Guanyin Huang
Current Organizations / Institutes
The organizations/institutes from the scholar's latest article
Guanyin Huang has a total of 58 co-authors. Here are the top co-authors by number of shared publications:
- Xin Hong
Southern University of Science and Technology 1 Department of Biochemistry, SUSTech Homeostatic Medicine Institute, School of Medicine Shenzhen, China
100 shared publications - Xuefei Liu
Southern University of Science and Technology 1 Department of Biochemistry, SUSTech Homeostatic Medicine Institute, School of Medicine Shenzhen, China
100 shared publications - Hao Yu
Institute of Biomedical and Health Engineering, Shenzhen Institute of Advanced Technology, Chinese Academy of Sciences, Shenzhen, China
85 shared publications - Shuqian Zheng
Southern University of Science and Technology 1 Department of Biochemistry, SUSTech Homeostatic Medicine Institute, School of Medicine Shenzhen, China
85 shared publications - Chun Wu
State Key Laboratory of Oncology in South China 4 Department of Nasopharyngeal Carcinoma Guangdong Provincial Clinical Research Center for Cancer Guangzhou, China
78 shared publications - Feiqiu Wen
Southern University of Science and Technology 2 Department of Hematology and Oncology, Shenzhen Children’s Hospital and School of Medicine Shenzhen, China
78 shared publications
Latest Publications
- Open Access
- 2 July 2026
- Published by American Association for Cancer Research (AACR)
Supplementary Figure S11 from NMB+CXCL13+CD4+ T Cell–Derived Neuromedin B Promotes Neuropeptide S Receptor 1–Positive Malignant Cell Senescence and Malignancy
Supplementary Figure S11. Metastatic lesions in vivo.
- 2 July 2026
- Published by American Association for Cancer Research (AACR)
Open AccessSupplementary Figure S11 from NMB+CXCL13+CD4+ T Cell–Derived Neuromedin B Promotes Neuropeptide S Receptor 1–Positive Malignant Cell Senescence and Malignancy
Supplementary Figure S11. Metastatic lesions in vivo.
- Open Access
- 2 July 2026
- Published by American Association for Cancer Research (AACR)
Supplementary Figure S1 from NMB+CXCL13+CD4+ T Cell–Derived Neuromedin B Promotes Neuropeptide S Receptor 1–Positive Malignant Cell Senescence and Malignancy
Supplementary Figure S1. Comprehensive characterization of CD4+ T cells in CRC.
- 2 July 2026
- Published by American Association for Cancer Research (AACR)
Open AccessSupplementary Figure S1 from NMB+CXCL13+CD4+ T Cell–Derived Neuromedin B Promotes Neuropeptide S Receptor 1–Positive Malignant Cell Senescence and Malignancy
Supplementary Figure S1. Comprehensive characterization of CD4+ T cells in CRC.
- Open Access
- 2 July 2026
- Published by American Association for Cancer Research (AACR)
Supplementary Table S4 from NMB+CXCL13+CD4+ T Cell–Derived Neuromedin B Promotes Neuropeptide S Receptor 1–Positive Malignant Cell Senescence and Malignancy
Information of published scRNA-seq datasets used in Pan_CD4 single-cell atlas in this study.
- 2 July 2026
- Published by American Association for Cancer Research (AACR)
Open AccessSupplementary Table S4 from NMB+CXCL13+CD4+ T Cell–Derived Neuromedin B Promotes Neuropeptide S Receptor 1–Positive Malignant Cell Senescence and Malignancy
Information of published scRNA-seq datasets used in Pan_CD4 single-cell atlas in this study.
- Open Access
- 2 July 2026
- Published by American Association for Cancer Research (AACR)
Supplementary Figure S2 from NMB+CXCL13+CD4+ T Cell–Derived Neuromedin B Promotes Neuropeptide S Receptor 1–Positive Malignant Cell Senescence and Malignancy
Supplementary Figure S2. Comprehensive characterization of CD4+ T cells in Pan_cancer.
- 2 July 2026
- Published by American Association for Cancer Research (AACR)
Open AccessSupplementary Figure S2 from NMB+CXCL13+CD4+ T Cell–Derived Neuromedin B Promotes Neuropeptide S Receptor 1–Positive Malignant Cell Senescence and Malignancy
Supplementary Figure S2. Comprehensive characterization of CD4+ T cells in Pan_cancer.
- Open Access
- 2 July 2026
- Published by American Association for Cancer Research (AACR)
Supplementary Figure S8 from NMB+CXCL13+CD4+ T Cell–Derived Neuromedin B Promotes Neuropeptide S Receptor 1–Positive Malignant Cell Senescence and Malignancy
Supplementary Figure S8. NMB + CXCL13+CD4+ T cells induce tumor cell malignancy.
- 2 July 2026
- Published by American Association for Cancer Research (AACR)
Open AccessSupplementary Figure S8 from NMB+CXCL13+CD4+ T Cell–Derived Neuromedin B Promotes Neuropeptide S Receptor 1–Positive Malignant Cell Senescence and Malignancy
Supplementary Figure S8. NMB + CXCL13+CD4+ T cells induce tumor cell malignancy.
- Open Access
- 2 July 2026
- Published by American Association for Cancer Research (AACR)
Supplementary Figure S9 from NMB+CXCL13+CD4+ T Cell–Derived Neuromedin B Promotes Neuropeptide S Receptor 1–Positive Malignant Cell Senescence and Malignancy
Supplementary Figure S9. NPSR1+ senescent tumor cells recruit and disrupt endothelial cells.
- 2 July 2026
- Published by American Association for Cancer Research (AACR)
Open AccessSupplementary Figure S9 from NMB+CXCL13+CD4+ T Cell–Derived Neuromedin B Promotes Neuropeptide S Receptor 1–Positive Malignant Cell Senescence and Malignancy
Supplementary Figure S9. NPSR1+ senescent tumor cells recruit and disrupt endothelial cells.
- Open Access
- 2 July 2026
- Published by American Association for Cancer Research (AACR)
Supplementary Figure S4 from NMB+CXCL13+CD4+ T Cell–Derived Neuromedin B Promotes Neuropeptide S Receptor 1–Positive Malignant Cell Senescence and Malignancy
Supplementary Figure S4. NMB expression correlates with poor CRC patient prognosis but is independent of ICI response.
- 2 July 2026
- Published by American Association for Cancer Research (AACR)
Open AccessSupplementary Figure S4 from NMB+CXCL13+CD4+ T Cell–Derived Neuromedin B Promotes Neuropeptide S Receptor 1–Positive Malignant Cell Senescence and Malignancy
Supplementary Figure S4. NMB expression correlates with poor CRC patient prognosis but is independent of ICI response.
- Open Access
- 2 July 2026
- Published by American Association for Cancer Research (AACR)
Supplementary Table S5 from NMB+CXCL13+CD4+ T Cell–Derived Neuromedin B Promotes Neuropeptide S Receptor 1–Positive Malignant Cell Senescence and Malignancy
The specially expressed genes in each subclusters of CRC CXCL13+CD4+ T cell.
- 2 July 2026
- Published by American Association for Cancer Research (AACR)
Open AccessSupplementary Table S5 from NMB+CXCL13+CD4+ T Cell–Derived Neuromedin B Promotes Neuropeptide S Receptor 1–Positive Malignant Cell Senescence and Malignancy
The specially expressed genes in each subclusters of CRC CXCL13+CD4+ T cell.
- Open Access
- 2 July 2026
- Published by American Association for Cancer Research (AACR)
Data from NMB+CXCL13+CD4+ T Cell–Derived Neuromedin B Promotes Neuropeptide S Receptor 1–Positive Malignant Cell Senescence and Malignancy
Colorectal cancer with liver metastases remains a clinical challenge. CXCL13 is widely recognized as a biomarker of immunotherapy response. However, the functional heterogeneity (protumor vs. antitumor) of CXCL13+CD4+ T-cell subsets has long been controversial. Through integrated analysis of single-cell RNA sequencing data from colorectal cancer clinical samples and pan-cancer datasets, combined with experimental validations, we first identified a prometastatic neuromedin B+ (NMB+)CXCL13+CD4+ T-cell subset and uncovered a mechanism by which this subset regulates tumor cell “senescence-malignant transition,” the NMB–NPSR1 axis. These NMB+CXCL13+CD4+ T cells induced senescence in NPSR1+ malignant cells via NMB secretion, leading to enhanced invasiveness and migration despite reduced proliferation. Activation of NPSR1 triggered the Wnt signaling pathway and epithelial–mesenchymal transition, thereby enhancing cellular malignancy. This NPSR1+ senescent subpopulation also recruited endothelial cells and disrupted tight junction integrity, fostering a prometastatic microenvironment. As a proof-of-principle study, the combination of the NPSR1 inhibitor SHA68 and anti–PD-1 demonstrated remarkable antitumor effects using mouse models of colorectal cancer metastasis. Overall, this study uncovered the role of NMB+CXCL13+CD4+ T cells in promoting tumor cell senescence while influencing tumor metastasis, offering potential clinical implications for the diagnosis and treatment of metastatic colorectal cancer.
- 2 July 2026
- Published by American Association for Cancer Research (AACR)
Open AccessData from NMB+CXCL13+CD4+ T Cell–Derived Neuromedin B Promotes Neuropeptide S Receptor 1–Positive Malignant Cell Senescence and Malignancy
Colorectal cancer with liver metastases remains a clinical challenge. CXCL13 is widely recognized as a biomarker of immunotherapy response. However, the functional heterogeneity (protumor vs. antitumor) of CXCL13+CD4+ T-cell subsets has long been controversial. Through integrated analysis of single-cell RNA sequencing data from colorectal cancer clinical samples and pan-cancer datasets, combined with experimental validations, we first identified a prometastatic neuromedin B+ (NMB+)CXCL13+CD4+ T-cell subset and uncovered a mechanism by which this subset regulates tumor cell “senescence-malignant transition,” the NMB–NPSR1 axis. These NMB+CXCL13+CD4+ T cells induced senescence in NPSR1+ malignant cells via NMB secretion, leading to enhanced invasiveness and migration despite reduced proliferation. Activation of NPSR1 triggered the Wnt signaling pathway and epithelial–mesenchymal transition, thereby enhancing cellular malignancy. This NPSR1+ senescent subpopulation also recruited endothelial cells and disrupted tight junction integrity, fostering a prometastatic microenvironment. As a proof-of-principle study, the combination of the NPSR1 inhibitor SHA68 and anti–PD-1 demonstrated remarkable antitumor effects using mouse models of colorectal cancer metastasis. Overall, this study uncovered the role of NMB+CXCL13+CD4+ T cells in promoting tumor cell senescence while influencing tumor metastasis, offering potential clinical implications for the diagnosis and treatment of metastatic colorectal cancer.
- Open Access
- 2 July 2026
- Published by American Association for Cancer Research (AACR)
Supplementary Table S3 from NMB+CXCL13+CD4+ T Cell–Derived Neuromedin B Promotes Neuropeptide S Receptor 1–Positive Malignant Cell Senescence and Malignancy
Information of published scRNA-seq datasets used in CD4 single-cell atlas in this study.
- 2 July 2026
- Published by American Association for Cancer Research (AACR)
Open AccessSupplementary Table S3 from NMB+CXCL13+CD4+ T Cell–Derived Neuromedin B Promotes Neuropeptide S Receptor 1–Positive Malignant Cell Senescence and Malignancy
Information of published scRNA-seq datasets used in CD4 single-cell atlas in this study.