Genetic Dissection of PTEN Signaling Mechanisms in Prostate Cancer

2005 ◽  
Author(s):  
Megan E. Keniry ◽  
Greg Hannon ◽  
Ramon Parsons
Keyword(s):  
Prostate Cancer ◽  
Genetic Dissection ◽  
Signaling Mechanisms

scholarly journals The many ways to make a luminal cell and a prostate cancer cell

2015 ◽  
Vol 22 (6) ◽  
pp. T187-T197 ◽  
Author(s):  
Douglas W Strand ◽  
Andrew S Goldstein
Keyword(s):  
Prostate Cancer ◽  
Stem Cell ◽  
Prostate Cancer Cell ◽  
Stem Cell Differentiation ◽  
Cell Populations ◽  
Self Renewal ◽  
Signaling Mechanisms ◽  
Cancer Initiation ◽  
The Many ◽  
Multiple Cells

Research in the area of stem/progenitor cells has led to the identification of multiple stem-like cell populations implicated in prostate homeostasis and cancer initiation. Given that there are multiple cells that can regenerate prostatic tissue and give rise to prostate cancer, our focus should shift to defining the signaling mechanisms that drive differentiation and progenitor self-renewal. In this article, we will review the literature, present the evidence and raise important unanswered questions that will help guide the field forward in dissecting critical mechanisms regulating stem-cell differentiation and tumor initiation.

scholarly journals Molecular Alterations during Progression of Prostate Cancer to Androgen Independence

2011 ◽  
Vol 57 (10) ◽  
pp. 1366-1375 ◽  
Author(s):  
Punit Saraon ◽  
Keith Jarvi ◽  
Eleftherios P Diamandis
Keyword(s):  
Prostate Cancer ◽  
Molecular Mechanisms ◽  
Therapeutic Strategies ◽  
Androgen Independence ◽  
Molecular Alterations ◽  
Signaling Mechanisms ◽  
Hormonal Therapies ◽  
Epigenetic Signatures ◽  
Key Pathways ◽  
Androgen Independent

BACKGROUND Prostate cancer is the most commonly diagnosed cancer among men in North America and is a leading cause of death. Standard treatments include androgen deprivation therapy, which leads to improved clinical outcomes. However, over time, most tumors become androgen independent and no longer respond to hormonal therapies. Several mechanisms have been implicated in the progression of prostate cancer to androgen independence. CONTENT Most tumors that have become androgen independent still rely on androgen receptor (AR) signaling. Mechanisms that enhance AR signaling in androgen-depleted conditions include: AR gene amplification, AR mutations, changes in the balance of AR cofactors, increases in steroidogenic precursors, and activation via “outlaw” pathways. Along with AR signaling, various other AR-independent “bypass” pathways have been shown to operate aberrantly during androgen independence. Changes in the epigenetic signatures and microRNA concentrations have also been implicated in the development of androgen-independent prostate cancer. SUMMARY Understanding of the molecular mechanisms that lead to the development of androgen-independent prostate cancer will allow for improved therapeutic strategies that target key pathways and molecules that are essential for these cells to survive.

scholarly journals Chemo-Preventive Effect of 1-Piperoyl Piperidine (Piperine) Is Mediated Through Intrinsic Signaling Mechanisms In Human Prostate Cancer Cells (Pc-3) In Vitro

2021 ◽  
Vol 5 (2) ◽  
Author(s):  
◽  
Nalini D ◽  
Ponnulakshmi R ◽  
Monisha Prasad ◽  
Lakshmi Priya ◽  
...  
Keyword(s):  
Prostate Cancer ◽  
Protein Expression ◽  
Cancer Cells ◽  
Human Prostate ◽  
Piper Nigrum ◽  
Human Prostate Cancer ◽  
Prostate Cancer Cells ◽  
Antitumor Effects ◽  
Signaling Mechanisms ◽  
Apoptotic Proteins

Background: Prostate cancer is a heterogeneous disease and it is second deadliest malignancy in men and the most commonly diagnosed cancer among men. Current chemo-therapies are limited due to considerable side effects. Recently, many kinds of bioactive phytochemicals have contributed significantly to developing new therapies for chemo-resistant prostate cancer due to their structural diversity. Piperine, a natural alkaloid found in the fruit of black (Piper nigrum Linn) and long (Piper longum Linn), has shown antitumor activities toward various cancer cell lines. However, the antitumor effects of piperine on intrinsic and extrinsic signaling mechanisms in breast cancer has not been elucidated so far. Aim: The study aimed to assess the anticancer activity of piperine in human prostate cancer cells through intrinsic signaling pathways. Methodology: Prostate cancer (PC3) cells were treated with different concentrations of piperine (100 & 200µg/ml) to analyze Bcl-2, p53, case pase-3 and caspase-9 protein expression in PC-3 cells. Cell viability was done using MTT in order to find the optimal dose. Results: MTT assay exhibited that piperine showed cell death at the concentration of 100 and 200µg. It significantly decreased the mRNA and protein expression of anti-apoptotic proteins (Bcl-2 and p-Bcl-2) and increased the levels of p53, casepase-3 and 9 protein expression in both concentrations used. Conclusion: Our present findings show that piperine induces apoptosis in PC-3 cells by inhibition the expression of anti-apoptotic proteins with concomitant increase in the tumor suppressor proteins effectively. Hence, piperine can be considered as a potential phototherapeutic drug for the treatment of prostate cancer which may lead to clinical utility.

scholarly journals PROLACTIN АND SEROTONIN

2015 ◽  
Vol 69 (1-2) ◽  
pp. 38-45
Author(s):  
A. E. Lychkova ◽  
A. M. Puzikov
Keyword(s):  
Breast Cancer ◽  
Prostate Cancer ◽  
Nervous System ◽  
Risk Factor ◽  
Clinical Use ◽  
Vegetative Nervous System ◽  
Genetic Characteristics ◽  
Signaling Mechanisms ◽  
Breast And Prostate Cancer

An overview of the results of studies on prolactin (PRL) is given. The molecular and genetic characteristics of PRL and its receptor (PRLR) are presented. The PRLR polymorphism in patients with tumors of the breast is described. Synthesized analogues of human PRL inhibited its peripheral effects. The vegetative nervous system modulate PRL secretion. PRL is a risk factor for breast and prostate cancer. The signaling mechanisms of PRL and its possible clinical use in therapy of breast cancer are characterized.

scholarly journals TBX2 Drives Neuroendocrine Prostate Cancer through Exosome-Mediated Repression of miR-200c-3p

Cancers ◽  
2021 ◽  
Vol 13 (19) ◽  
pp. 5020
Author(s):  
Girijesh Kumar Patel ◽  
Sayanika Dutta ◽  
Mosharaf Mahmud Syed ◽  
Sabarish Ramachandran ◽  
Monica Sharma ◽  
...  
Keyword(s):  
Prostate Cancer ◽  
Therapeutic Strategies ◽  
Signaling Mechanisms ◽  
Neuroendocrine Prostate Cancer ◽  
Signaling Axis ◽  
Castrate Resistant Prostate Cancer ◽  
Castrate Resistant ◽  
Novel Therapeutic Strategies ◽  
Tbx2 Expression ◽  
Aggressive Subtype

Deciphering the mechanisms that drive transdifferentiation to neuroendocrine prostate cancer (NEPC) is crucial to identifying novel therapeutic strategies against this lethal and aggressive subtype of advanced prostate cancer (PCa). Further, the role played by exosomal microRNAs (miRs) in mediating signaling mechanisms that propagate the NEPC phenotype remains largely elusive. The unbiased differential miR expression profiling of human PCa cells genetically modulated for TBX2 expression led to the identification of miR-200c-3p. Our findings have unraveled the TBX2/miR-200c-3p/SOX2/N-MYC signaling axis in NEPC transdifferentiation. Mechanistically, we found that: (1) TBX2 binds to the promoter and represses the expression of miR-200c-3p, a miR reported to be lost in castrate resistant prostate cancer (CRPC), and (2) the repression of miR-200c-3p results in the increased expression of its targets SOX2 and N-MYC. In addition, the rescue of mir-200c-3p in the context of TBX2 blockade revealed that miR-200c-3p is the critical intermediary effector in TBX2 regulation of SOX2 and N-MYC. Further, our studies show that in addition to the intracellular mode, TBX2/miR-200c-3p/SOX2/N-MYC signaling can promote NEPC transdifferentiation via exosome-mediated intercellular mechanism, an increasingly recognized and key mode of propagation of the NEPC phenotype.

scholarly journals Genomic Analysis Highlights the Role of the JAK-STAT Signaling in the Anti-Proliferative Effects of Dietary Flavonoid—‘Ashwagandha’ in Prostate Cancer Cells

2010 ◽  
Vol 7 (2) ◽  
pp. 177-187 ◽  
Author(s):  
Ravikumar Aalinkeel ◽  
Zihua Hu ◽  
Bindukumar B. Nair ◽  
Donald E. Sykes ◽  
Jessica L. Reynolds ◽  
...  
Keyword(s):  
Prostate Cancer ◽  
Protein Expression ◽  
Cancer Cells ◽  
Cancer Progression ◽  
Molecular Signaling ◽  
Prostate Cancer Cells ◽  
Carcinogenic Agent ◽  
Signaling Mechanisms ◽  
Gene And Protein Expression ◽  
Insight Into

Phytochemicals are dietary phytoestrogens that may play a role in prostate cancer prevention. Forty percent of Americans use complementary and alternative medicines (CAM) for disease prevention and therapy. Ashwagandha (Withania somnifera) contains flavonoids and active ingredients like alkaloids and steroidal lactones which are called ‘Withanolides’. We hypothesize that the immunomodulatory and anti-inflammatory properties of Ashwagandha might contribute to its overall effectiveness as an anti-carcinogenic agent. The goal of our study was gain insight into the general biological and molecular functions and immunomodulatory processes that are altered as a result of Ashwagandha treatment in prostate cancer cells, and to identify the key signaling mechanisms that are involved in the regulation of these physiological effects using genomic microarray analysis in conjunction with quantitative real-time PCR and western blot analysis. Ashwagandha treatment significantly downregulated the gene and protein expression of proinflammatory cytokines IL-6, IL-1β, chemokine IL-8, Hsp70 and STAT-2, while a reciprocal upregulation was observed in gene and protein expression of p38 MAPK, PI3K, caspase 6, Cyclin D and c-myc. Furthermore, Ashwagandha treatment significantly modulated the JAK-STAT pathway which regulates both the apoptosis process as well as the MAP kinase signaling. These studies outline several functionally important classes of genes, which are associated with immune response, signal transduction, cell signaling, transcriptional regulation, apoptosis and cell cycle regulation and provide insight into the molecular signaling mechanisms that are modulated by Ashwagandha, thereby highlighting the use of this bioflavanoid as effective chemopreventive agent relevant to prostate cancer progression.

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