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147 results on '"Gao, Allen C."'

1. Proteostasis perturbation of N-Myc leveraging HSP70 mediated protein turnover improves treatment of neuroendocrine prostate cancer

Author

Xu, Pengfei, Yang, Joy C., Chen, Bo, Ning, Shu, Zhang, Xiong, Wang, Leyi, Nip, Christopher, Shen, Yuqiu, Johnson, Oleta T., Grigorean, Gabriela, Phinney, Brett, Liu, Liangren, Wei, Qiang, Corey, Eva, Tepper, Clifford G., Chen, Hong-Wu, Evans, Christopher P., Dall’Era, Marc A., Gao, Allen C., Gestwicki, Jason E., and Liu, Chengfei

Published
2024
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11. MEK-ERK signaling is a therapeutic target in metastatic castration resistant prostate cancer

Author

Nickols, Nicholas G., Nazarian, Ramin, Zhao, Shuang G., Tan, Victor, Uzunangelov, Vladislav, Xia, Zheng, Baertsch, Robert, Neeman, Elad, Gao, Allen C., Thomas, George V., Howard, Lauren, De Hoedt, Amanda M., Stuart, Josh, Goldstein, Theodore, Chi, Kim, Gleave, Martin E., Graff, Julie N., Beer, Tomasz M., Drake, Justin M., Evans, Christopher P., Aggarwal, Rahul, Foye, Adam, Feng, Felix Y., Small, Eric J., Aronson, William J., Freedland, Stephen J., Witte, Owen N., Huang, Jiaoti, Alumkal, Joshi J., Reiter, Robert E., and Rettig, Matthew B.

Published
2019
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13. KDM8/JMJD5 as a dual coactivator of AR and PKM2 integrates AR/EZH2 network and tumor metabolism in CRPC

Author

Wang, Hung-Jung, Pochampalli, Mamata, Wang, Ling-Yu, Zou, June X, Li, Pei-Shan, Hsu, Sheng-Chieh, Wang, Bi-Juan, Huang, Shih-Han, Yang, Ping, Yang, Joy C., Chu, Cheng-Ying, Hsieh, Chia-Ling, Sung, Shian-Ying, Li, Chien-Feng, Tepper, Clifford G., Ann, David K., Gao, Allen C., Evans, Christopher P., Izumiya, Yoshihiro, Chuu, Chi-Pin, Wang, Wen-Ching, Chen, Hong-Wu, and Kung, Hsing-Jien

Published
2019
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15. Therapeutic Resistance Models and Treatment Sequencing in Advanced Prostate Cancer.

Author

Schaaf, Zachary A., Ning, Shu, Leslie, Amy R., Sharifi, Masuda, Han, Xianrui, Armstrong, Cameron, Lou, Wei, Lombard, Alan P., Liu, Chengfei, and Gao, Allen C.

Subjects
THERAPEUTIC use of antineoplastic agents, BIOLOGICAL models, ENERGY metabolism, ANTIANDROGENS, SEQUENCE analysis, ABIRATERONE acetate, CABAZITAXEL, APOPTOSIS, CASTRATION-resistant prostate cancer, TREATMENT effectiveness, CELLULAR signal transduction, RESEARCH funding, DOCETAXEL, GENE expression profiling, TRANSFERASES, CELL lines, DRUG resistance in cancer cells, ENZYME inhibitors, EVALUATION
Abstract

Simple Summary: Castration-resistant prostate cancer (CRPC) treatments include next-generation anti-androgen therapies (NGATs), taxane therapy, and PARP inhibitors (PARPi). However, resistance often occurs across and within therapeutic classes, which can complicate sequential treatment options. We developed acquired resistant models to study therapeutic resistance. Our findings indicate that while NGAT-resistant cells are cross-resistant to other NGATs, they remain sensitive to taxanes and olaparib. Cells resistant to docetaxel display cross-resistance to cabazitaxel and olaparib but respond to NGATs. Olaparib-resistant cells are cross-resistant to other PARPi but still sensitive to NGATs and docetaxel. Our research underscores the significance of rationale drug sequencing in CRPC treatment and underlying mechanisms of resistance. Current common treatments for castration-resistant prostate cancer (CRPC) typically belong to one of three major categories: next-generation anti-androgen therapies (NGAT) including enzalutamide, abiraterone acetate, apalutamide, and darolutamide; taxane therapy represented by docetaxel; and PARP inhibitors (PARPi) like olaparib. Although these treatments have shown efficacy and have improved outcomes for many patients, some do not survive due to the emergence of therapeutic resistance. The clinical landscape is further complicated by limited knowledge about how the sequence of treatments impacts the development of therapeutic cross-resistance in CRPC. We have developed multiple CRPC models of acquired therapeutic resistance cell sublines from C4-2B cells. These include C4-2B MDVR, C4-2B AbiR, C4-2B ApaR, C4-2B DaroR, TaxR, and 2B-olapR, which are resistant to enzalutamide, abiraterone, apalutamide, darolutamide, docetaxel, and olaparib, respectively. These models are instrumental for analyzing gene expression and assessing responses to various treatments. Our findings reveal distinct cross-resistance characteristics among NGAT-resistant cell sublines. Specifically, resistance to enzalutamide induces resistance to abiraterone and vice versa, while maintaining sensitivity to taxanes and olaparib. Conversely, cells with acquired resistance to docetaxel exhibit cross-resistance to both cabazitaxel and olaparib but retain sensitivity to NGATs like enzalutamide and abiraterone. OlapR cells, significantly resistant to olaparib compared to parental cells, are still responsive to NGATs and docetaxel. Moreover, OlapR models display cross-resistance to other clinically relevant PARP inhibitors, including rucaparib, niraparib, and talazoparib. RNA-sequencing analyses have revealed a complex network of altered gene expressions that influence signaling pathways, energy metabolism, and apoptotic signaling, pivotal to cancer's evolution and progression. The data indicate that resistance mechanisms are distinct among different drug classes. Notably, NGAT-resistant sublines exhibited a significant downregulation of androgen-regulated genes, contrasting to the stable expression noted in olaparib and docetaxel-resistant sublines. These results may have clinical implications by showing that treatments of one class can be sequenced with those from another class, but caution should be taken when sequencing drugs of the same class. [ABSTRACT FROM AUTHOR]

Published
2023
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18. ROR-γ drives androgen receptor expression and represents a therapeutic target in castration-resistant prostate cancer

Author

Wang, Junjian, Zou, June X., Xue, Xiaoqian, Cai, Demin, Zhang, Yan, Duan, Zhijian, Xiang, Qiuping, Yang, Joy C., Louie, Maggie C., Borowsky, Alexander D., Gao, Allen C., Evans, Christopher P., Lam, Kit S., Xu, Jianzhen, Kung, Hsing-Jien, Evans, Ronald M., Xu, Yong, and Chen, Hong-Wu

Subjects
Gene expression -- Health aspects, Prostate cancer -- Genetic aspects -- Development and progression, Hormone receptors -- Properties, Molecular targeted therapy -- Innovations, Biological sciences, Health
Abstract

The androgen receptor (AR) is overexpressed and hyperactivated in human castration-resistant prostate cancer (CRPC). However, the determinants of AR overexpression in CRPC are poorly defined. Here we show that retinoic acid receptorrelated orphan receptor g (ROR-γ) is overexpressed and amplified in metastatic CRPC tumors, and that ROR-γ drives AR expression in the tumors. ROR-γ recruits nuclear receptor coactivator 1 and 3 (NCOA1 and NCOA3, also known as SRC-1 and SRC-3) to an AR-ROR response element (RORE) to stimulate AR gene transcription. ROR-γ antagonists suppress the expression of both AR and its variant AR-V7 in prostate cancer (PCa) cell lines and tumors. ROR-γ antagonists also markedly diminish genomewide AR binding, H3K27ac abundance and expression of the AR target gene network. Finally, ROR-γ antagonists suppressed tumor growth in multiple AR-expressing, but not AR-negative, xenograft PCa models, and they effectively sensitized CRPC tumors to enzalutamide, without overt toxicity, in mice. Taken together, these results establish ROR-γ as a key player in CRPC by acting upstream of AR and as a potential therapeutic target for advanced PCa., Persistent or reactivated signaling by the androgen receptor (AR), a member of the nuclear receptor (NR) superfamily, drives the progression of prostate cancer to a deadly form of the disease, [...]

Published
2016
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30. Stat3 activation of NF-[kappa]B p100 processing involves CBP/p300-mediated acetylation

Author

Nadiminty, Nagalakshmi, Lou, Wei, Lee, Soo Ok, Lin, Xin, Trump, Donald L., and Gao, Allen C.

Subjects
Apoptosis -- Research, Apoptosis -- Diagnosis, Cellular signal transduction -- Analysis, Prostate cancer -- Diagnosis, Science and technology
Abstract

Activation of the noncanonical NF-[kappa]B signaling pathway involved in the proteolytic processing of NF-[kappa]B p100 to p52 is tightly regulated, and overproduction of p52 leads to lymphocyte hyperplasia and transformation. We have demonstrated that active but not latent Stat3, expressed in many types of human cancers involved in cell proliferation and survival, induces p100 processing to p52 by activation of IKK[alpha] and subsequent phosphorylation of p100. The Stat3-mediated p100 processing to p52 requires activation of Stat3 by the acetyltransferase activity of cAMP-response element-binding protein (CREB)-binding protein (CBP)/p300. A mutant of Stat3 defective in acetylation blocked Stat3-mediated p100 processing to p52 and acted as a dominant negative in blocking the production of p52. Furthermore, overexpression of p52 protected ceils from apoptotic cell death. Thus, activation of the processing of p100 to p52 by Stat3 may represent one of the common pathways used by cancer cells to survive and escape therapy. apoptosis | cancer | cell signal | prostate

Published
2006

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