scholarly journals MicroRNA-4287 is a novel tumor suppressor microRNA controlling epithelial-to mesenchymal transition in prostate cancer

Oncotarget ◽  
2020 ◽  
Vol 11 (51) ◽  
pp. 4681-4692
Author(s):  
Divya Bhagirath ◽  
Thao Ly Yang ◽  
Theresa Akoto ◽  
Nikhil Patel ◽  
Laura Z. Tabatabai ◽  
...  
Keyword(s):  
Prostate Cancer ◽  
Tumor Suppressor ◽  
Epithelial To Mesenchymal Transition ◽  
Mesenchymal Transition

scholarly journals miR-154* and miR-379 in the DLK1-DIO3 MicroRNA Mega-Cluster Regulate Epithelial to Mesenchymal Transition and Bone Metastasis of Prostate Cancer

2014 ◽  
Vol 20 (24) ◽  
pp. 6559-6569 ◽  
Author(s):  
Murali Gururajan ◽  
Sajni Josson ◽  
Gina Chia-Yi Chu ◽  
Chia-Lun Lu ◽  
Yi-Tsung Lu ◽  
...  
Keyword(s):  
Prostate Cancer ◽  
Bone Metastasis ◽  
Epithelial To Mesenchymal Transition ◽  
Mesenchymal Transition

scholarly journals PPAR-gamma induced AKT3 expression increases levels of mitochondrial biogenesis driving prostate cancer

Oncogene ◽  
2021 ◽  
Vol 40 (13) ◽  
pp. 2355-2366
Author(s):  
Laura C. A. Galbraith ◽  
Ernest Mui ◽  
Colin Nixon ◽  
Ann Hedley ◽  
David Strachan ◽  
...  
Keyword(s):  
Prostate Cancer ◽  
Mitochondrial Biogenesis ◽  
Nuclear Export ◽  
Epithelial To Mesenchymal Transition ◽  
Ppar Gamma ◽  
Peroxisome Proliferator ◽  
Serine Threonine Kinase ◽  
Peroxisome Proliferator Activated Receptor ◽  
Mesenchymal Transition ◽  
And Function

AbstractPeroxisome Proliferator-Activated Receptor Gamma (PPARG) is one of the three members of the PPAR family of transcription factors. Besides its roles in adipocyte differentiation and lipid metabolism, we recently demonstrated an association between PPARG and metastasis in prostate cancer. In this study a functional effect of PPARG on AKT serine/threonine kinase 3 (AKT3), which ultimately results in a more aggressive disease phenotype was identified. AKT3 has previously been shown to regulate PPARG co-activator 1 alpha (PGC1α) localisation and function through its action on chromosome maintenance region 1 (CRM1). AKT3 promotes PGC1α localisation to the nucleus through its inhibitory effects on CRM1, a known nuclear export protein. Collectively our results demonstrate how PPARG over-expression drives an increase in AKT3 levels, which in turn has the downstream effect of increasing PGC1α localisation within the nucleus, driving mitochondrial biogenesis. Furthermore, this increase in mitochondrial mass provides higher energetic output in the form of elevated ATP levels which may fuel the progression of the tumour cell through epithelial to mesenchymal transition (EMT) and ultimately metastasis.

PHENOTYPIC HETEROGENEITY IN DISSEMINATED PROSTATE CANCER TUMOR CELLS: IMPLICATIONS IN EPITHELIAL TO MESENCHYMAL TRANSITION

2009 ◽  
Vol 181 (4S) ◽  
pp. 756-756
Author(s):  
Theodore D Koreckij ◽  
Todd M Morgan ◽  
Paul H Lange ◽  
Ilsa Coleman ◽  
Roger Coleman ◽  
...  
Keyword(s):  
Prostate Cancer ◽  
Tumor Cells ◽  
Epithelial To Mesenchymal Transition ◽  
Phenotypic Heterogeneity ◽  
Mesenchymal Transition ◽  
Cancer Tumor

scholarly journals miR-204 Shifts the Epithelial to Mesenchymal Transition in Concert with the Transcription Factors RUNX2, ETS1, and cMYB in Prostate Cancer Cell Line Model

2014 ◽  
Vol 2014 ◽  
pp. 1-14 ◽  
Author(s):  
Krassimira Todorova ◽  
Diana Zasheva ◽  
Kristiyan Kanev ◽  
Soren Hayrabedyan
Keyword(s):  
Prostate Cancer ◽  
Transcription Factors ◽  
Cancer Cell ◽  
Epithelial To Mesenchymal Transition ◽  
Prostate Cancer Cell ◽  
Cancer Cell Line ◽  
Prostate Cancer Cell Line ◽  
Mesenchymal Transition ◽  
Cell Line Model ◽  
E Cadherin

Epithelial to mesenchymal transition is an essential step in advanced cancer development. Many master transcription factors shift their expression to drive this process, while noncoding RNAs families like miR-200 are found to restrict it. In this study we investigated how the tumor suppressor miR-204 and several transcription factors modulate main markers of mesenchymal transformation like E- and N-cadherin, SLUG, VEGF, and SOX-9 in prostate cancer cell line model (LNCaP, PC3, VCaP, and NCI-H660). We found that SLUG, E-cadherin, and N-cadherin are differentially modulated by miR-204, using miR-204 specific mimics and inhibitors and siRNA gene silencing (RUNX2, ETS-1, and cMYB). The genome perturbation associated TMPRSS2-ERG fusion coincided with shift from tumor-suppressor to tumor-promoting activity of this miRNA. The ability of miR-204 to suppress cancer cell viability and migration was lost in the fusion harboring cell lines. We found differential E-cadherin splicing corroborating to miR-204 modulatory effects. RUNX2, ETS1, and cMYB are involved in the regulation of E-cadherin, N-cadherin, and VEGFA expression. RUNX2 knockdown results in SOX9 downregulation, while ETS1 and cMYB silencing result in SOX9 upregulation in VCaP cells. Their expression was found to be also methylation dependent. Our study provides means for understanding cancer heterogeneity in regard to adapted therapeutic approaches development.

scholarly journals Alleviation of Multidrug Resistance by Flavonoid and Non-Flavonoid Compounds in Breast, Lung, Colorectal and Prostate Cancer

2020 ◽  
Vol 21 (2) ◽  
pp. 401 ◽  
Author(s):  
Teodora Costea ◽  
Oana Cezara Vlad ◽  
Luminita-Claudia Miclea ◽  
Constanta Ganea ◽  
János Szöllősi ◽  
...  
Keyword(s):  
Prostate Cancer ◽  
Multidrug Resistance ◽  
Phenolic Compounds ◽  
Epithelial To Mesenchymal Transition ◽  
Inflammatory Responses ◽  
Inhibition Of Proliferation ◽  
Mesenchymal Transition ◽  
Beneficial Effects ◽  
Different Types ◽  
Phenolcarboxylic Acids

The aim of the manuscript is to discuss the influence of plant polyphenols in overcoming multidrug resistance in four types of solid cancers (breast, colorectal, lung and prostate cancer). Effective treatment requires the use of multiple toxic chemotherapeutic drugs with different properties and targets. However, a major cause of cancer treatment failure and metastasis is the development of multidrug resistance. Potential mechanisms of multidrug resistance include increase of drug efflux, drug inactivation, detoxification mechanisms, modification of drug target, inhibition of cell death, involvement of cancer stem cells, dysregulation of miRNAs activity, epigenetic variations, imbalance of DNA damage/repair processes, tumor heterogeneity, tumor microenvironment, epithelial to mesenchymal transition and modulation of reactive oxygen species. Taking into consideration that synthetic multidrug resistance agents have failed to demonstrate significant survival benefits in patients with different types of cancer, recent research have focused on beneficial effects of natural compounds. Several phenolic compounds (flavones, phenolcarboxylic acids, ellagitannins, stilbens, lignans, curcumin, etc.) act as chemopreventive agents due to their antioxidant capacity, inhibition of proliferation, survival, angiogenesis, and metastasis, modulation of immune and inflammatory responses or inactivation of pro-carcinogens. Moreover, preclinical and clinical studies revealed that these compounds prevent multidrug resistance in cancer by modulating different pathways. Additional research is needed regarding the role of phenolic compounds in the prevention of multidrug resistance in different types of cancer.

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