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36 results on '"Yan, Honghua"'

6. Abstract A31: C-MYC Targeting by Degradation: Novel Dual c-MYC/GSPT1 Degrader GT19715 Induces TP53-independent Cell Death in MYC-amplified Acute Myeloid Leukemia and Lymphomas

Author

Nishida, Yuki, primary, Scruggs, Darah A, additional, Ayoub, Edward, additional, Ostermann, Lauren B, additional, Patsilevas, Tallie, additional, Ruvolo, Vivian R, additional, Mak, Po Yee, additional, Carter, Bing Z., additional, Boettcher, Steffen, additional, Maiti, Abhishek, additional, Sasaki, Koji, additional, Zhou, Qianxiang, additional, Yang, Zhaohui, additional, Yan, Honghua, additional, Ma, Liandong, additional, and Andreeff, Michael, additional

Published
2023
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10. C-MYC Targeting By Degradation: Novel Dual c-Myc/GSPT1 Degrader GT19715 Induces TP53-Independent Cell Death in Acute Myeloid Leukemia and Lymphomas

Author

Nishida, Yuki, primary, Scruggs, Darah A, additional, Ayoub, Edward, additional, Patsilevas, Tallie, additional, Ruvolo, Vivian, additional, Mak, Po Yee, additional, Carter, Bing Z, additional, Boettcher, Steffen, additional, Maiti, Abhishek, additional, Zhou, Qianxiang, additional, Yang, Zhaohui, additional, Yan, Honghua, additional, Ma, Liandong, additional, and Andreeff, Michael, additional

Published
2022
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13. Poster: AML-147 C-MYC Targeting by Degradation: Novel Dual c-Myc/GSPT1 Degrader GT19715 Exerts Profound Cell Kill In Vitro and In Vivo in Acute Myeloid Leukemia and Lymphomas

Author

Nishida, Yuki, primary, Scruggs, Darah A, additional, Ayoub, Edward, additional, Patsilevas, Tallie, additional, Ruvolo, Vivian R, additional, Mak, Po Yee, additional, Carter, Bing Z, additional, Boettcher, Steffen, additional, Maiti, Abhishek, additional, Zhou, Qianxiang, additional, Yang, Zhaohui, additional, Yan, Honghua, additional, Ma, Liandong, additional, and Andreeff, Michael, additional

Published
2022
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18. C-MYC Targeting by Degradation: Novel Dual c-Myc/GSPT1 Degrader GT19715 Exerts Profound Cell Kill in vitro and in vivo in Acute Myeloid Leukemia and Lymphomas

Author

Nishida, Yuki, primary, Scruggs, Darah A., additional, Ayoub, Edward, additional, Patsilevas, Tallie, additional, Ostermann, Lauren, additional, Ruvolo, Vivian R., additional, Mak, Po Yee, additional, Carter, Bing Z., additional, Boettcher, Steffan, additional, Maiti, Abhishek, additional, Zhou, Qianxiang, additional, Yang, Zhaohui, additional, Yan, Honghua, additional, Ma, Liandong, additional, and Andreeff, Michael, additional

Published
2022
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24. Preclinical profile and phase I clinical trial of a novel androgen receptor antagonist GT0918 in castration-resistant prostate cancer

Author

Zhou, Tie, primary, Xu, Weidong, additional, Zhang, Wei, additional, Sun, Ye, additional, Yan, Honghua, additional, Gao, Xu, additional, Wang, Fubo, additional, Zhou, Qianxiang, additional, Hou, Jianguo, additional, Ren, Shancheng, additional, Yang, Qing, additional, Yang, Bo, additional, Xu, Chuanliang, additional, Zhou, Qingqing, additional, Wang, Meiyu, additional, Chen, Chunyun, additional, and Sun, Yinghao, additional

Published
2020
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25. Suppression of Androgen Receptor (AR)-ACE2/TMPRSS2 Axis by AR Antagonists May Be Therapeutically Beneficial for Male COVID-19 Patients

Author

Wu, Siqi, primary, Miao, Liyan, additional, Zhou, Qianxiang, additional, Gao, Chang, additional, Liu, Jialin, additional, Zhan, Qingyuan, additional, Guo, Binbin, additional, Li, Fang, additional, Wang, Yirong, additional, Xu, Hongyang, additional, Yan, Honghua, additional, Wu, Rui, additional, Zhang, Shenghua, additional, Zheng, Jiangnan, additional, Yang, Jianfei, additional, Wang, Shanshan, additional, Yu, Wenkui, additional, Niu, Haitao, additional, Li, Fengyuan, additional, Yang, Ling, additional, Huang, Jianan, additional, Lu, Xiaoting, additional, Chen, Jiahao, additional, Tong, Youzhi, additional, Ma, Liandong, additional, Zhou, Yifeng, additional, and Guo, Qiang, additional

Published
2020
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29. An ethyl acetate fraction of Artemisia capillaris (ACE-63) induced apoptosis and anti-angiogenesis via inhibition of PI3K/AKT signaling in hepatocellular carcinoma.

Author

Jung, Kyung Hee, Rumman, Marufa, Yan, Honghua, Cheon, Min Ji, Choi, Jin Gyu, Jin, Xing, Park, Sunghouk, Oh, Myung Sook, Hong, Soon‐Sun, and Hong, Soon-Sun

Subjects
PROTEIN metabolism, ANIMALS, APOPTOSIS, CELL lines, CELL physiology, CELLULAR signal transduction, EPITHELIAL cells, HEPATOCELLULAR carcinoma, LIVER tumors, MICE, NEOVASCULARIZATION inhibitors, PHOSPHOTRANSFERASES, PROTEINS, PSYCHOLOGICAL tests, RESEARCH funding, TRANSFERASES, WORMWOOD, PLANT extracts, VASCULAR endothelial growth factors, PLANT anatomy, PATHOLOGIC neovascularization, CHEMICAL inhibitors, PHARMACODYNAMICS
Abstract

In cancer treatment, herbal medicines may be a good choice because of the reduced risk of adverse side effects. Artemisia capillaris has been recognized as a promising candidate due to its hepatoprotective effects. Herein, we investigated whether A. capillaris-derived fraction (ACE-63) could inhibit the progression of hepatocellular carcinoma (HCC) and its underlying mechanism. In this study, ACE-63 effectively inhibited the growth and proliferation of HCC cells. ACE-63 induced apoptosis, as observed using Terminal deoxynucleotidyl transferase dUTP nick end labeling (TUNEL) staining, which was accompanied with increases in cleaved Poly (ADP-ribose) polymerase (PARP) and caspase-3 in HCC cells. Additionally, the pro-apoptotic effect of ACE-63 was demonstrated by a decrease in the expression of the X-linked inhibitor of apoptosis protein (XIAP) and survivin via a loss of mitochondrial membrane potential. In an ex vivo model, ACE-63 significantly inhibited tumor cell growth and induced apoptosis by increasing the expression of cleaved caspase-3 and DNA fragmentation. In addition, ACE-63 decreased the expression of hypoxia-inducible factor-1α and vascular endothelial growth factor and inhibited tube formation of human umbilical vein endothelial cells. A mechanistic study revealed that ACE-63 effectively suppressed the PI3K/AKT/mTOR signaling pathways, which were observed as a target signaling by phosphokinase array. Taken together, our findings demonstrate that ACE-63 could not only efficiently induce apoptosis but also inhibit the growth/angiogenesis of human HCC cells by blocking the PI3K/AKT/mTOR signaling pathway, suggesting that ACE-63 may be a new chemotherapeutic candidate against HCC. [ABSTRACT FROM AUTHOR]

Published
2018
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36. Proxalutamide reduces SARS-CoV-2 infection and associated inflammatory response.

Author

Qiao Y, Wotring JW, Zheng Y, Zhang CJ, Zhang Y, Jiang X, Pretto CD, Eyunni S, Parolia A, He T, Cheng C, Cao X, Wang R, Su F, Ellison SJ, Wang Y, Qin J, Yan H, Zhou Q, Ma L, Sexton JZ, and Chinnaiyan AM

Subjects
Male, Humans, Animals, Mice, SARS-CoV-2 metabolism, Androgens, Androgen Antagonists therapeutic use, Pandemics, Peptidyl-Dipeptidase A metabolism, Interferon-gamma therapeutic use, COVID-19, Prostatic Neoplasms drug therapy
Abstract

Early in the COVID-19 pandemic, data suggested that males had a higher risk of developing severe disease and that androgen deprivation therapy might be associated with protection. Combined with the fact that TMPRSS2 ( transmembrane serine protease 2 ), a host entry factor for the SARS-CoV-2 virus, was a well-known androgen-regulated gene, this led to an upsurge of research investigating androgen receptor (AR)-targeting drugs. Proxalutamide, an AR antagonist, was shown in initial clinical studies to benefit COVID-19 patients; however, further validation is needed as one study was retracted. Due to continued interest in proxalutamide, which is in phase 3 trials, we examined its ability to impact SARS-CoV-2 infection and downstream inflammatory responses. Proxalutamide exerted similar effects as enzalutamide, an AR antagonist prescribed for advanced prostate cancer, in decreasing AR signaling and expression of TMPRSS2 and angiotensin-converting enzyme 2 (ACE2) , the SARS-CoV-2 receptor. However, proxalutamide led to degradation of AR protein, which was not observed with enzalutamide. Proxalutamide inhibited SARS-CoV-2 infection with an IC 50 value of 97 nM, compared to 281 nM for enzalutamide. Importantly, proxalutamide inhibited infection by multiple SARS-CoV-2 variants and synergized with remdesivir. Proxalutamide protected against cell death in response to tumor necrosis factor alpha and interferon gamma, and overall survival of mice was increased with proxalutamide treatment prior to cytokine exposure. Mechanistically, we found that proxalutamide increased levels of NRF2, an essential transcription factor that mediates antioxidant responses, and decreased lung inflammation. These data provide compelling evidence that proxalutamide can prevent SARS-CoV-2 infection and cytokine-induced lung damage, suggesting that promising clinical data may emerge from ongoing phase 3 trials.

Published
2023
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