Junjie T. Hua
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View article: Genome-scale CRISPR screens identify PTGES3 as a direct modulator of androgen receptor function in advanced prostate cancer
Genome-scale CRISPR screens identify PTGES3 as a direct modulator of androgen receptor function in advanced prostate cancer Open
The androgen receptor (AR) is a critical driver of prostate cancer (PCa). Here, to study regulators of AR protein levels and oncogenic activity, we developed a live-cell quantitative endogenous AR fluorescent reporter. Leveraging this AR r…
View article: 778 CRISPR screens reveal innate immune checkpoints regulating NK cell sensitivity across solid tumors
778 CRISPR screens reveal innate immune checkpoints regulating NK cell sensitivity across solid tumors Open
View article: Lipid-Coated Mesoporous Silica Particles for pH-Sensitive Tumor-Targeted Paclitaxel: Development, Characterization
Lipid-Coated Mesoporous Silica Particles for pH-Sensitive Tumor-Targeted Paclitaxel: Development, Characterization Open
Nanoparticle carriers can selectively deliver the drug cargo to tumor cells, thus having the ability to prevent early drug release, reduce non-specific cell binding, and prolong in vivo drug retention. We constructed paclitaxel (PTX…
View article: Exploitable mechanisms of antibody and CAR mediated macrophage cytotoxicity
Exploitable mechanisms of antibody and CAR mediated macrophage cytotoxicity Open
Macrophages infiltrate solid tumors and either support survival or induce cancer cell death through phagocytosis or cytotoxicity. To uncover regulators of macrophage cytotoxicity towards cancer cells, we perform two co-culture CRISPR scree…
View article: Genome-wide CRISPR screens identify PTGES3 as a novel AR modulator
Genome-wide CRISPR screens identify PTGES3 as a novel AR modulator Open
The androgen receptor (AR) is a critical driver of prostate cancer (PCa). To study regulators of AR protein levels and oncogenic activity, we created the first live cell quantitative endogenous AR fluorescent reporters. Leveraging this nov…
View article: Supplementary Figure 7 from Androgen Receptor Inhibition Increases MHC Class I Expression and Improves Immune Response in Prostate Cancer
Supplementary Figure 7 from Androgen Receptor Inhibition Increases MHC Class I Expression and Improves Immune Response in Prostate Cancer Open
Supplementary Figure 7 is a graphical abstract of how AR regulates MHCI expression in prostate tumor cells.
View article: Supplementary Tables 1-7 from Androgen Receptor Inhibition Increases MHC Class I Expression and Improves Immune Response in Prostate Cancer
Supplementary Tables 1-7 from Androgen Receptor Inhibition Increases MHC Class I Expression and Improves Immune Response in Prostate Cancer Open
Table S1: List of top 20 significant (p< 0.05) genes from a whole-genome CRISPRi FACS-based screen which increased or decreased MHC Class I expression upon knockdown. Genes that were indicated as common essential by DepMap were removed fro…
View article: Supplementary Figure 1 from Androgen Receptor Inhibition Increases MHC Class I Expression and Improves Immune Response in Prostate Cancer
Supplementary Figure 1 from Androgen Receptor Inhibition Increases MHC Class I Expression and Improves Immune Response in Prostate Cancer Open
Supplementary Figure 1 shows sgRNA validation and MHCI protein expression on tumor cell lines.
View article: Supplementary Figure 5 from Androgen Receptor Inhibition Increases MHC Class I Expression and Improves Immune Response in Prostate Cancer
Supplementary Figure 5 from Androgen Receptor Inhibition Increases MHC Class I Expression and Improves Immune Response in Prostate Cancer Open
Supplementary Figure 5 provides in vivo validation of enhanced T cell responses and enhanced tumor control after AR knockdown.
View article: Supplementary Figure 3 from Androgen Receptor Inhibition Increases MHC Class I Expression and Improves Immune Response in Prostate Cancer
Supplementary Figure 3 from Androgen Receptor Inhibition Increases MHC Class I Expression and Improves Immune Response in Prostate Cancer Open
Supplementary Figure 3 shows validation of AR binding in MHC regulatory genes of interest +/- AR inhibition with enzalutamide.
View article: Supplementary Figure 6 from Androgen Receptor Inhibition Increases MHC Class I Expression and Improves Immune Response in Prostate Cancer
Supplementary Figure 6 from Androgen Receptor Inhibition Increases MHC Class I Expression and Improves Immune Response in Prostate Cancer Open
Supplementary Figure 6 shows clinical data analysis of neoadjuvant androgen axis inhibition in primary prostate cancer as well as expression analysis of AR, MHCI, and IFNG activity in mHSPC clinical samples.
View article: Supplementary Figure 4 from Androgen Receptor Inhibition Increases MHC Class I Expression and Improves Immune Response in Prostate Cancer
Supplementary Figure 4 from Androgen Receptor Inhibition Increases MHC Class I Expression and Improves Immune Response in Prostate Cancer Open
Supplementary Figure 4 shows a co-culture of tumor-antigen specific T cell mediated killing of tumor cells +/- AR inhibition or MHCI inhibition.
View article: Supplementary Figure 2 from Androgen Receptor Inhibition Increases MHC Class I Expression and Improves Immune Response in Prostate Cancer
Supplementary Figure 2 from Androgen Receptor Inhibition Increases MHC Class I Expression and Improves Immune Response in Prostate Cancer Open
Supplementary Figure 2 demonstrates MHC expression following pharmacologic inhibition of AR and/or ligand withdrawal.
View article: Supplementary Figure 1 from Androgen Receptor Inhibition Increases MHC Class I Expression and Improves Immune Response in Prostate Cancer
Supplementary Figure 1 from Androgen Receptor Inhibition Increases MHC Class I Expression and Improves Immune Response in Prostate Cancer Open
Supplementary Figure 1 shows sgRNA validation and MHCI protein expression on tumor cell lines.
View article: Supplementary Figure 3 from Androgen Receptor Inhibition Increases MHC Class I Expression and Improves Immune Response in Prostate Cancer
Supplementary Figure 3 from Androgen Receptor Inhibition Increases MHC Class I Expression and Improves Immune Response in Prostate Cancer Open
Supplementary Figure 3 shows validation of AR binding in MHC regulatory genes of interest +/- AR inhibition with enzalutamide.
View article: Supplementary Figure 7 from Androgen Receptor Inhibition Increases MHC Class I Expression and Improves Immune Response in Prostate Cancer
Supplementary Figure 7 from Androgen Receptor Inhibition Increases MHC Class I Expression and Improves Immune Response in Prostate Cancer Open
Supplementary Figure 7 is a graphical abstract of how AR regulates MHCI expression in prostate tumor cells.
View article: Supplementary Figure 4 from Androgen Receptor Inhibition Increases MHC Class I Expression and Improves Immune Response in Prostate Cancer
Supplementary Figure 4 from Androgen Receptor Inhibition Increases MHC Class I Expression and Improves Immune Response in Prostate Cancer Open
Supplementary Figure 4 shows a co-culture of tumor-antigen specific T cell mediated killing of tumor cells +/- AR inhibition or MHCI inhibition.
View article: Supplementary Figure 5 from Androgen Receptor Inhibition Increases MHC Class I Expression and Improves Immune Response in Prostate Cancer
Supplementary Figure 5 from Androgen Receptor Inhibition Increases MHC Class I Expression and Improves Immune Response in Prostate Cancer Open
Supplementary Figure 5 provides in vivo validation of enhanced T cell responses and enhanced tumor control after AR knockdown.
View article: Supplementary Figure 2 from Androgen Receptor Inhibition Increases MHC Class I Expression and Improves Immune Response in Prostate Cancer
Supplementary Figure 2 from Androgen Receptor Inhibition Increases MHC Class I Expression and Improves Immune Response in Prostate Cancer Open
Supplementary Figure 2 demonstrates MHC expression following pharmacologic inhibition of AR and/or ligand withdrawal.
View article: Supplementary Tables 1-7 from Androgen Receptor Inhibition Increases MHC Class I Expression and Improves Immune Response in Prostate Cancer
Supplementary Tables 1-7 from Androgen Receptor Inhibition Increases MHC Class I Expression and Improves Immune Response in Prostate Cancer Open
Table S1: List of top 20 significant (p< 0.05) genes from a whole-genome CRISPRi FACS-based screen which increased or decreased MHC Class I expression upon knockdown. Genes that were indicated as common essential by DepMap were removed fro…
View article: Supplementary Figure 6 from Androgen Receptor Inhibition Increases MHC Class I Expression and Improves Immune Response in Prostate Cancer
Supplementary Figure 6 from Androgen Receptor Inhibition Increases MHC Class I Expression and Improves Immune Response in Prostate Cancer Open
Supplementary Figure 6 shows clinical data analysis of neoadjuvant androgen axis inhibition in primary prostate cancer as well as expression analysis of AR, MHCI, and IFNG activity in mHSPC clinical samples.
View article: Data from Androgen Receptor Inhibition Increases MHC Class I Expression and Improves Immune Response in Prostate Cancer
Data from Androgen Receptor Inhibition Increases MHC Class I Expression and Improves Immune Response in Prostate Cancer Open
Tumors escape immune detection and elimination through a variety of mechanisms. Here, we used prostate cancer as a model to examine how androgen-dependent tumors undergo immune evasion through downregulation of the major histocompatibility…
View article: Androgen Receptor Inhibition Increases MHC Class I Expression and Improves Immune Response in Prostate Cancer
Androgen Receptor Inhibition Increases MHC Class I Expression and Improves Immune Response in Prostate Cancer Open
Tumors escape immune detection and elimination through a variety of mechanisms. Here, we used prostate cancer as a model to examine how androgen-dependent tumors undergo immune evasion through downregulation of the major histocompatibility…
View article: Recent advances in understanding DNA methylation of prostate cancer
Recent advances in understanding DNA methylation of prostate cancer Open
Epigenetic modifications, such as DNA methylation, is widely studied in cancer. DNA methylation patterns have been shown to distinguish between benign and malignant tumors in various cancers, including prostate cancer. It may also contribu…
View article: Supplementary Figures from LSD1-Mediated Epigenetic Reprogramming Drives CENPE Expression and Prostate Cancer Progression
Supplementary Figures from LSD1-Mediated Epigenetic Reprogramming Drives CENPE Expression and Prostate Cancer Progression Open
Figures S1-2: LSD1 reprogramming in CRPC. Figure S3: Clinical relevance of CENPE in CRPC. Figures S4-8: Regulation and Function of CENPE in CRPC. Figure S9: Inhibition of CENPE in xenograft model.
View article: Data from LSD1-Mediated Epigenetic Reprogramming Drives CENPE Expression and Prostate Cancer Progression
Data from LSD1-Mediated Epigenetic Reprogramming Drives CENPE Expression and Prostate Cancer Progression Open
Androgen receptor (AR) signaling is a key driver of prostate cancer, and androgen-deprivation therapy (ADT) is a standard treatment for patients with advanced and metastatic disease. However, patients receiving ADT eventually develop incur…
View article: Supplementary Tables from LSD1-Mediated Epigenetic Reprogramming Drives CENPE Expression and Prostate Cancer Progression
Supplementary Tables from LSD1-Mediated Epigenetic Reprogramming Drives CENPE Expression and Prostate Cancer Progression Open
Table S1: Primers and siRNA sequences used in this study. Table S2-9: GO analysis of LSD1 and CENPE target genes in LNCaP and abl Cells.
View article: Supplementary Tables from LSD1-Mediated Epigenetic Reprogramming Drives CENPE Expression and Prostate Cancer Progression
Supplementary Tables from LSD1-Mediated Epigenetic Reprogramming Drives CENPE Expression and Prostate Cancer Progression Open
Table S1: Primers and siRNA sequences used in this study. Table S2-9: GO analysis of LSD1 and CENPE target genes in LNCaP and abl Cells.
View article: Data from LSD1-Mediated Epigenetic Reprogramming Drives CENPE Expression and Prostate Cancer Progression
Data from LSD1-Mediated Epigenetic Reprogramming Drives CENPE Expression and Prostate Cancer Progression Open
Androgen receptor (AR) signaling is a key driver of prostate cancer, and androgen-deprivation therapy (ADT) is a standard treatment for patients with advanced and metastatic disease. However, patients receiving ADT eventually develop incur…
View article: Supplementary Figures from LSD1-Mediated Epigenetic Reprogramming Drives CENPE Expression and Prostate Cancer Progression
Supplementary Figures from LSD1-Mediated Epigenetic Reprogramming Drives CENPE Expression and Prostate Cancer Progression Open
Figures S1-2: LSD1 reprogramming in CRPC. Figure S3: Clinical relevance of CENPE in CRPC. Figures S4-8: Regulation and Function of CENPE in CRPC. Figure S9: Inhibition of CENPE in xenograft model.