13 Papers
112 Citations
Rui Li is an academic researcher from University of Texas Southwestern Medical Center. The author has contributed to research in topics: Prostate cancer & Androgen receptor. The author has an hindex of 12, co-authored 13 publications. Previous affiliations of Rui Li include University of Texas at Dallas.
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Papers
Dihydrotestosterone synthesis bypasses testosterone to drive castration-resistant prostate cancer
Kai Hsiung Chang,Rui Li,Mahboubeh Papari-Zareei,Lori M Watumull,Yan D. Zhao,Richard J. Auchus,Nima Sharifi +6 more
TL;DR: It is shown that the dominant route of DHT synthesis in CRPC bypasses testosterone, and instead requires 5α-reduction of androstenedione by SRD5A1 to 5 α-androstanedione, which is then converted to DHT.
362
A Gain-of-Function Mutation in DHT Synthesis in Castration-Resistant Prostate Cancer
Kai Hsiung Chang,Rui Li,Barbara Kuri,Yair Lotan,Claus G. Roehrborn,JJ Liu,Robert L. Vessella,Peter S. Nelson,Payal Kapur,Xiaofeng Guo,Hamid Mirzaei,Richard J. Auchus,Nima Sharifi +12 more
TL;DR: It is shown that CRPC sometimes expresses a gain-of-stability mutation that leads to a gain of function in 3β-hydroxysteroid dehydrogenase type 1 (3βHSD1), which catalyzes the initial rate-limiting step in conversion of the adrenal-derived steroid dehydroepiandrosterone to DHT.
310
BRD4 Promotes DNA Repair and Mediates the Formation of TMPRSS2-ERG Gene Rearrangements in Prostate Cancer
Xiangyi Li,Guem Hee Baek,Susmita G. Ramanand,Adam Sharp,Yunpeng Gao,Wei Yuan,Jon Welti,Daniel Nava Rodrigues,David Dolling,Ines Figueiredo,Semini Sumanasuriya,Mateus Crespo,Adam Aslam,Rui Li,Yi Yin,Bipasha Mukherjee,Mohammed Kanchwala,Ashley M. Hughes,Wendy S. Halsey,Cheng Ming Chiang,Chao Xing,Ganesh V. Raj,Sandeep Burma,Johann S. de Bono,Ram Shankar Mani +24 more
TL;DR: It is shown that BRD4 is essential for the repair of DNA double-strand breaks (DSBs) and mediates the formation of oncogenic gene rearrangements by engaging the non-homologous end joining (NHEJ) pathway.
123
Androgen receptor-mediated non-genomic regulation of prostate cancer cell proliferation.
TL;DR: The data suggest that therapeutic strategies aimed at preventing AR nuclear translocation and genomic AR signaling alone may not completely abrogate AR signaling, and elucidation of mechanisms that underlie non-genomic AR signaling may identify potential mechanisms of resistance to current anti-androgens and help developing novel therapies that abolish all AR signaling in prostate cancer.
3β-Hydroxysteroid Dehydrogenase Is a Possible Pharmacological Target in the Treatment of Castration-Resistant Prostate Cancer
TL;DR: It is demonstrated that DHEA and A5diol must be metabolized by 3betaHSD to activate AR in these models of CRPC, and suggests that 3 betaHSD may be exploited as a pharmacologic target in the treatment ofCRPC.