor–Immune Cell Interactions and Suppressing CD8+ T-cell Infiltration
Supplemental Table 14. Mean expression values of marker genes for T-cell subclusters in subcutaneous tumor scRNA-seq data.
- Open Access
- 8 January 2026
- Published by American Association for Cancer Research (AACR)
Figure S4 from HNRNPA2B1 Orchestrates Immune Evasion in Colorectal Cancer by Rewiring Tumor–Immune Cell Interactions and Suppressing CD8+ T-cell Infiltration
Flow cytometry analysis of the tumor immune microenvironment following Hnrnpa2b1 deletion.
- 8 January 2026
- Published by American Association for Cancer Research (AACR)
Open AccessFigure S4 from HNRNPA2B1 Orchestrates Immune Evasion in Colorectal Cancer by Rewiring Tumor–Immune Cell Interactions and Suppressing CD8+ T-cell Infiltration
Flow cytometry analysis of the tumor immune microenvironment following Hnrnpa2b1 deletion.
- Open Access
- 8 January 2026
- Published by American Association for Cancer Research (AACR)
Supplementary Table 2 from HNRNPA2B1 Orchestrates Immune Evasion in Colorectal Cancer by Rewiring Tumor–Immune Cell Interactions and Suppressing CD8+ T-cell Infiltration
Supplemental Table 2. List of antibodies used in this study, including sources and dilutions.
- 8 January 2026
- Published by American Association for Cancer Research (AACR)
Open AccessSupplementary Table 2 from HNRNPA2B1 Orchestrates Immune Evasion in Colorectal Cancer by Rewiring Tumor–Immune Cell Interactions and Suppressing CD8+ T-cell Infiltration
Supplemental Table 2. List of antibodies used in this study, including sources and dilutions.
- Open Access
- 8 January 2026
- Published by American Association for Cancer Research (AACR)
Figure S6 from HNRNPA2B1 Orchestrates Immune Evasion in Colorectal Cancer by Rewiring Tumor–Immune Cell Interactions and Suppressing CD8+ T-cell Infiltration
Altered cellular interactions in the tumor microenvironment following Hnrnpa2b1 deletion.
- 8 January 2026
- Published by American Association for Cancer Research (AACR)
Open AccessFigure S6 from HNRNPA2B1 Orchestrates Immune Evasion in Colorectal Cancer by Rewiring Tumor–Immune Cell Interactions and Suppressing CD8+ T-cell Infiltration
Altered cellular interactions in the tumor microenvironment following Hnrnpa2b1 deletion.
- Open Access
- 8 January 2026
- Published by American Association for Cancer Research (AACR)
Supplementary Table 8 from HNRNPA2B1 Orchestrates Immune Evasion in Colorectal Cancer by Rewiring Tumor–Immune Cell Interactions and Suppressing CD8+ T-cell Infiltration
Supplemental Table 8. Mean expression values of marker genes delineating major cell types in the scRNA-seq dataset of subcutaneous tumors in mice.
- 8 January 2026
- Published by American Association for Cancer Research (AACR)
Open AccessSupplementary Table 8 from HNRNPA2B1 Orchestrates Immune Evasion in Colorectal Cancer by Rewiring Tumor–Immune Cell Interactions and Suppressing CD8+ T-cell Infiltration
Supplemental Table 8. Mean expression values of marker genes delineating major cell types in the scRNA-seq dataset of subcutaneous tumors in mice.
- Open Access
- 8 January 2026
- Published by American Association for Cancer Research (AACR)
Supplementary Table 12 from HNRNPA2B1 Orchestrates Immune Evasion in Colorectal Cancer by Rewiring Tumor–Immune Cell Interactions and Suppressing CD8+ T-cell Infiltration
Supplemental Table 12. KEGG pathway enrichment analysis of genes upregulated in T cells isolated from Hnrnpa2b1-depleted CRC tumors.
- 8 January 2026
- Published by American Association for Cancer Research (AACR)
Open AccessSupplementary Table 12 from HNRNPA2B1 Orchestrates Immune Evasion in Colorectal Cancer by Rewiring Tumor–Immune Cell Interactions and Suppressing CD8+ T-cell Infiltration
Supplemental Table 12. KEGG pathway enrichment analysis of genes upregulated in T cells isolated from Hnrnpa2b1-depleted CRC tumors.
- Open Access
- 8 January 2026
- Published by American Association for Cancer Research (AACR)
Data from HNRNPA2B1 Orchestrates Immune Evasion in Colorectal Cancer by Rewiring Tumor–Immune Cell Interactions and Suppressing CD8+ T-cell Infiltration
Immune checkpoint blockade (ICB) has transformed colorectal cancer therapy, yet the majority of microsatellite-stable colorectal cancers remain refractory because of insufficient tumor–immune cell cross-talk. Identifying molecular regulators that modulate the tumor immune microenvironment (TIME) is crucial for expanding ICB efficacy. In this study, we identified HNRNPA2B1, an RNA-binding protein prominently upregulated in colorectal cancer, as a key driver of immune evasion. Despite low cytotoxicity to normal cells, HNRNPA2B1 rewired the TIME by suppressing Cxcl9/Cxcl10–Cxcr3 signaling, CD8+ T-cell infiltration, and MHC class I antigen presentation, resulting in a noninflamed (“cold”) tumor state. HNRNPA2B1 deletion reprogramed the TIME, enhanced CD8+ T cell–mediated tumor clearance, and sensitized microsatellite-stable colorectal cancers to ICB. A computational A2B1 score was developed to quantify HNRNPA2B1’s impact on tumor–immune interactions, and it strongly correlated with immune infiltration, epithelial–mesenchymal transition status, and patient prognosis, supporting its potential role as a biomarker for ICB responsiveness in colorectal cancer.
- 8 January 2026
- Published by American Association for Cancer Research (AACR)
Open AccessData from HNRNPA2B1 Orchestrates Immune Evasion in Colorectal Cancer by Rewiring Tumor–Immune Cell Interactions and Suppressing CD8+ T-cell Infiltration
Immune checkpoint blockade (ICB) has transformed colorectal cancer therapy, yet the majority of microsatellite-stable colorectal cancers remain refractory because of insufficient tumor–immune cell cross-talk. Identifying molecular regulators that modulate the tumor immune microenvironment (TIME) is crucial for expanding ICB efficacy. In this study, we identified HNRNPA2B1, an RNA-binding protein prominently upregulated in colorectal cancer, as a key driver of immune evasion. Despite low cytotoxicity to normal cells, HNRNPA2B1 rewired the TIME by suppressing Cxcl9/Cxcl10–Cxcr3 signaling, CD8+ T-cell infiltration, and MHC class I antigen presentation, resulting in a noninflamed (“cold”) tumor state. HNRNPA2B1 deletion reprogramed the TIME, enhanced CD8+ T cell–mediated tumor clearance, and sensitized microsatellite-stable colorectal cancers to ICB. A computational A2B1 score was developed to quantify HNRNPA2B1’s impact on tumor–immune interactions, and it strongly correlated with immune infiltration, epithelial–mesenchymal transition status, and patient prognosis, supporting its potential role as a biomarker for ICB responsiveness in colorectal cancer.