Mani Roshan‐Moniri

ORCID: 0000-0003-4172-7348
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About
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Research Areas
  • Prostate Cancer Treatment and Research
  • Estrogen and related hormone effects
  • Cancer, Hypoxia, and Metabolism
  • RNA Interference and Gene Delivery
  • Angiogenesis and VEGF in Cancer
  • Molecular Biology Techniques and Applications
  • Cancer, Lipids, and Metabolism
  • Computational Drug Discovery Methods
  • FOXO transcription factor regulation
  • Hormonal and reproductive studies
  • Melanoma and MAPK Pathways
  • Nitric Oxide and Endothelin Effects
  • Nuclear Receptors and Signaling
  • Marine and coastal ecosystems
  • Cancer Cells and Metastasis
  • Analytical Chemistry and Chromatography
  • Cholesterol and Lipid Metabolism
  • Ubiquitin and proteasome pathways
  • Extracellular vesicles in disease
  • Mitochondrial Function and Pathology
  • Veterinary Equine Medical Research
  • Clusterin in disease pathology
  • Enzyme function and inhibition
  • Lipid metabolism and disorders
  • Cardiac Imaging and Diagnostics

University of British Columbia
2010-2017

// Elham Hosseini-Beheshti 1, 3 , Wendy Choi Louis-Bastien Weiswald 4 Geetanjali Kharmate Mazyar Ghaffari Mani Roshan-Moniri Mohamed D. Hassona Leslie Chan Mei Yieng Chin Isabella T. Tai Paul S. Rennie 2, Ladan Fazli Emma Tomlinson Guns 1 Department of Experimental Medicine University British Columbia, Vancouver, V6H 3Z6, Canada 2 Urologic Sciences The Vancouver Prostate Centre Division Gastroenterology, Correspondence to: Guns, e-mail: eguns@prostatecentre.com Keywords: exosomes, cancer...

10.18632/oncotarget.7052 article EN Oncotarget 2016-01-28

Recent evidence has implicated the transmembrane co-receptor neuropilin-1 (NRP1) in cancer progression. Primarily known as a regulator of neuronal guidance and angiogenesis, NRP1 is also expressed multiple human malignancies, where it promotes tumor angiogenesis. However, non-angiogenic roles progression remain poorly characterized. In this study, we define an androgen-repressed gene whose expression elevated during adaptation prostate tumors to androgen-targeted therapies (ATTs), subsequent...

10.1038/onc.2016.482 article EN cc-by-nc-nd Oncogene 2017-01-16

Treatment-induced neuroendocrine transdifferentiation (NEtD) complicates therapies for metastatic prostate cancer (PCa). Based on evidence that PCa cells can transdifferentiate to other neuroectodermally-derived cell lineages in vitro, we proposed NEtD requires first an intermediary reprogramming metastable stem-like (CSCs) of a neural class and demonstrate several different AR+/PSA+ lines were efficiently reprogrammed to, maintained propagated as CSCs by growth androgen-free neural/neural...

10.18632/oncotarget.14850 article EN Oncotarget 2017-01-27

Genomic alterations involving translocations of the ETS-related gene ERG occur in approximately half prostate cancer cases. These result aberrant, androgen-regulated production protein variants that directly contribute to disease development and progression. This study describes discovery characterization a new class small molecule antagonists identified through rational silico methods. are designed sterically block DNA binding by ETS domain thereby disrupt transcriptional activity. We...

10.18632/oncotarget.17124 article EN Oncotarget 2017-04-15

Human androgen receptor (AR) is a hormone-activated transcription factor that an important drug target in the treatment of prostate cancer. Current small-molecule AR antagonists, such as enzalutamide, compete with androgens bind to steroid-binding pocket ligand-binding domain (LBD). In castration-resistant cancer (CRPC), resistance can manifest through AR-LBD mutations convert antagonists into agonists, or by expression variants lacking LBD. Such underscores importance novel ways targeting...

10.1158/1535-7163.mct-17-0259 article EN Molecular Cancer Therapeutics 2017-08-04

Abstract The development of new antiandrogens, such as enzalutamide, or androgen synthesis inhibitors like abiraterone has improved patient outcomes in the treatment advanced prostate cancer. However, due to drug resistance and tumor cell survival, a majority these patients progress refractory state castration-resistant cancer (CRPC). Thus, newer therapeutic agents better understanding their mode action are needed for treating CRPC patients. We demonstrated previously that targeting Binding...

10.1158/1535-7163.mct-16-0354 article EN Molecular Cancer Therapeutics 2016-10-08

Like most teleosts, sablefish (Anoplopoma fimbria Pallas 1814) blood exhibits a moderate Root effect (~35% maximal desaturation), where reduction in pH dramatically reduces O(2) carrying capacity, mechanism important for oxygenating the eye and filling swim bladder (SB) teleosts. Although lack SB, we observed well-defined choroid rete at eye. The adrenergically mediated cell swelling typically associated with functional red (RBC) beta-adrenergic Na(+)/H(+) exchanger (betaNHE), which would...

10.1242/jeb.038844 article EN Journal of Experimental Biology 2010-04-16

Purpose Angiopoietin-like 4 (ANGPTL4) is known to play a variety of roles in the response exercise, and more recently has been shown enhance healing tendon, fibrous load-bearing tissue required for efficient movement. The objective current study was further explore mechanisms ANGPTL4's effect on tendon cells using gene array approach. Methods Human fibroblasts were treated with recANGPTL4 their global transcriptome analyzed after 24 h. We also conducted functional studies derived from human...

10.1249/mss.0000000000001294 article EN Medicine & Science in Sports & Exercise 2017-04-11

Clusterin (CLU) is a chaperone-like protein and plays protective role against renal ischemia-reperfusion injury (IRI); however, the molecular pathways for its functions in kidney are not fully understood. This study was designed to investigate CLU-mediating cells by using bioinformatics analysis. CLU null tubular epithelial (TECs) expressing human cDNA (TEC-CLU(hCLU) ) or empty vector (TEC-CLU(-/-) were exposed normoxia hypoxia (1% O2 ). Transcriptome profiling with significant twofold...

10.1002/jcp.25415 article EN Journal of Cellular Physiology 2016-05-08

VOLUME 289 (2014) PAGES 26417–26429 A symbol was omitted to designate that Drs. Artem Cherkasov and Paul S. Rennie are equal senior authors.

10.1074/jbc.a115.553818 article EN cc-by Journal of Biological Chemistry 2015-10-01

Abstract The androgen receptor (AR) is a hormone-activated transcription factor implicated in the development and progression of prostate cancer. AR contains an N-terminal domain (NTD), followed by DNA binding (DBD) ligand-binding (LBD) domains. Upon androgens to LBD, moves into nucleus where it interacts with target genes via conserved AR-DBD. Prostate cancer treatment involves use small-molecules block production or compete for AR-LBD. Drug-resistance occurs when LBD mutations render...

10.1158/1538-7445.am2015-1778 article EN Cancer Research 2015-08-01

Abstract Aims: Androgen-targeted therapies (ATTs) are the mainstay treatment for metastatic prostate cancer (PCa). However, ATTs promote adaptation of tumour cells and lead to castration resistant disease (CRPC). We have recently identified cell surface receptor, Neuropilin-1 (NRP1) as increased during EMT in CRPC. role NRP1 epithelium is poorly understood. This study aims determine whether inhibition will be a feasible therapeutic strategy blocking PCa metastasis therapy resistance....

10.1158/1538-7445.am2017-4908 article EN Cancer Research 2017-07-01

Abstract Genomic alterations involving translocations of the ETS-related gene ERG occur in approximately half prostate cancer cases. These result aberrant, androgen-regulated production protein variants that directly contribute to disease development and progression. This study describes discovery characterization a new class small molecule antagonists identified through rational silico methods. are designed sterically block DNA binding by ETS domain thereby disrupt transcriptional activity....

10.1158/1538-7445.am2017-130 article EN Cancer Research 2017-07-01

Abstract Prostate cancer (PCa) is one of the leading causes cancer-related death in men worldwide. The common treatment option for recurring and advanced PCa focuses on inhibiting androgen receptor (AR). Unfortunately, despite an initial response to this treatment, drug resistance occurs, relapses incurable, castration-resistant form; thus, there a pressing need new therapeutics. Previous research has shown that up 50% all prostate cases, cause disease may be attributed genomic...

10.1158/1538-7445.am2015-1652 article EN Cancer Research 2015-08-01

Abstract The androgen receptor (AR) is a hormone inducible transcription factor that continues to be an important drug-target prevent or slow the progression of prostate cancer. Current small molecule inhibitors, such as Enzalutamide (anti-androgens), compete with naturally occurring steroids bind binding pocket AR ligand domain (LBD). In advanced castration resistant cancer (CRPC), mutations in LBD confer drug-resistance by converting anti-androgens into agonists, prompting research develop...

10.1158/1538-7445.am2016-4644 article EN Cancer Research 2016-07-15

<p>Supplementary Table S1: Cloning and RT-PCR primers used in this study; Supplementary Figure Luciferase cell viability experiments with MR49C PC3 cells; S2: ITC control experiment between AR-DBD dsDNA; S3: ChIP-PCR analysis; S4: Quality for ChIP experiments</p>

10.1158/1535-7163.22508866.v1 preprint EN cc-by 2023-04-03

<p>Supplementary Table S1: Cloning and RT-PCR primers used in this study; Supplementary Figure Luciferase cell viability experiments with MR49C PC3 cells; S2: ITC control experiment between AR-DBD dsDNA; S3: ChIP-PCR analysis; S4: Quality for ChIP experiments</p>

10.1158/1535-7163.22508866 preprint EN cc-by 2023-04-03

<div>Abstract<p>Human androgen receptor (AR) is a hormone-activated transcription factor that an important drug target in the treatment of prostate cancer. Current small-molecule AR antagonists, such as enzalutamide, compete with androgens bind to steroid-binding pocket ligand–binding domain (LBD). In castration-resistant cancer (CRPC), resistance can manifest through AR-LBD mutations convert antagonists into agonists, or by expression variants lacking LBD. Such underscores...

10.1158/1535-7163.c.6539128 preprint EN 2023-04-03
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