scholarly journals Effect of PTEN loss on metabolic reprogramming in prostate cancer cells

2019 ◽  
Author(s):  
Xin Zhou ◽  
Xu Yang ◽  
Xiang Sun ◽  
Xinyuan Xu ◽  
Xi'an Li ◽  
...  
Keyword(s):  
Prostate Cancer ◽  
Cancer Cells ◽  
Metabolic Reprogramming ◽  
Prostate Cancer Cells ◽  
Pten Loss

Abstract 1467: Metabolic reprogramming fuels prostate cancer cells towards enzalutamide resistance

2020 ◽  
Author(s):  
Shiv S. Verma ◽  
Eswar Shankar ◽  
Rajnee Kanwal ◽  
Ricky Chan ◽  
Sanjay Gupta
Keyword(s):  
Prostate Cancer ◽  
Cancer Cells ◽  
Metabolic Reprogramming ◽  
Prostate Cancer Cells

scholarly journals Metabolic Reprogramming and Predominance of Solute Carrier Genes during Acquired Enzalutamide Resistance in Prostate Cancer

Cells ◽  
2020 ◽  
Vol 9 (12) ◽  
pp. 2535
Author(s):  
Shiv Verma ◽  
Eswar Shankar ◽  
E. Ricky Chan ◽  
Sanjay Gupta
Keyword(s):  
Prostate Cancer ◽  
Drug Resistance ◽  
Cancer Cells ◽  
Standard Of Care ◽  
Resistant Cell ◽  
Metabolic Reprogramming ◽  
Differentially Expressed ◽  
Pcr Analysis ◽  
Prostate Cancer Cells ◽  
Solute Carrier

Androgen deprivation therapy (ADT) is standard-of-care for advanced-stage prostate cancer, and enzalutamide (Xtandi®, Astellas, Northbrook, IL, USA), a second generation antiandrogen, is prescribed in this clinical setting. The response to this medication is usually temporary with the rapid emergence of drug resistance. A better understanding of gene expression changes associated with enzalutamide resistance will facilitate circumventing this problem. We compared the transcriptomic profile of paired enzalutamide-sensitive and resistant LNCaP and C4-2B prostate cancer cells for identification of genes involved in drug resistance by performing an unbiased bioinformatics analysis and further validation. Next-Gen sequencing detected 9409 and 7757 genes differentially expressed in LNCaP and C4-2B cells, compared to their parental counterparts. A subset of differentially expressed genes were validated by qRT-PCR. Analysis by the i-pathway revealed membrane transporters including solute carrier proteins, ATP-binding cassette transporters, and drug metabolizing enzymes as the most prominent genes dysregulated in resistant cell lines. RNA-Seq data demonstrated predominance of solute carrier genes SLC12A5, SLC25A17, and SLC27A6 during metabolic reprogramming and development of drug resistance. Upregulation of these genes were associated with higher uptake of lactic/citric acid and lower glucose intake in resistant cells. Our data suggest the predominance of solute carrier genes during metabolic reprogramming of prostate cancer cells in an androgen-deprived environment, thus signifying them as potentially attractive therapeutic targets.

Abstract 4757: TNFAIP8 facilitates metabolic reprogramming in prostate cancer cells

2020 ◽  
Author(s):  
Suryakant Niture ◽  
Minghui Lin ◽  
Joab O. Odera ◽  
John Moore ◽  
Deepak Kumar
Keyword(s):  
Prostate Cancer ◽  
Cancer Cells ◽  
Metabolic Reprogramming ◽  
Prostate Cancer Cells

scholarly journals Targeting Mitochondrial Metabolism in Prostate Cancer with Triterpenoids

2021 ◽  
Vol 22 (5) ◽  
pp. 2466
Author(s):  
Kenza Mamouni ◽  
Georgios Kallifatidis ◽  
Bal L. Lokeshwar
Keyword(s):  
Prostate Cancer ◽  
Cell Survival ◽  
Cancer Cells ◽  
Cancer Cell ◽  
Mitochondrial Metabolism ◽  
Metabolic Reprogramming ◽  
Prostate Cancer Cells ◽  
Normal Prostate ◽  
Cancer Cell Survival ◽  
The Impact

Metabolic reprogramming is a hallmark of malignancy. It implements profound metabolic changes to sustain cancer cell survival and proliferation. Although the Warburg effect is a common feature of metabolic reprogramming, recent studies have revealed that tumor cells also depend on mitochondrial metabolism. Due to the essential role of mitochondria in metabolism and cell survival, targeting mitochondria in cancer cells is an attractive therapeutic strategy. However, the metabolic flexibility of cancer cells may enable the upregulation of compensatory pathways, such as glycolysis, to support cancer cell survival when mitochondrial metabolism is inhibited. Thus, compounds capable of targeting both mitochondrial metabolism and glycolysis may help overcome such resistance mechanisms. Normal prostate epithelial cells have a distinct metabolism as they use glucose to sustain physiological citrate secretion. During the transformation process, prostate cancer cells consume citrate to mainly power oxidative phosphorylation and fuel lipogenesis. A growing number of studies have assessed the impact of triterpenoids on prostate cancer metabolism, underlining their ability to hit different metabolic targets. In this review, we critically assess the metabolic transformations occurring in prostate cancer cells. We will then address the opportunities and challenges in using triterpenoids as modulators of prostate cancer cell metabolism.

scholarly journals Model-driven discovery of long-chain fatty acid metabolic reprogramming in heterogeneous prostate cancer cells

2018 ◽  
Vol 14 (1) ◽  
pp. e1005914 ◽  
Author(s):  
Igor Marín de Mas ◽  
Esther Aguilar ◽  
Erika Zodda ◽  
Cristina Balcells ◽  
Silvia Marin ◽  
...  
Keyword(s):  
Prostate Cancer ◽  
Fatty Acid ◽  
Cancer Cells ◽  
Chain Fatty Acid ◽  
Metabolic Reprogramming ◽  
Prostate Cancer Cells ◽  
Long Chain Fatty Acid ◽  
Model Driven ◽  
Long Chain

scholarly journals PDHA1 gene knockout in prostate cancer cells results in metabolic reprogramming towards greater glutamine dependence

Oncotarget ◽  
2016 ◽  
Vol 7 (33) ◽  
pp. 53837-53852 ◽  
Author(s):  
Yaqing Li ◽  
Xiaoran Li ◽  
Xiaoli Li ◽  
Yali Zhong ◽  
Yasai Ji ◽  
...  
Keyword(s):  
Prostate Cancer ◽  
Cancer Cells ◽  
Gene Knockout ◽  
Metabolic Reprogramming ◽  
Prostate Cancer Cells

279: Inhibition of Cyclooxygenase-2 Pathway Overcomes the Heat-Resistance in Prostate Cancer Cells

2007 ◽  
Vol 177 (4S) ◽  
pp. 93-93
Author(s):  
Makoto Sumitomo ◽  
Kenji Kuroda ◽  
Takako Asano ◽  
Akio Horiguchi ◽  
Keiichi Ito ◽  
...  
Keyword(s):  
Prostate Cancer ◽  
Heat Resistance ◽  
Cancer Cells ◽  
Cyclooxygenase 2 ◽  
Prostate Cancer Cells
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