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407 results on '"Yu, Jindan"'

7. Activation of MAPK Signaling by CXCR7 Leads to Enzalutamide Resistance in Prostate Cancer

Author

Li, Shangze, Fong, Ka-wing, Gritsina, Galina, Zhang, Ali, Zhao, Jonathan C, Kim, Jung, Sharp, Adam, Yuan, Wei, Aversa, Caterina, Yang, Ximing J, Nelson, Peter S, Feng, Felix Y, Chinnaiyan, Arul M, de Bono, Johann S, Morrissey, Colm, Rettig, Matthew B, and Yu, Jindan

Subjects
Cancer, Urologic Diseases, Aging, Prostate Cancer, 5.1 Pharmaceuticals, Development of treatments and therapeutic interventions, Animals, Antineoplastic Agents, Benzamides, Cell Division, Cell Line, Tumor, Cell Survival, Drug Resistance, Neoplasm, HEK293 Cells, Humans, MAP Kinase Signaling System, Male, Mice, Mice, Inbred BALB C, Mice, Nude, Neoplasm Invasiveness, Nitriles, Phenylthiohydantoin, Prostatic Neoplasms, Castration-Resistant, Pyridones, Pyrimidinones, Receptors, CXCR, Xenograft Model Antitumor Assays, Oncology and Carcinogenesis, Oncology & Carcinogenesis
Abstract

Castration-resistant prostate cancer (CRPC) that has developed resistance to the new-generation androgen receptor (AR) antagonist enzalutamide is a lethal disease. Transcriptome analysis of multiple prostate cancer models identified CXCR7, an atypical chemokine receptor, as one of the most upregulated genes in enzalutamide-resistant cells. AR directly repressed CXCR7 by binding to an enhancer 110 kb downstream of the gene and expression was restored upon androgen deprivation. We demonstrate that CXCR7 is a critical regulator of prostate cancer sensitivity to enzalutamide and is required for CRPC growth in vitro and in vivo. Elevated CXCR7 activated MAPK/ERK signaling through ligand-independent, but β-arrestin 2-dependent mechanisms. Examination of patient specimens showed that CXCR7 and pERK levels increased significantly from localized prostate cancer to CRPC and further upon enzalutamide resistance. Preclinical studies revealed remarkable efficacies of MAPK/ERK inhibitors in suppressing enzalutamide-resistant prostate cancer. Overall, these results indicate that CXCR7 may serve as a biomarker of resistant disease in patients with prostate cancer and that disruption of CXCR7 signaling may be an effective strategy to overcome resistance. SIGNIFICANCE: These findings identify CXCR7-mediated MAPK activation as a mechanism of resistance to second-generation antiandrogen therapy, highlighting the therapeutic potential of MAPK/ERK inhibitors in CRPC.

Published
2019

9. Genotypic and phenotypic features of 39 Chinese patients with glycogen storage diseases type I, VI, and IX.

Author

Yu, Jindan, Ling, Xiuxin, Chen, Lingli, Fang, Youhong, Lin, Haihua, Lou, Jingan, Ren, Yanqi, and Chen, Jie

Subjects
*GLYCOGEN storage disease, *PROTEIN deficiency, *GENETIC mutation, *CHINESE people, *HEARING disorders
Abstract

Glycogen storage diseases (GSDs) are abnormally inherited glycogen metabolism mainly affecting the liver, muscles, and heart. Deficiency of proteins involved in glycogen metabolism caused by genetic mutations are responsible for different subtype of GSDs. However, there are still some challenges in diagnosing GSD. This study includes 39 suspected GSDs patients from unrelated families in China. Next‐generation sequencing (NGS) was used to investigate the reason for their diseases at the genetic level. Finally, all 39 patients were diagnosed with GSDs, including 20 GSD‐Ia, 4 GSD‐VI, and 15 GSD IX (12 GSD‐IXa patients and 3 GSD‐IXb patients). Thirty‐two mutations in G6PC1, PYGL, PHKA2, and PHKB genes were identified, with 14 of them being novel variants. The pathogenicity of novel variants was classified according to ACMG guildlines and predicted by in slico algorithms. Mutations p.L216L and p.R83H in G6PC1 gene may be the hot spot mutation in Chinese. Hearing impairment is a rare clinical feature of GSD Ia, which has also been observed in our cohort. The severity of GSD VI and IX was indicated by our patients. Close follow‐up should be applied to GSD VI and IX patients. Our findings provided evidence for building the phenotype–genotype of GSDs and expanded the mutation spectrum of related genes. [ABSTRACT FROM AUTHOR]

Published
2024
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12. Ferroptosis: the vulnerability within a cancer monster

Author

Xie, Wanqing, Agarwal, Shivani, and Yu, Jindan

Subjects
Health care industry
Abstract

Treatment-resistant cancer, such as neuroendocrine prostate cancer (NEPC), is a lethal disease with limited therapeutic options. RB1 is a tumor suppressor gene that is lost in a majority of NEPC tumors. In this issue of the JCI, Wang and colleagues examined how RB1 loss may sensitize cancer cells to ferroptosis inducers through elevation of ACSL4, a key enzyme that promotes lipid peroxidation and triggers ferroptosis. We discuss a high potential of RBI-deficient cells to undergo ferroptosis due to the elevation of ACSL4. This is normally kept in check by abundant expression of GPX4, an antioxidant enzyme, in cancer cells. This balance, however, is tilted by GPX4 inhibitors, leading to massive ferroptosis. We highlight possible therapeutic strategies that exploit this inherent vulnerability for targeting RBI-deficient, treatment-resistant cancer., Emerging roles of ferroptosis in cancer and treatment resistance Ferroptosis is a recently identified, iron-dependent form of programmed cell death that is distinct from other cell death pathways, such as [...]

Published
2023
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14. Myeloid differentiation factor-2/LY96, a potential predictive biomarker of metastasis and poor outcomes in prostate cancer: clinical implications as a potential therapeutic target

Author

Ferrari, Marina G., primary, Jimenez-Uribe, Alexis P., additional, Wang, Li, additional, Hoeppner, Luke H., additional, Murugan, Paari, additional, Hahm, Eunsil, additional, Yu, Jindan, additional, Kuzel, Timothy M., additional, Gradilone, Sergio A., additional, and Mansini, Adrian P., additional

Published
2023
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20. N-Myc-mediated epigenetic reprogramming drives lineage plasticity in advanced prostate cancer

Author

Berger, Adeline, Brady, Nicholas J., Bareja, Rohan, Robinson, Brian, Conteduca, Vincenza, Augello, Michael A., Puca, Loredana, Ahmed, Adnan, Dardenne, Etienne, Lu, Xiaodong, Hwang, Inah, Bagadion, Alyssa M., Sboner, Andrea, Elemento, Olivier, Paik, Jihye, Yu, Jindan, Barbieri, Christopher E., Dephoure, Noah, Beltran, Himisha, and Rickman, David S.

Subjects
Thermo Fisher Scientific Inc., Epigenetic inheritance -- Analysis -- Health aspects, Genes -- Analysis -- Health aspects, Prostate cancer -- Development and progression -- Prognosis -- Analysis -- Health aspects, Scientific equipment industry -- Analysis -- Health aspects, Death, Androgens, Tumors, Health care industry
Abstract

Despite recent therapeutic advances, prostate cancer remains a leading cause of cancer-related death. A subset of castration-resistant prostate cancers become androgen receptor (AR) signaling independent and develop neuroendocrine prostate cancer (NEPC) features through lineage plasticity. These NEPC tumors, associated with aggressive disease and poor prognosis, are driven, in part, by aberrant expression of N-Myc, through mechanisms that remain unclear. Integrative analysis of the N-Myc transcriptome, cistrome, and interactome using in vivo, in vitro, and ex vivo models (including patient-derived organoids) identified a lineage switch towards a neural identity associated with epigenetic reprogramming. N-Myc and known AR cofactors (e.g., FOXA1 and HOXB13) overlapped, independently of AR, at genomic loci implicated in neural lineage specification. Moreover, histone marks specifically associated with lineage- defining genes were reprogrammed by N-Myc. We also demonstrated that the N-Myc-induced molecular program accurately classifies our cohort of patients with advanced prostate cancer. Finally, we revealed the potential for enhancer of zeste homolog 2 (EZH2) inhibition to reverse the N-Myc-induced suppression of epithelial lineage genes. Altogether, our data provide insights into how N-Myc regulates lineage plasticity and epigenetic reprogramming associated with lineage specification. The N-Myc signature we defined could also help predict the evolution of prostate cancer and thus better guide the choice of future therapeutic strategies., Introduction Lineage plasticity, a process by which differentiated cells lose their identity and acquire an alternative lineage program, has recently been identified as an emerging mechanism of resistance to targeted [...]

Published
2019
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21. Targeting FOXAI-mediated repression of TGF-[beta] signaling suppresses castration-resistant prostate cancer progression

Author

Song, Bing, Park, Su-Hong, Zhao, Jonathan C., Fong, Ka-Wing, Li, Shangze, Lee, Yongik, Yang, Yeqing A., Sridhar, Subhasree, Lu, Xiaodong, Abdulkadir, Sarki A., Vessella, Robert L., Morrissey, Colm, Kuzel, Timothy M., Catalona, William, Yang, Ximing, and Yu, Jindan

Subjects
Cellular signal transduction -- Research, Drug resistance -- Research, Enzalutamide -- Dosage and administration, Prostate cancer -- Development and progression -- Drug therapy, Transforming growth factors -- Research, Antiandrogens, DNA microarrays, Bone morphogenetic proteins, Occupancy, Stem cells, Tumors, Genes, Cancer metastasis, Transcription (Genetics), B cells, Health care industry
Abstract

Prostate cancer (PC) progressed to castration resistance (CRPC) is a fatal disease. CRPC tumors develop resistance to new-generation antiandrogen enzalutamide through lineage plasticity, characterized by epithelial-mesenchymal transition (EMT) and a basal-like phenotype. FOXA1 is a transcription factor essential for epithelial lineage differentiation. Here, we demonstrate that FOXA1 loss leads to remarkable upregulation of transforming growth factor beta 3 (TGFB3), which encodes a ligand of the TGF-[beta] pathway. Mechanistically, this is due to genomic occupancy of FOXA1 on an upstream enhancer of the TGFB3 gene to directly inhibit its transcription. Functionally, FOXA1 downregulation induces TGF-[beta] signaling, EMT, and cell motility, which is effectively blocked by the TGF-[beta] receptor I inhibitor galunisertib (LY2157299). Tissue microarray analysis confirmed reduced levels of FOXA1 protein and a concordant increase in TGF-[beta] signaling, indicated by SMAD2 phosphorylation, in CRPC as compared with primary tumors. Importantly, combinatorial LY2157299 treatment sensitized PC cells to enzalutamide, leading to synergistic effects in inhibiting cell invasion in vitro and xenograft CRPC tumor growth and metastasis in vivo. Therefore, our study establishes FOXA1 as an important regulator of lineage plasticity mediated in part by TGF-[beta] signaling, and supports a novel therapeutic strategy to control lineage switching and potentially extend clinical response to antiandrogen therapies., Introduction Prostate cancer (PC) is the third leading cause of cancer-related death among men in the United States, where 1 in 8 men are expected to be diagnosed with PC [...]

Published
2019
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22. Chemokine receptor CXCR7 activates Aurora Kinase A and promotes neuroendocrine prostate cancer growth

Author

Gritsina, Galina, primary, Fong, Ka-wing, additional, Lu, Xiaodong, additional, Lin, Zhuoyuan, additional, Xie, Wanqing, additional, Agarwal, Shivani, additional, Lin, Dong, additional, Schiltz, Gary E., additional, Beltran, Himisha, additional, Corey, Eva, additional, Morrissey, Colm, additional, Wang, Yuzhuo, additional, Zhao, Jonathan C., additional, Hussain, Maha, additional, and Yu, Jindan, additional

Published
2023
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28. Data from Activation of MAPK Signaling by CXCR7 Leads to Enzalutamide Resistance in Prostate Cancer

Author

Li, Shangze, primary, Fong, Ka-wing, primary, Gritsina, Galina, primary, Zhang, Ali, primary, Zhao, Jonathan C., primary, Kim, Jung, primary, Sharp, Adam, primary, Yuan, Wei, primary, Aversa, Caterina, primary, Yang, Ximing J., primary, Nelson, Peter S., primary, Feng, Felix Y., primary, Chinnaiyan, Arul M., primary, de Bono, Johann S., primary, Morrissey, Colm, primary, Rettig, Matthew B., primary, and Yu, Jindan, primary

Published
2023
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29. Supplementary Table from A Genome-Wide CRISPR Activation Screen Identifies PRRX2 as a Regulator of Enzalutamide Resistance in Prostate Cancer

Author

Rodríguez, Yara, primary, Unno, Kenji, primary, Truica, Mihai I., primary, Chalmers, Zachary R., primary, Yoo, Young A., primary, Vatapalli, Rajita, primary, Sagar, Vinay, primary, Yu, Jindan, primary, Lysy, Barbara, primary, Hussain, Maha, primary, Han, Huiying, primary, and Abdulkadir, Sarki A., primary

Published
2023
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30. Supplementary Data from Activation of MAPK Signaling by CXCR7 Leads to Enzalutamide Resistance in Prostate Cancer

Author

Li, Shangze, primary, Fong, Ka-wing, primary, Gritsina, Galina, primary, Zhang, Ali, primary, Zhao, Jonathan C., primary, Kim, Jung, primary, Sharp, Adam, primary, Yuan, Wei, primary, Aversa, Caterina, primary, Yang, Ximing J., primary, Nelson, Peter S., primary, Feng, Felix Y., primary, Chinnaiyan, Arul M., primary, de Bono, Johann S., primary, Morrissey, Colm, primary, Rettig, Matthew B., primary, and Yu, Jindan, primary

Published
2023
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32. Supplementary Data from A Genome-Wide CRISPR Activation Screen Identifies PRRX2 as a Regulator of Enzalutamide Resistance in Prostate Cancer

Author

Rodríguez, Yara, primary, Unno, Kenji, primary, Truica, Mihai I., primary, Chalmers, Zachary R., primary, Yoo, Young A., primary, Vatapalli, Rajita, primary, Sagar, Vinay, primary, Yu, Jindan, primary, Lysy, Barbara, primary, Hussain, Maha, primary, Han, Huiying, primary, and Abdulkadir, Sarki A., primary

Published
2023
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33. Supplementary Table 5 from Autoantibody Profiles Reveal Ubiquilin 1 as a Humoral Immune Response Target in Lung Adenocarcinoma

Author

Chen, Guoan, primary, Wang, Xiaoju, primary, Yu, Jianjun, primary, Varambally, Sooryanarayana, primary, Yu, Jindan, primary, Thomas, Dafydd G., primary, Lin, Mu-Yen, primary, Vishnu, Prakash, primary, Wang, Zhuwen, primary, Wang, Rui, primary, Fielhauer, Jeff, primary, Ghosh, Debashis, primary, Giordano, Thomas J., primary, Giacherio, Donald, primary, Chang, Andrew C., primary, Orringer, Mark B., primary, El-Hefnawy, Talal, primary, Bigbee, William L., primary, Beer, David G., primary, and Chinnaiyan, Arul M., primary

Published
2023
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36. Supplementary Data, Methods, Figures 1-5, Tables 1-5 from A Polycomb Repression Signature in Metastatic Prostate Cancer Predicts Cancer Outcome

Author

Yu, Jindan, primary, Yu, Jianjun, primary, Rhodes, Daniel R., primary, Tomlins, Scott A., primary, Cao, Xuhong, primary, Chen, Guoan, primary, Mehra, Rohit, primary, Wang, Xiaoju, primary, Ghosh, Debashis, primary, Shah, Rajal B., primary, Varambally, Sooryanarayana, primary, Pienta, Kenneth J., primary, and Chinnaiyan, Arul M., primary

Published
2023
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37. Supplementary Data from Autoantibody Profiles Reveal Ubiquilin 1 as a Humoral Immune Response Target in Lung Adenocarcinoma

Author

Chen, Guoan, primary, Wang, Xiaoju, primary, Yu, Jianjun, primary, Varambally, Sooryanarayana, primary, Yu, Jindan, primary, Thomas, Dafydd G., primary, Lin, Mu-Yen, primary, Vishnu, Prakash, primary, Wang, Zhuwen, primary, Wang, Rui, primary, Fielhauer, Jeff, primary, Ghosh, Debashis, primary, Giordano, Thomas J., primary, Giacherio, Donald, primary, Chang, Andrew C., primary, Orringer, Mark B., primary, El-Hefnawy, Talal, primary, Bigbee, William L., primary, Beer, David G., primary, and Chinnaiyan, Arul M., primary

Published
2023
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38. Data from A Fluorescence In situ Hybridization Screen for E26 Transformation–Specific Aberrations: Identification of DDX5-ETV4 Fusion Protein in Prostate Cancer

Author

Han, Bo, primary, Mehra, Rohit, primary, Dhanasekaran, Saravana M., primary, Yu, Jindan, primary, Menon, Anjana, primary, Lonigro, Robert J., primary, Wang, Xiaosong, primary, Gong, Yusong, primary, Wang, Lei, primary, Shankar, Sunita, primary, Laxman, Bharathi, primary, Shah, Rajal B., primary, Varambally, Sooryanarayana, primary, Palanisamy, Nallasivam, primary, Tomlins, Scott A., primary, Kumar-Sinha, Chandan, primary, and Chinnaiyan, Arul M., primary

Published
2023
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40. Supplementary Table 1, Figures 1-3 from A Fluorescence In situ Hybridization Screen for E26 Transformation–Specific Aberrations: Identification of DDX5-ETV4 Fusion Protein in Prostate Cancer

Author

Han, Bo, primary, Mehra, Rohit, primary, Dhanasekaran, Saravana M., primary, Yu, Jindan, primary, Menon, Anjana, primary, Lonigro, Robert J., primary, Wang, Xiaosong, primary, Gong, Yusong, primary, Wang, Lei, primary, Shankar, Sunita, primary, Laxman, Bharathi, primary, Shah, Rajal B., primary, Varambally, Sooryanarayana, primary, Palanisamy, Nallasivam, primary, Tomlins, Scott A., primary, Kumar-Sinha, Chandan, primary, and Chinnaiyan, Arul M., primary

Published
2023
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43. Supplementary Methods, Tables 1-2, Figures 1-6 from Definition of a FoxA1 Cistrome That Is Crucial for G1 to S-Phase Cell-Cycle Transit in Castration-Resistant Prostate Cancer

Author

Zhang, Chunpeng, primary, Wang, Liguo, primary, Wu, Dayong, primary, Chen, Hongyan, primary, Chen, Zhong, primary, Thomas-Ahner, Jennifer M., primary, Zynger, Debra L., primary, Eeckhoute, Jérôme, primary, Yu, Jindan, primary, Luo, Jun, primary, Brown, Myles, primary, Clinton, Steven K., primary, Nephew, Kenneth P., primary, Huang, Tim H.-M., primary, Li, Wei, primary, and Wang, Qianben, primary

Published
2023
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49. Data from Autoantibody Profiles Reveal Ubiquilin 1 as a Humoral Immune Response Target in Lung Adenocarcinoma

Author

Chen, Guoan, primary, Wang, Xiaoju, primary, Yu, Jianjun, primary, Varambally, Sooryanarayana, primary, Yu, Jindan, primary, Thomas, Dafydd G., primary, Lin, Mu-Yen, primary, Vishnu, Prakash, primary, Wang, Zhuwen, primary, Wang, Rui, primary, Fielhauer, Jeff, primary, Ghosh, Debashis, primary, Giordano, Thomas J., primary, Giacherio, Donald, primary, Chang, Andrew C., primary, Orringer, Mark B., primary, El-Hefnawy, Talal, primary, Bigbee, William L., primary, Beer, David G., primary, and Chinnaiyan, Arul M., primary

Published
2023
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50. Data from Definition of a FoxA1 Cistrome That Is Crucial for G1 to S-Phase Cell-Cycle Transit in Castration-Resistant Prostate Cancer

Author

Zhang, Chunpeng, primary, Wang, Liguo, primary, Wu, Dayong, primary, Chen, Hongyan, primary, Chen, Zhong, primary, Thomas-Ahner, Jennifer M., primary, Zynger, Debra L., primary, Eeckhoute, Jérôme, primary, Yu, Jindan, primary, Luo, Jun, primary, Brown, Myles, primary, Clinton, Steven K., primary, Nephew, Kenneth P., primary, Huang, Tim H.-M., primary, Li, Wei, primary, and Wang, Qianben, primary

Published
2023
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