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

Year 2018, Volume: 4 Issue: 4, 266 - 274, 04.10.2018

Ömer Faruk Karataş Michael Ittmann

https://doi.org/10.18621/eurj.380619

Cited By: 1

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. 

Keywords

Prostate cancer, microRNA, miR-33a, cholesterol, sttatins

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