scholarly journals Inhibition of Phospholipase D1 mRNA Expression Slows Down the Proliferation Rate of Prostate Cancer Cells That Have Transited to Androgen Independence

2018 ◽  
Vol 9 (19) ◽  
pp. 3620-3625 ◽  
Author(s):  
Wu Zhou ◽  
Keqing Shi ◽  
Lili Ji ◽  
Ruihao Wu ◽  
Yuehui Chen ◽  
...  
Keyword(s):  
Prostate Cancer ◽  
Mrna Expression ◽  
Cancer Cells ◽  
Proliferation Rate ◽  
Prostate Cancer Cells ◽  
Androgen Independence ◽  
Phospholipase D1

scholarly journals SHH-N non-canonically sustains androgen receptor activity in androgen-independent prostate cancer cells

2021 ◽  
Vol 11 (1) ◽  
Author(s):  
Diana Trnski ◽  
Maja Sabol ◽  
Sanja Tomić ◽  
Ivan Štefanac ◽  
Milanka Mrčela ◽  
...  
Keyword(s):  
Prostate Cancer ◽  
Androgen Receptor ◽  
Cancer Cells ◽  
Therapy Resistance ◽  
Androgen Deprivation ◽  
Prostate Cancer Cells ◽  
Androgen Independence ◽  
Androgen Receptor Activity ◽  
Signaling Activation ◽  
Androgen Independent

AbstractProstate cancer is the second most frequent cancer diagnosed in men worldwide. Localized disease can be successfully treated, but advanced cases are more problematic. After initial effectiveness of androgen deprivation therapy, resistance quickly occurs. Therefore, we aimed to investigate the role of Hedgehog-GLI (HH-GLI) signaling in sustaining androgen-independent growth of prostate cancer cells. We found various modes of HH-GLI signaling activation in prostate cancer cells depending on androgen availability. When androgen was not deprived, we found evidence of non-canonical SMO signaling through the SRC kinase. After short-term androgen deprivation canonical HH-GLI signaling was activated, but we found little evidence of canonical HH-GLI signaling activity in androgen-independent prostate cancer cells. We show that in androgen-independent cells the pathway ligand, SHH-N, non-canonically binds to the androgen receptor through its cholesterol modification. Inhibition of this interaction leads to androgen receptor signaling downregulation. This implies that SHH-N activates the androgen receptor and sustains androgen-independence. Targeting this interaction might prove to be a valuable strategy for advanced prostate cancer treatment. Also, other non-canonical aspects of this signaling pathway should be investigated in more detail and considered when developing potential therapies.

scholarly journals ERβ and NFκB—Modulators of Zearalenone-Induced Oxidative Stress in Human Prostate Cancer Cells

Toxins ◽  
2020 ◽  
Vol 12 (3) ◽  
pp. 199 ◽  
Author(s):  
Karolina Kowalska ◽  
Dominika Ewa Habrowska-Górczyńska ◽  
Kamila Domińska ◽  
Kinga Anna Urbanek ◽  
Agnieszka Wanda Piastowska-Ciesielska
Keyword(s):  
Oxidative Stress ◽  
Prostate Cancer ◽  
Cancer Cells ◽  
Prostate Cancer Cells ◽  
M Cell ◽  
Androgen Independence ◽  
Prostate Carcinogenesis ◽  
Cycle Arrest ◽  
Light Chain Enhancer

Nuclear factor kappa-light-chain-enhancer of activated B cells (NFκB) is commonly expressed in prostate cancer (PCa) cells and is associated with increased proliferation, metastases and androgen independence. Zearalenone (ZEA) is one of the most common mycotoxins contaminating food, which might mimic estrogens and bind to estrogen receptors (ERs). The ratio of androgens to estrogens in men decreases physiologically with age, and is believed to participate in prostate carcinogenesis. In this study, we evaluated the role of NFκB and ERβ in the induction of oxidative stress in human PCa cells by ZEA. As observed, ZEA at a dose of 30 µM induces oxidative stress in PCa cells associated with DNA damage and G2/M cell cycle arrest. We also observed that the inhibition of ERβ and NFΚB via specific inhibitors (PHTPP and BAY 117082) significantly increased ZEA-induced oxidative stress, although the mechanism seems to be different for androgen-dependent and androgen-independent cells. Based on our findings, it is possible that the activation of ERβ and NFΚB in PCa might protect cancer cells from ZEA-induced oxidative stress. We therefore shed new light on the mechanism of ZEA toxicity in human cells.

Phenethyl isothiocyanate in combination with dibenzoylmethane inhibits the androgen-independent growth of prostate cancer cells

2018 ◽  
Vol 9 (4) ◽  
pp. 2398-2408 ◽  
Author(s):  
Huarong Huang ◽  
Yan He ◽  
Lanyue Zhang ◽  
Hongping Xiang ◽  
Dongli Li ◽  
...  
Keyword(s):  
Prostate Cancer ◽  
Cancer Cells ◽  
Inhibitory Effect ◽  
Phenethyl Isothiocyanate ◽  
Prostate Cancer Cells ◽  
Prostate Tumors ◽  
Androgen Independence ◽  
Androgen Independent

This study investigates the inhibitory effect of PEITC and DBM in combination on the progression of androgen-dependent VCaP prostate tumors to androgen independence.

scholarly journals Silibinin inhibits aberrant lipid metabolism, proliferation and emergence of androgen-independence in prostate cancer cells via primarily targeting the sterol response element binding protein 1

Oncotarget ◽  
2014 ◽  
Vol 5 (20) ◽  
pp. 10017-10033 ◽  
Author(s):  
Dhanya K. Nambiar ◽  
Gagan Deep ◽  
Rana P. Singh ◽  
Chapla Agarwal ◽  
Rajesh Agarwal
Keyword(s):  
Prostate Cancer ◽  
Lipid Metabolism ◽  
Cancer Cells ◽  
Binding Protein ◽  
Prostate Cancer Cells ◽  
Response Element ◽  
Androgen Independence ◽  
Element Binding Protein

scholarly journals Possibility of using mRNA expression levels for nucleic acid-metabolizing enzymes within prostate cancer cells as indices for prognostic factors

2010 ◽  
Vol 1 (6) ◽  
pp. 1049-1053 ◽  
Author(s):  
AKIRA YANO ◽  
YOSHINORI SHIGEMATSU ◽  
HIROYUKI KITANO ◽  
AKI HANAYAMA ◽  
AKIRA OZAWA ◽  
...  
Keyword(s):  
Prostate Cancer ◽  
Prognostic Factors ◽  
Nucleic Acid ◽  
Mrna Expression ◽  
Cancer Cells ◽  
Prostate Cancer Cells ◽  
Metabolizing Enzymes ◽  
Expression Levels ◽  
Mrna Expression Levels

Longitudinal analysis of androgen deprivation of prostate cancer cells identifies pathways to androgen independence

The Prostate ◽  
2008 ◽  
Vol 68 (7) ◽  
pp. 698-714 ◽  
Author(s):  
Jason M. D'Antonio ◽  
Changqing Ma ◽  
Federico A. Monzon ◽  
Beth R. Pflug
Keyword(s):  
Prostate Cancer ◽  
Cancer Cells ◽  
Longitudinal Analysis ◽  
Androgen Deprivation ◽  
Prostate Cancer Cells ◽  
Androgen Independence

scholarly journals Switch to full-length of XAF1 mRNA expression in prostate cancer cells by the DNA methylation inhibitor

2006 ◽  
Vol 118 (10) ◽  
pp. 2485-2489 ◽  
Author(s):  
Xiaolei Fang ◽  
Zhaoxu Liu ◽  
Yidong Fan ◽  
Chengyun Zheng ◽  
Sten Nilson ◽  
...  
Keyword(s):  
Prostate Cancer ◽  
Dna Methylation ◽  
Mrna Expression ◽  
Cancer Cells ◽  
Full Length ◽  
Prostate Cancer Cells ◽  
Methylation Inhibitor ◽  
Dna Methylation Inhibitor

scholarly journals Emblicanin-A Inhibits Cell Growth in Human Prostate Cancer Cells (PC-3) By Modulating Apoptotic Signaling Molecules

2020 ◽  
Vol 10 (5) ◽  
Author(s):  
Jayaraman Selvaraj ◽  
Rajagopal Ponnulakshmi ◽  
V Vishnupriya ◽  
Myneni Sindhura ◽  
Kamineni Sai Ravi Teja ◽  
...  
Keyword(s):  
Prostate Cancer ◽  
Mrna Expression ◽  
Cancer Cells ◽  
Caspase 3 ◽  
Treatment Options ◽  
B Cell Lymphoma ◽  
Multi Drug Resistance ◽  
Mrna Levels ◽  
Prostate Cancer Cells ◽  
Apoptotic Signaling

Cancer is a one of the leading causes of death in the world, continue to be worldwide dreadful disease. Prostate cancer is the most common cancer diagnosed in men. Multi-drug resistance (MDR) is a major problem with the current treatment options. It is now widely believed that many herbal dietary products are available as chemo-preventive agents against commonly occurring cancer types such as prostate cancer. Emblicanin-A, a hydrolyzable tannins has been isolated from the fruit of Emblicaofficinalis. The present study was aimedto find out whether emblicanin-A can inhibit growth of the prostate cancer cells (PC-3) through the regulation of apoptotic signaling mechanisms. Hence, PC-3 cells were treated with different concentrations of emblicanin-A (10, 25, 50, 100 and 150µM) for the analysis of B-cell lymphoma 2 (Bcl-2), Tumor suppressor protein (p53), Caspase-3 and caspase-9 mRNA expression in PC-3 cells. Cell viability was done using MTT in order to find the optimal dose. MTT assay exhibited that emblicanin-A showed cell death at the concentration of 100 and 150µM. It significantly (p<0.05) decreased the mRNA expression of anti apoptotic proteins (Bcl-2) while it upregulated the p53, caspase-3 and cas-9 mRNA levels effectively (p<0.05) in PC-3 cells which clearly indicates that emblicanin-A induces apoptosis in PC-3 cells by modulating intrinsic signalling mechanisms. To best of our knowledge, the present findings are the first to report anticancer activity of a bioactive compound from E.officinalis. Our study concludes that emblicanin-A may serve as a potential chemotherapeutic agent for the treatment of prostate cancer. Further studies on the effect of Emblicanin-A on the protein expression of further downstream signalling mechanisms is warranted in order to ascertain its potential mechanisms action towards clinical utility.

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