Journals / Celal Bayar Üniversitesi Sağlık Bilimleri Enstitüsü Dergisi / 2021 / Cilt: 8 - Sayı: 2

The Effect Of Epigallocatechin-3-Gallate On Transcriptional Regulation Of Migration And Inflammation Related Genes In Benign Prostate Hyperplasia Cells

Epigallokateşin-3-gallat'ın benign prostat hiperplazi hücrelerinde migrasyon ve enflamasyon ile ilişkili genlerin transkripsiyonel regülasyonuna etkisi

Pages
323–330
DOI
—
🏛️Bibliographic metadata and full text access for this article are provided via DergiPark.
DergiPark Record ↗
✨

AI Summary & Key Takeaways

AI Insight
⚡ TL;DR(Too Long; Didn't Read)

These results show that EGCG probably reduces the activity of FAK and NFκB signaling pathways by altering the protein function without affecting mRNA levels.

📌 3 Key Takeaways

🎯
Objective & Hypothesis:Objective: This study was aimed to evaluate the role of epigallocatechin-3-gallate (EGCG) in the transcriptional regulation of genes associated with migration and inflammation in benign prostate hyperplasia (BPH-1) cells.
📊
Key Findings & Data:Material and Methods: Effect of EGCG treatment on expressions of FAK, PXN, RhoA, Rac1, Cdc42, PAK1, ROCK1, WASL genes related to migration and IL-8, IL-6, NFκB p50, NFκB p65, IκBα genes related to inflammation were determined by quantitative real time-polymerase chain reaction (qRT-PCR).
💡
Conclusion & Impact:These results show that EGCG probably reduces the activity of FAK and NFκB signaling pathways by altering the protein function without affecting mRNA levels.
🔬Design:Research Article
📍Scope:Comprehensive Sample
⚙️Variables:EGCG · migrasyon · enflamasyon

Abstract

Objective: This study was aimed to evaluate the role of epigallocatechin-3-gallate (EGCG) in the transcriptional regulation of genes associated with migration and inflammation in benign prostate hyperplasia (BPH-1) cells. Material and Methods: Effect of EGCG treatment on expressions of FAK, PXN, RhoA, Rac1, Cdc42, PAK1, ROCK1, WASL genes related to migration and IL-8, IL-6, NFκB p50, NFκB p65, IκBα genes related to inflammation were determined by quantitative real time-polymerase chain reaction (qRT-PCR). Results: It was determined that EGCG treatment did not significantly change the expressions of investigated genes over 2 fold in terms of mRNA levels. EGCG, which effectively suppresses protein phosphorylations and levels, does not play a role in transcriptional regulation of migration and inflammation-related genes. These results show that EGCG probably reduces the activity of FAK and NFκB signaling pathways by altering the protein function without affecting mRNA levels. Conclusion: It is thought that EGCG may be useful in the treatment of premalignant lesions such as LUTS (lower urinary tract symptoms) and BPH, and its mechanism of action can be predominantly realized at post-translational level.

Özet

Giriş ve Amaç: Bu çalışmada epigallokateşin-3-gallat’ın (EGCG) benign prostat hiperplazisi hücrelerinde migrasyon ve inflamasyon ile ilişkili genlerin transkripsiyonel regülasyonundaki rolünün araştırılması amaçlanmıştır. Gereç ve Yöntemler: EGCG uygulamasının migrasyon ile ilişkili FAK, PXN, RhoA, Rac1, Cdc42, PAK1, ROCK1, WASL genlerinin ve inflamasyon ile ilişkili IL-8, IL-6, NFκB p50, NFκB p65, IκBα genlerinin ekspresyonları üzerine etkisi kantitatif gerçek zamanlı-polimeraz zincir reaksiyonu (qRT-PCR) kullanılarak tespit edildi. Bulgular: EGCG uygulamasının araştırılan genlerin mRNA seviyelerinde 2 kattan fazla anlamlı bir değişikliğe yol açmadığı belirlendi. Protein fosforilasyonlarını ve seviyelerini etkili bir şekilde baskılayan EGCG’nin, migrasyon ve inflamasyon ile ilişkili genlerin transkripsiyonel regülasyonunda rol oynamadığı belirlenmiştir. Elde edilen sonuçlar, EGCG’nin büyük olasılıkla mRNA seviyelerini etkilemeden protein fonksiyonunu değiştirerek FAK ve NFκB sinyal yolaklarınının aktivitesini azalttığını göstermektedir. Sonuç: EGCG’nin alt idrar yolu semptomları ve BPH gibi premalign lezyonların tedavisinde faydalı olabileceği ve etki mekanizmasının baskın olarak post-translasyonel seviyede gerçekleştiği düşünülmektedir.

🔖

Cite This Article

TEPEDELEN, B. E. (2021). The Effect Of Epigallocatechin-3-Gallate On Transcriptional Regulation Of Migration And Inflammation Related Genes In Benign Prostate Hyperplasia Cells. Celal Bayar Üniversitesi Sağlık Bilimleri Enstitüsü Dergisi, Cilt: 8 - Sayı: 2, 323–330. https://ajindex.com/articles/351816

📄 Full Text PDF Viewer

📄

PDF görüntüleyici hazırlanıyor...

References (14)

  1. Ke, Z.B, Cai, H, et al., Identification of key genes and pathways in benign prostatic hyperplasia, Journal of Cellular Physiology, 2019, 234(11), 19942-19950.
  2. Zhou, J, Lei, Y, Chen, J, Zhou, X, Potential ameliorative effects of epigallocatechin-gallate against testosterone-induced benign prostatic hyperplasia and fibrosis in rats, International Immunopharmacology, 2018, 64, 162-169.
  3. Penna, G, Fibbi, B, et al., The Vitamin D Receptor Agonist Elocalcitol Inhibits IL-8-Dependent Benign Prostatic Hyperplasia Stromal Cell Proliferation and Inflammatory Response by Targeting the RhoA/RhoKinase and NF-kB Pathways, The Prostate, 2009, 69, 480-493.
  4. Iglesias-Gato, D, Carsten, T, et al., Androgen-independent effects of Serenoa repens extract (Prostasan®) on prostatic epithelial cell proliferation and inflammation, Phytotherapy Research: PTR, 2012, 26(2), 259-264.
  5. Eleazu, C, Eleazu, K, Kalu, W, Management of Benign Prostatic Hyperplasia: could dietary polyphenols be an alternative to existing therapies?, Frontiers and Pharmacology, 2017, 8(234), 1-11.
  6. Briganti, A, Capitanio, U, et al., Benign prostatic hyperplasia and its etiologies, European Urology Supplements, 2009, 8, 865-71.
  7. De Nunzio, C, Kramer, G, et al., The controversial relationship between benign prostatic hyperplasia and prostate cancer: the role of inflammation, European Urology, 2011, 60, 106–117.
  8. Untergasser, G, Madersbacher, S, Berger, P, Benign prostatic hyperplasia: age-related tissue-remodeling, Experimental Gerontology, 2005, 40, 121–128.
  9. Roberts, R.O, Jacobson, D.J, Rhodes, T, Klee, G.G, Leiber, M.M, Jacobsen, S.J, Serum sex hormones and measures of benign prostatic hyperplasia, Prostate, 2004, 61(2), 124-131.
  10. Giri, D, Ittmann, M. Interleukin-8 is a paracrine inducer of fibroblast growth factor 2, a stromal and epithelial growth factor in benign prostatic hyperplasia, The American Journal of Pathology, 2001, 159, 139-147.
  11. Chughtai, B, Lee, R, Te, A, Kaplan, S, Role of Inflammation in Benign Prostatic Hyperplasia, Reviews in Urology, 2011, 13, 147-150.
  12. Minciullo, P.L, Inferrera, A, Navarra, M, Calapai, G, Magno, C, Gangemi, S, Oxidative stress in benign prostatic hyperplasia: a systematic review, Urologia Internationalis, 2015, 94(3), 249–254.
  13. Wang, L, Yang, J.R, Yang, L.Y, Liu, Z.T, Chronic inflammation in benign prostatic hyperplasia: implications for therapy, Medical Hypotheses, 2008, 70(5), 1021-1023.
  14. Erbaykent Tepedelen, B, Soya, E, Korkmaz, M, Epigallocatechin-3-gallate reduces the proliferat