A5101692044- Prostate Cancer Treatment and Research
- Cancer, Stress, Anesthesia, and Immune Response
- Epigenetics and DNA Methylation
- Ferroptosis and cancer prognosis
- Nanoplatforms for cancer theranostics
- Cancer Immunotherapy and Biomarkers
- Genetics, Bioinformatics, and Biomedical Research
- Cancer Cells and Metastasis
- PARP inhibition in cancer therapy
- Lung Cancer Research Studies
- RNA modifications and cancer
- Biological Research and Disease Studies
- Cancer-related gene regulation
- Cancer Research and Treatments
- Renal cell carcinoma treatment
- Fluorine in Organic Chemistry
- DNA Repair Mechanisms
- Renal and related cancers
- Histone Deacetylase Inhibitors Research
- Genomics and Chromatin Dynamics
- Immune cells in cancer
- Ubiquitin and proteasome pathways
Second Military Medical University
2017-2023
General Hospital of Guangzhou Military Command
2023
Shanghai Pudong New Area Gongli Hospital
2023
81th Hospital of PLA
2023
Eastern Hepatobiliary Surgery Hospital
2021
Changhai Hospital
2017-2019
The University of Texas MD Anderson Cancer Center
2015-2018
Purpose: Cancer stem-like cells (CSC) contribute to the progression and androgen deprivation therapy (ADT) resistance of prostate cancer. As CSCs depend on their specific niche, including tumor-associated macrophages (TAM), elucidating network between TAMs may help effectively inhibit ADT cancer.Experimental Design: The underlying intracellular mechanism that sustains characteristics in cancer was assessed via RNA sequencing, co-immunoprecipitation, chromatin immunoprecipitation, other...
Purpose: Androgen deprivation therapy (ADT), including enzalutamide, induces resistance in prostate cancer; ADT is associated with neuroendocrine differentiation (NED) and tumor-associated macrophages (TAM). This study aimed to investigate the association between enzalutamide-induced NED TAMs its mechanism.Experimental Design: The was investigated by IHC using cancer tissues, enzalutamide-resistant mouse xenografts, a coculture system. underlying mechanisms were assessed vitro cytokine...
Increasing evidence reveals that the interaction between tumor cells and tumor-associated macrophages (TAMs) facilitates progression of prostate cancer, but related mechanisms remained unclear. This study determined how gankyrin, a component 19S regulatory complex 26S proteasome, regulates androgen deprivation therapy (ADT) resistance cancer through cell-TAM interactions. In vitro functional experiments in vivo subcutaneous models were used to explore biological role molecular gankyrin 234...
Metastasis accounts for 90% of deaths caused by solid tumors, but the multitude mechanisms underlying tumor metastasis remains poorly understood. CARMIL1 and 2 proteins are capping protein (CP) interactants multidomain regulators actin-based mobility. However, CARMIL3's function has not been explored. Through bioinformatic metadata analysis, we find that high CARMIL3 expression correlates with poor survival patients breast prostate cancer. Functional studies in murine xenograft models...
Although many intratumoral biomarkers have been reported to predict clear cell renal carcinoma (ccRCC) patient prognosis, combining and clinical indicators could ccRCC prognosis more accurately than any of these markers alone. This study mainly examined the prognostic value HECT, C2 WW domain-containing E3 ubiquitin protein ligase 1 (HECW1) expression in patients combination with established indicators.The level HECW1 was screened out by data-independent acquisition mass spectrometry...
<p>Supplementary Figures S1-S5. NPRL2/TUSC4 up-regulation doesn't correlate with patient survival (S1); Microarray analysis of knockdown cells (S2); The expression NPRL2/TUSC4-deficient genes are correlated canonical pathways changes (S3); Histogram cell cycle distribution for control and NPRL2/TUSC4-deficiency (S4); Colony formation assay overexpression (S5).</p>
<p>Supplementary Figures S1-S5. NPRL2/TUSC4 up-regulation doesn't correlate with patient survival (S1); Microarray analysis of knockdown cells (S2); The expression NPRL2/TUSC4-deficient genes are correlated canonical pathways changes (S3); Histogram cell cycle distribution for control and NPRL2/TUSC4-deficiency (S4); Colony formation assay overexpression (S5).</p>
<p>Supplementary Figures and Legends (S1-S6)</p>
<p>Supplementary Figures and Figure Legends</p>
<div>Abstract<p><b>Purpose:</b> Androgen deprivation therapy (ADT), including enzalutamide, induces resistance in prostate cancer; ADT is associated with neuroendocrine differentiation (NED) and tumor-associated macrophages (TAM). This study aimed to investigate the association between enzalutamide-induced NED TAMs its mechanism.</p><p><b>Experimental Design:</b> The was investigated by IHC using cancer tissues, enzalutamide-resistant mouse...
<div>Abstract<p><b>Purpose:</b> Cancer stem-like cells (CSC) contribute to the progression and androgen deprivation therapy (ADT) resistance of prostate cancer. As CSCs depend on their specific niche, including tumor-associated macrophages (TAM), elucidating network between TAMs may help effectively inhibit ADT cancer.</p><p><b>Experimental Design:</b> The underlying intracellular mechanism that sustains characteristics in cancer was assessed...
<div>Abstract<p><b>Purpose:</b> Androgen deprivation therapy (ADT), including enzalutamide, induces resistance in prostate cancer; ADT is associated with neuroendocrine differentiation (NED) and tumor-associated macrophages (TAM). This study aimed to investigate the association between enzalutamide-induced NED TAMs its mechanism.</p><p><b>Experimental Design:</b> The was investigated by IHC using cancer tissues, enzalutamide-resistant mouse...
<div>Abstract<p><b>Purpose:</b> Cancer stem-like cells (CSC) contribute to the progression and androgen deprivation therapy (ADT) resistance of prostate cancer. As CSCs depend on their specific niche, including tumor-associated macrophages (TAM), elucidating network between TAMs may help effectively inhibit ADT cancer.</p><p><b>Experimental Design:</b> The underlying intracellular mechanism that sustains characteristics in cancer was assessed...
<p>Supplementary Figures and Legends (S1-S6)</p>
<p>Supplementary Figures and Figure Legends</p>
<p>Supplementary Figure 1, CARIML3 expression is upregulated among various types of cancer. Related to 1. A. CARMIL3 copy number variance (CNV) level across cancer in TCGA. B. mRNA (RNA-Seq) different samples compared with their normal counterpart C. Analysis (RNA-seq) TCGA-BRCA cohort grouped by major subclasses (with TNBC). D. Immunohistochemistry (IHC) staining image breast patient sample (ID: 2565). The was from Human Protein Atlas (HPA) database. E. analysis prostate patients,...
<p>Supplementary Figure 1, CARIML3 expression is upregulated among various types of cancer. Related to 1. A. CARMIL3 copy number variance (CNV) level across cancer in TCGA. B. mRNA (RNA-Seq) different samples compared with their normal counterpart C. Analysis (RNA-seq) TCGA-BRCA cohort grouped by major subclasses (with TNBC). D. Immunohistochemistry (IHC) staining image breast patient sample (ID: 2565). The was from Human Protein Atlas (HPA) database. E. analysis prostate patients,...