Collagen I and III and metalloproteinase gene and protein expression in prostate cancer in relation to Gleason score

Abstract Background The prevalence and molecular characteristics of deficient mismatch repair prostate cancer in the Japanese population have scarcely been investigated. Methods Immunohistochemistry for mismatch repair proteins (MLH1, MSH2, MSH6 and PMS2) was performed in formalin-fixed paraffin-embedded sections prepared from resected primary prostate cancers in patients who underwent prostatectomy at our institution between January 2001 and May 2016. Genetic and/or epigenetic alterations of mismatch repair genes were investigated in patients with any loss of mismatch repair protein expression in the tumour. Results Of the 337 patients, four (1.2%) showed loss of mismatch repair protein expression on immunohistochemistry. All four patients showed loss of both MSH2 and MSH6 protein expression. Genetic testing was performed in two of the four patients, demonstrating no pathogenic germline alterations were present. In each of these two patients, at least one somatic alteration inactivating MSH2 without MSH2 hypermethylation was identified, leading to the diagnosis of supposed ‘Lynch-like syndrome’. Patients with deficient mismatch repair prostate cancer were at a significantly higher stage (pT2pN0 vs. pT3-4pN0/pTanypN1, P = 0.02) and had a greater Gleason score (<8 vs. ≥8, P < 0.01) than those with proficient mismatch repair prostate cancer. Conclusions The prevalence of deficient mismatch repair prostate cancer in the Japanese hospital-based prostatectomized population was extremely low. To improve screening efficacy for deficient mismatch repair prostate cancer, screening candidates can be limited to patients with locally advanced, node-positive and/or Gleason score of 8 or greater prostate cancer. Universal tumour screening for Lynch syndrome seems ineffective in patients with prostate cancer.

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Enoxacin Exerts Anti-Tumor Effects Against Prostate Cancer Through Inducing Apoptosis

Technology in Cancer Research & Treatment ◽

10.1177/1533033821995284 ◽

2021 ◽

Vol 20 ◽

pp. 153303382199528

Author(s):

Hongyan Xu ◽

Minghuan Mao ◽

Rui Zhao ◽

Qing Zhao

Keyword(s):

Prostate Cancer ◽

Protein Expression ◽

Molecular Mechanisms ◽

Tumor Model ◽

Annexin V ◽

Stress Markers ◽

Gene And Protein Expression ◽

Xenograft Tumor Model ◽

Cancer Types ◽

Apoptotic Proteins

Background: Prostate cancer is the most commonly diagnosed cancer and second leading cause of cancer death in men. Enoxacin, a third-generation fluoroquinolone antibiotic, was found with anti-proliferative effects against many cancer types. This study was to further investigate its effects against prostate cancer and explore the underlying molecular mechanisms. Methods: PC-3 cells were treated with Enoxacin at different concentrations. Tumor model was established by subcutaneously injecting PC-3 cells into nude mice. MTT assay was used to detect cell viability. ELISA assay, Annexin V/PI staining and TUNEL assay were used to detect apoptosis. RT-qPCR and western blot were used to detect the gene and protein expression, respectively. Results: Our data showed that Enoxacin inhibited PC-3 cell proliferation and induced the apoptosis through up-regulating the expression of pro-apoptotic proteins, while down-regulating expression levels of anti-apoptotic proteins. Moreover, Enoxacin increased the gene and protein expression of the autophagy and endoplasmic reticulum stress markers. Treating tumor-bearing mice with Enoxacin significantly inhibited tumor growth in xenograft tumor model. Conclusion: Our results suggested that Enoxacin could be developed as a potential anti-tumor agent against prostate carcinoma.

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Phospholipase D2 in prostate cancer: protein expression changes with Gleason score

British Journal of Cancer ◽

10.1038/s41416-019-0610-7 ◽

2019 ◽

Vol 121 (12) ◽

pp. 1016-1026 ◽

Cited By ~ 1

Author(s):

Amanda R. Noble ◽

Karen Hogg ◽

Rakesh Suman ◽

Daniel M. Berney ◽

Sylvain Bourgoin ◽

...

Keyword(s):

Prostate Cancer ◽

Protein Expression ◽

Cell Viability ◽

Gleason Score ◽

Cell Movement ◽

Western World ◽

Prostate Cell ◽

Prostate Epithelial Cells ◽

Downstream Effects ◽

Castrate Resistant

Abstract Background Phospholipases D1 and D2 (PLD1/2) are implicated in tumorigenesis through their generation of the signalling lipid phosphatidic acid and its downstream effects. Inhibition of PLD1 blocks prostate cell growth and colony formation. Here a role for PLD2 in prostate cancer (PCa), the major cancer of men in the western world, is examined. Methods PLD2 expression was analysed by immunohistochemistry and western blotting. The effects of PLD2 inhibition on PCa cell viability and cell motility were measured using MTS, colony forming and wound-healing assays. Results PLD2 protein is expressed about equally in luminal and basal prostate epithelial cells. In cells from different Gleason-scored PCa tissue PLD2 protein expression is generally higher than in non-tumorigenic cells and increases in PCa tissue scored Gleason 6–8. PLD2 protein is detected in the cytosol and nucleus and had a punctate appearance. In BPH tissue stromal cells as well as basal and luminal cells express PLD2. PLD2 protein co-expresses with chromogranin A in castrate-resistant PCa tissue. PLD2 inhibition reduces PCa cell viability, colony forming ability and directional cell movement. Conclusions PLD2 expression correlates with increasing Gleason score to GS8. PLD2 inhibition has the potential to reduce PCa progression.

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ERG protein expression reflects hormonal treatment response and is associated with Gleason score and prostate cancer specific mortality

European Journal of Cancer ◽

10.1016/j.ejca.2012.01.001 ◽

2012 ◽

Vol 48 (4) ◽

pp. 538-546 ◽

Cited By ~ 47

Author(s):

Tarek A. Bismar ◽

Michael Dolph ◽

Liang-Hong Teng ◽

Shuhong Liu ◽

Bryan Donnelly

Keyword(s):

Prostate Cancer ◽

Protein Expression ◽

Treatment Response ◽

Gleason Score ◽

Hormonal Treatment ◽

Specific Mortality ◽

Cancer Specific Mortality

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Human kallikrein-2 gene and protein expression predicts prostate cancer at repeat biopsy

SpringerPlus ◽

10.1186/2193-1801-3-295 ◽

2014 ◽

Vol 3 (1) ◽

pp. 295 ◽

Cited By ~ 3

Author(s):

Raj Satkunasivam ◽

William Zhang ◽

John Trachtenberg ◽

Ants Toi ◽

Changhong Yu ◽

...

Keyword(s):

Prostate Cancer ◽

Protein Expression ◽

Repeat Biopsy ◽

Gene And Protein Expression ◽

Human Kallikrein 2 ◽

Kallikrein 2

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

Evidence-based Complementary and Alternative Medicine ◽

10.1093/ecam/nem184 ◽

2010 ◽

Vol 7 (2) ◽

pp. 177-187 ◽

Cited By ~ 35

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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