Huinian Zhou
Current Organizations / Institutes
The organizations/institutes from the scholar's latest article
Research Subjects
Huinian Zhou has a total of 60 co-authors. Here are the top co-authors by number of shared publications:
- Long Qin
Cuiying Biomedical Research Center, The Second Hospital & Clinical Medical School, Lanzhou University, Lanzhou, People’s Republic of China
23 shared publications - Wengui Shi
Cuiying Biomedical Research Center, The Second Hospital & Clinical Medical School, Lanzhou University, Lanzhou, People’s Republic of China
23 shared publications - Zuoyi Jiao
Gansu Provincial Center for Basic Research in Cancer Immunology, Lanzhou University, Lanzhou, People’s Republic of China
23 shared publications - Xiangyan Jiang
Department of General Surgery, Lanzhou University Second Hospital, Lanzhou, Gansu, China
22 shared publications - Zeyuan Yu
Department of General Surgery, Lanzhou University Second Hospital, Lanzhou, Gansu, China
22 shared publications - Yuman Dong
Cuiying Biomedical Research Center, The Second Hospital & Clinical Medical School, Lanzhou University, Lanzhou, People’s Republic of China
19 shared publications
Latest Publications
- Open Access
- 17 June 2026
- Published by American Association for Cancer Research (AACR)
Supplementary Data from Targeting SHCBP1 Inhibits Tumor Progression by Restoring Ciliogenesis in Ductal Carcinoma
Supplementary Figures and Tables
- 17 June 2026
- Published by American Association for Cancer Research (AACR)
Open AccessSupplementary Data from Targeting SHCBP1 Inhibits Tumor Progression by Restoring Ciliogenesis in Ductal Carcinoma
Supplementary Figures and Tables
- Open Access
- 17 June 2026
- Published by American Association for Cancer Research (AACR)
Data from Targeting SHCBP1 Inhibits Tumor Progression by Restoring Ciliogenesis in Ductal Carcinoma
Primary cilia detect and transmit environmental signals into cells. Primary cilia are absent in a subset of ductal carcinomas characterized by distinctive biological activities, and recovery of cilia with normal functionality has been shown to have therapeutic potential in some cancer types. Therefore, elucidation of the underlying mechanism and clinical significance of ciliary loss in ductal carcinomas could help develop effective treatment strategies. Here, we identified a link between Shc1-binding protein (SHCBP1) and cilia in ductal carcinomas. Shcbp1 knockout in transgenic mice profoundly impeded tumor progression and metastasis, prolonging survival. Single-cell transcriptome analysis revealed a functional connection between SHCBP1 deficiency and increased tumor ciliogenesis. SHCBP1 ablation restored ciliogenesis in unciliated ductal carcinoma by promoting the proximity between the midbody remnant (MBR) and centrosome through enhanced Rab8 GTPase activity and Rab8GTP positioning within the MBR. Inhibition of tumor progression by SHCBP1 loss relied on the recovery of ciliogenesis. Analysis of a large cohort of patients with ductal carcinoma revealed a negative correlation between SHCBP1-induced ciliary loss and patient prognosis. Restoring ciliogenesis via SHCBP1 ablation elicited therapeutic effects in patient-derived xenograft models. Together, this study delineates that induction of MBR-centrosome proximity through SHCBP1-deficiency reactivates ciliogenesis, offering unique opportunities for the treatment of unciliated ductal carcinomas.Significance:SHCBP1 depletion rescues tumor ciliogenesis by enhancing Rab8 GTPase activity to restore the proximity of the midbody remnant to the centrosome, which impedes progression of ductal carcinomas and suggests potential therapeutic strategies.
- 17 June 2026
- Published by American Association for Cancer Research (AACR)
Open AccessData from Targeting SHCBP1 Inhibits Tumor Progression by Restoring Ciliogenesis in Ductal Carcinoma
Primary cilia detect and transmit environmental signals into cells. Primary cilia are absent in a subset of ductal carcinomas characterized by distinctive biological activities, and recovery of cilia with normal functionality has been shown to have therapeutic potential in some cancer types. Therefore, elucidation of the underlying mechanism and clinical significance of ciliary loss in ductal carcinomas could help develop effective treatment strategies. Here, we identified a link between Shc1-binding protein (SHCBP1) and cilia in ductal carcinomas. Shcbp1 knockout in transgenic mice profoundly impeded tumor progression and metastasis, prolonging survival. Single-cell transcriptome analysis revealed a functional connection between SHCBP1 deficiency and increased tumor ciliogenesis. SHCBP1 ablation restored ciliogenesis in unciliated ductal carcinoma by promoting the proximity between the midbody remnant (MBR) and centrosome through enhanced Rab8 GTPase activity and Rab8GTP positioning within the MBR. Inhibition of tumor progression by SHCBP1 loss relied on the recovery of ciliogenesis. Analysis of a large cohort of patients with ductal carcinoma revealed a negative correlation between SHCBP1-induced ciliary loss and patient prognosis. Restoring ciliogenesis via SHCBP1 ablation elicited therapeutic effects in patient-derived xenograft models. Together, this study delineates that induction of MBR-centrosome proximity through SHCBP1-deficiency reactivates ciliogenesis, offering unique opportunities for the treatment of unciliated ductal carcinomas.Significance:SHCBP1 depletion rescues tumor ciliogenesis by enhancing Rab8 GTPase activity to restore the proximity of the midbody remnant to the centrosome, which impedes progression of ductal carcinomas and suggests potential therapeutic strategies.
- Open Access
- 2 February 2026
- Published by American Association for Cancer Research (AACR)
Supplementary Figure 8 from USP20-Driven Cholesterol Metabolism Links Inflammatory Signaling to Malignancy and Stromal Coevolution in Pancreatic Cancer
USP20 deletion suppresses PDAC progression
- 2 February 2026
- Published by American Association for Cancer Research (AACR)
Open AccessSupplementary Figure 8 from USP20-Driven Cholesterol Metabolism Links Inflammatory Signaling to Malignancy and Stromal Coevolution in Pancreatic Cancer
USP20 deletion suppresses PDAC progression
- Open Access
- 2 February 2026
- Published by American Association for Cancer Research (AACR)
Supplementary Figure 11 from USP20-Driven Cholesterol Metabolism Links Inflammatory Signaling to Malignancy and Stromal Coevolution in Pancreatic Cancer
GSK2643943A enhances cadonilimab efficacy in PDXs
- 2 February 2026
- Published by American Association for Cancer Research (AACR)
Open AccessSupplementary Figure 11 from USP20-Driven Cholesterol Metabolism Links Inflammatory Signaling to Malignancy and Stromal Coevolution in Pancreatic Cancer
GSK2643943A enhances cadonilimab efficacy in PDXs
- Open Access
- 2 February 2026
- Published by American Association for Cancer Research (AACR)
Supplementary Figure 2 from USP20-Driven Cholesterol Metabolism Links Inflammatory Signaling to Malignancy and Stromal Coevolution in Pancreatic Cancer
Inflammation promotes ECM-like characteristics of malignant cells and communication with CAFs
- 2 February 2026
- Published by American Association for Cancer Research (AACR)
Open AccessSupplementary Figure 2 from USP20-Driven Cholesterol Metabolism Links Inflammatory Signaling to Malignancy and Stromal Coevolution in Pancreatic Cancer
Inflammation promotes ECM-like characteristics of malignant cells and communication with CAFs
- Open Access
- 2 February 2026
- Published by American Association for Cancer Research (AACR)
Supplementary Figure 6 from USP20-Driven Cholesterol Metabolism Links Inflammatory Signaling to Malignancy and Stromal Coevolution in Pancreatic Cancer
Simvastatin suppresses PDAC progression
- 2 February 2026
- Published by American Association for Cancer Research (AACR)
Open AccessSupplementary Figure 6 from USP20-Driven Cholesterol Metabolism Links Inflammatory Signaling to Malignancy and Stromal Coevolution in Pancreatic Cancer
Simvastatin suppresses PDAC progression
- Open Access
- 2 February 2026
- Published by American Association for Cancer Research (AACR)
Supplementary Figure 4 from USP20-Driven Cholesterol Metabolism Links Inflammatory Signaling to Malignancy and Stromal Coevolution in Pancreatic Cancer
CP organoids exhibit more proliferation ability, ECM-like characteristics and activation of inflammatory signaling
- 2 February 2026
- Published by American Association for Cancer Research (AACR)
Open AccessSupplementary Figure 4 from USP20-Driven Cholesterol Metabolism Links Inflammatory Signaling to Malignancy and Stromal Coevolution in Pancreatic Cancer
CP organoids exhibit more proliferation ability, ECM-like characteristics and activation of inflammatory signaling
- Open Access
- 2 February 2026
- Published by American Association for Cancer Research (AACR)
Supplementary Figure 5 from USP20-Driven Cholesterol Metabolism Links Inflammatory Signaling to Malignancy and Stromal Coevolution in Pancreatic Cancer
Simvastatin inhibits CAF activation by suppressing YAP/TAZ signaling in cancer cells
- 2 February 2026
- Published by American Association for Cancer Research (AACR)
Open AccessSupplementary Figure 5 from USP20-Driven Cholesterol Metabolism Links Inflammatory Signaling to Malignancy and Stromal Coevolution in Pancreatic Cancer
Simvastatin inhibits CAF activation by suppressing YAP/TAZ signaling in cancer cells
- Open Access
- 2 February 2026
- Published by American Association for Cancer Research (AACR)
Supplementary Table 1 from USP20-Driven Cholesterol Metabolism Links Inflammatory Signaling to Malignancy and Stromal Coevolution in Pancreatic Cancer
Correlation between USP20 level and age, sex, tumor diameter, AJCC (American Joint Committee on Cancer) stage, differentiation degree, and CA19-9 value
- 2 February 2026
- Published by American Association for Cancer Research (AACR)
Open AccessSupplementary Table 1 from USP20-Driven Cholesterol Metabolism Links Inflammatory Signaling to Malignancy and Stromal Coevolution in Pancreatic Cancer
Correlation between USP20 level and age, sex, tumor diameter, AJCC (American Joint Committee on Cancer) stage, differentiation degree, and CA19-9 value
- Open Access
- 2 February 2026
- Published by American Association for Cancer Research (AACR)
Supplementary Figure 3 from USP20-Driven Cholesterol Metabolism Links Inflammatory Signaling to Malignancy and Stromal Coevolution in Pancreatic Cancer
TNFSF13B-positive macrophages promote tumor cell inflammatory signaling
- 2 February 2026
- Published by American Association for Cancer Research (AACR)
Open AccessSupplementary Figure 3 from USP20-Driven Cholesterol Metabolism Links Inflammatory Signaling to Malignancy and Stromal Coevolution in Pancreatic Cancer
TNFSF13B-positive macrophages promote tumor cell inflammatory signaling