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

POD-04.01: Purine-Rich Element Binding Protein Alpha Induces Cell Stress and Differentiation Pathways in Prostate Cancer Cells

Urology ◽  
2009 ◽  
Vol 74 (4) ◽  
pp. S10
Author(s):  
T. Inoue ◽  
A. Maeno ◽  
P. Kulkarni ◽  
Y. Zeng ◽  
D. Yeater ◽  
...  
Keyword(s):  
Prostate Cancer ◽  
Cancer Cells ◽  
Binding Protein ◽  
Cell Stress ◽  
Prostate Cancer Cells ◽  
Element Binding Protein ◽  
Differentiation Pathways

scholarly journals Ras responsive element binding protein-1 (RREB-1) down-regulates hZIP1 expression in prostate cancer cells

The Prostate ◽  
2009 ◽  
Vol 70 (3) ◽  
pp. 288-296 ◽  
Author(s):  
Beatrice C. Milon ◽  
Anthony Agyapong ◽  
Roderick Bautista ◽  
Leslie C. Costello ◽  
Renty B. Franklin
Keyword(s):  
Prostate Cancer ◽  
Cancer Cells ◽  
Binding Protein ◽  
Prostate Cancer Cells ◽  
Element Binding Protein ◽  
Responsive Element

PURINE-RICH ELEMENT BINDING PROTEIN ALPHA INDUCES CELL STRESS AND DIFFERENTIATION PATHWAYS IN PROSTATE CANCER CELLS

2009 ◽  
Vol 181 (4S) ◽  
pp. 189-189
Author(s):  
Takahiro Inoue ◽  
Atsushi Maeno ◽  
Prakash Kulkarni ◽  
Yu Zeng ◽  
David B Yeater ◽  
...  
Keyword(s):  
Prostate Cancer ◽  
Cancer Cells ◽  
Binding Protein ◽  
Cell Stress ◽  
Prostate Cancer Cells ◽  
Element Binding Protein ◽  
Differentiation Pathways

scholarly journals Inhibition of lipogenesis and induction of apoptosis by valproic acid in prostate cancer cells via the C/EBPα/SREBP-1 pathway

2021 ◽  
Author(s):  
B o Pang ◽  
Juanjuan Zhang ◽  
X i Zhang ◽  
Jihong Yuan ◽  
Yanan Shi ◽  
...  
Keyword(s):  
Prostate Cancer ◽  
Valproic Acid ◽  
Lipid Metabolism ◽  
Cell Viability ◽  
Cancer Cells ◽  
Lipid Accumulation ◽  
Binding Protein ◽  
B Cell Lymphoma ◽  
Lncap Cells ◽  
Prostate Cancer Cells

Abstract Lipid metabolism reprogramming is now accepted as a new hallmark of cancer. Hence, targeting the lipogenesis pathway may be a potential avenue for cancer treatment. Valproic acid (VPA) emerges as a promising drug for cancer therapy; however, the underlying mechanisms are not yet fully understood. In this study, we aimed to investigate the effects and mechanisms of VPA on cell viability, lipogenesis, and apoptosis in human prostate cancer PC-3 and LNCaP cells. The results showed that VPA significantly reduced lipid accumulation and induced apoptosis of PC-3 and LNCaP cells. Moreover, the expression of CCAAT/enhancer-binding protein α (C/EBPα), as well as sterol regulatory element-binding protein 1 (SREBP-1) and its downstream effectors, including fatty acid synthase (FASN), acetyl CoA carboxylase 1 (ACC1), and anti-apoptotic B-cell lymphoma 2 (Bcl-2), was markedly decreased in PC-3 and LNCaP cells after VPA administration. Mechanistically, the overexpression of C/EBPα rescued the levels of SREBP-1, FASN, ACC1, and Bcl-2, enhanced lipid accumulation, and attenuated apoptosis of VPA-treated PC-3 cells. Conversely, knockdown of C/EBPα by siRNA further decreased lipid accumulation, enhanced apoptosis, and reduced the levels of SREBP-1, FASN, ACC1, and Bcl-2. In addition, SREBP-1a and 1c enhanced the expressions of FASN and ACC1, but only SREBP-1a had a significant effect on Bcl-2 expression in VPA-treated PC-3 cells. Based on the results, we concluded that VPA significantly inhibits cell viability via decreasing lipogenesis and inducing apoptosis via the C/EBPα/SREBP-1 pathway in prostate cancer cells. Therefore, VPA that targets lipid metabolism and apoptosis is a promising candidate for PCa chemotherapy.

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 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

NOL8, the binding protein for beta-catenin, promoted the growth and migration of prostate cancer cells

2018 ◽  
Vol 294 ◽  
pp. 40-47 ◽  
Author(s):  
Shuo Gu ◽  
Peijin Hou ◽  
Kun Liu ◽  
Xiaobing Niu ◽  
Bingjian Wei ◽  
...  
Keyword(s):  
Prostate Cancer ◽  
Cancer Cells ◽  
Binding Protein ◽  
Beta Catenin ◽  
Prostate Cancer Cells ◽  
And Migration
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