Dergiler / The European Research Journal / 2018 / Cilt: 4 - Sayı: 4

MiR-33a and statins collaboratively reduce the proliferative capacity of prostate cancer cells

Sayfa
266–274
DOI
—
🏛️Bu makalenin bibliyografik verileri ve tam metin bağlantısı DergiPark üzerinden sağlanmıştır.
DergiPark Kaydı ↗
✨

Yapay Zeka Hızlı Bakış & Çıkarımlar

AI Insight
⚡ TL;DR(1 Cümlede Hızlı Çıkarım)

These findings suggest that statins alone and together with miR-33a might be a useful tool for effective and successful eradication of PCa cells.

📌 3 Maddede Bu Makale

🎯
Amaç & Hipotez:Objectives: Prostate cancer (PCa) is one of the leading causes of cancer deaths among men in the developed countries.
📊
Temel Bulgular & Veri:Besides,significant evidencesassociate increased serum cholesterol levels with PCa development and progression.In this study, we aimed at investigating the collaborative roles of cholesterol analogs, cholesterol-lowering drugs, and miR-33a, which is an important microRNA involved in regulation of cholesterol metabolism,on the cellular phenotypes associated with PCa progression.
💡
Sonuç & Katkı:These findings suggest that statins alone and together with miR-33a might be a useful tool for effective and successful eradication of PCa cells.
🔬Tür:Araştırma Makalesi
📍Kapsam:Genişletilmiş Akademik Örneklem
⚙️Değişkenler:Prostate cancer · microRNA · miR-33a

Abstract

Objectives: Prostate cancer (PCa) is one of the leading causes of cancer deaths among men in the developed countries. Accumulating data suggests a high-cholesterol Western diet as an important risk factor for PCa. Besides,significant evidencesassociate increased serum cholesterol levels with PCa development and progression.In this study, we aimed at investigating the collaborative roles of cholesterol analogs, cholesterol-lowering drugs, and miR-33a, which is an important microRNA involved in regulation of cholesterol metabolism,on the cellular phenotypes associated with PCa progression. Methods: We evaluated the effects of low-density lipoprotein (LDL) cholesterol, 25-hydroxycholesterol (25-HC), mevastatin and simvastatin on their ownand together with miR-33a on the proliferation, invasion and anchorage independent growthcapacity of PCa cells using Cell Counting Kit-8, Matrigel invasion, and soft agar assays, respectively. Results: We show that cholesterol analogs significantly promoted proliferative, invasive, and clonogenic potential of PCa cells, while cholesterol loweringstatins demonstrated opposite effects. Moreover, LDL and 25-HC reversed the tumor suppressive potential of miR-33a and statin treatment promoted the proliferation inhibitory effect of miR-33a on PCa cells. Conclusions: We demonstrated that statins inhibited the cellular phenotypes associated with PCa progression and miR-33a treatment strengthens the impacts of statins on cellular proliferation. These findings suggest that statins alone and together with miR-33a might be a useful tool for effective and successful eradication of PCa cells.

🔖

Bu Makaleye Atıf Yap

KARATAŞ, Ö. F., ITTMANN, M. (2018). MiR-33a and statins collaboratively reduce the proliferative capacity of prostate cancer cells. The European Research Journal, Cilt: 4 - Sayı: 4, 266–274. https://ajindex.com/articles/361360

Kaynakça (13)

  1. Yang B, Liao GQ, Wen XF, Chen WH, Cheng S, Stolzenburg JU, et al. Nuclear magnetic resonance spectroscopy as a new approach for improvement of early diagnosis and risk stratification of prostate cancer. J Zhejiang Univ Sci B 2017;18:921-33
  2. Brookman-Amissah N, Nariculam J, Freeman A, Willamson M, Kirby RS, Masters JR, et al. Allelic imbalance at 13q14.2 approximately q14.3 in localized prostate cancer is associated with early biochemical relapse. Cancer Genet Cytogenet 2007;179:118-26
  3. Barron N, Keenan J, Gammell P, Martinez VG, Freeman A, Masters JR, et al. Biochemical relapse following radical prostatectomy and miR-200a levels in prostate cancer. Prostate 2012;72:1193-9
  4. Bhatnagar N, Li X, Padi SK, Zhang Q, Tang MS, Guo B. Downregulation of miR-205 and miR-31 confers resistance to chemotherapy-induced apoptosis in prostate cancer cells. Cell Death Dis 2010;1:e105
  5. Masko EM, Alfaqih MA, Solomon KR, Barry WT, Newgard CB, Muehlbauer MJ, et al. Evidence for feedback regulation following cholesterol lowering therapy in a prostate cancer xenograft model. Prostate 2017;77:446-57
  6. Van Hemelrijck M, Walldius G, Jungner I, Hammar N, Garmo H, Binda E, et al. Low levels of apolipoprotein A-I and HDL are associated with risk of prostate cancer in the Swedish AMORIS study. Cancer Causes Control 2011;22:1011-9
  7. Farwell WR, D'Avolio LW, Scranton RE, Lawler EV, Gaziano JM. Statins and prostate cancer diagnosis and grade in a veterans population. J Natl Cancer Inst 2011;103:885-92
  8. Mondul A, Weinstein S, Virtamo J, Albanes D. Serum total and HDL cholesterol and risk of prostate cancer. Cancer Causes Control 2011;22:1545-52
  9. Allott EH, Howard LE, Cooperberg MR, Kane CJ, Aronson WJ, Terris MK, et al. Postoperative statin use and risk of biochemical recurrence following radical prostatectomy: results from the Shared Equal Access Regional Cancer Hospital (SEARCH) database. BJU Int 2014;114:661-6
  10. Dillard PR, Lin MF, Khan SA. Androgen-independent prostate cancer cells acquire the complete steroidogenic potential of synthesizing testosterone from cholesterol. Mol Cell Endocrinol 2008;295:115-20
  11. Murtola TJ, Tammela TL, Lahtela J, Auvinen A. Cholesterol-lowering drugs and prostate cancer risk: a population-based case-control study. Cancer Epidemiol Biomarkers Prev 2007;16:2226-32
  12. Graaf MR, Beiderbeck AB, Egberts AC, Richel DJ, Guchelaar HJ. The risk of cancer in users of statins. J Clin Oncol 2004;22:2388-94
  13. Platz EA, Lei