<?xml version="1.0" encoding="UTF-8"?>
<!DOCTYPE Articles SYSTEM "HBI_DTD">
<Articles><Article><Journal><PublisherName></PublisherName><JournalTitle>International Journal of Preventive Medicine (Int J Prev Med)</JournalTitle><Issn>2008-7802</Issn><Volume>10</Volume><Issue>10</Issue><PubDate PubStatus="epublish"><Year>2020</Year><Month>02</Month><Day>09</Day></PubDate></Journal><title locale="en_US">Antiproliferative and Anti‑invasion Effects of Carvacrol on PC3 Human Prostate Cancer Cells through Reducing pSTAT3, pAKT, and pERK1/2 Signaling Proteins</title><FirstPage>2147</FirstPage><LastPage>2147</LastPage><Language>EN</Language><AuthorList><Author><affiliation locale="en_US">Clinical Biochemistry Research Center, Basic Health Sciences Institute, Shahrekord University of Medical Sciences, Shahrekord</affiliation></Author><Author><affiliation locale="en_US">Cellular and Molecular Research Center, Basic Health Sciences Institute, Shahrekord University of Medical Sciences, Shahrekord</affiliation></Author></AuthorList><History><PubDate PubStatus="received"><Year>2020</Year><Month>01</Month><Day>19</Day></PubDate></History><abstract locale="en_US">&lt;p&gt;&lt;span class="fontstyle0"&gt;&lt;strong&gt;Background&lt;/strong&gt;: &lt;/span&gt;&lt;span class="fontstyle2"&gt;One of the most effective parameters in the progression of the prostate cancer is interleukin (IL)‑6 through affecting pSTAT3, pERK1/2, and pAKT cell signaling proteins. Carvacrol is an herbal antioxidant with antitumor effects. The purpose of this study was to investigate the effects of carvacrol on &lt;/span&gt;&lt;span class="fontstyle3"&gt;IL&lt;/span&gt;&lt;span class="fontstyle2"&gt;‑&lt;/span&gt;&lt;span class="fontstyle3"&gt;6 &lt;/span&gt;&lt;span class="fontstyle2"&gt;gene expression, pSTAT3, pAKT, pERK1/2 cellular signaling proteins, and invasion in human prostate cancer PC3 cells. &lt;/span&gt;&lt;/p&gt;&lt;p&gt;&lt;span class="fontstyle0"&gt;&lt;strong&gt;Methods&lt;/strong&gt;: &lt;/span&gt;&lt;span class="fontstyle2"&gt;PC3 cell viability was evaluated by MTT assay with different concentrations of carvacrol (0–800 &lt;/span&gt;&lt;span class="fontstyle4"&gt;µ&lt;/span&gt;&lt;span class="fontstyle2"&gt;M). &lt;/span&gt;&lt;span class="fontstyle3"&gt;IL‑6 &lt;/span&gt;&lt;span class="fontstyle2"&gt;gene expression and cellular concentration of pSTAT3, pERK1/2, and pAKT were investigated using the real‑time reverse transcription quantitative polymerase chain reaction (RT‑qPCR) and western blotting technic, respectively. PC3 cell invasion was determined by invasion assay test. &lt;/span&gt;&lt;/p&gt;&lt;p&gt;&lt;span class="fontstyle0"&gt;&lt;strong&gt;Results&lt;/strong&gt;: &lt;/span&gt;&lt;span class="fontstyle2"&gt;Carvacrol IC &lt;/span&gt;&lt;span class="fontstyle2" style="font-size: 5pt;"&gt;50 &lt;/span&gt;&lt;span class="fontstyle2"&gt;for PC3 prostate cancer cells was 360 &lt;/span&gt;&lt;span class="fontstyle4"&gt;µ&lt;/span&gt;&lt;span class="fontstyle2"&gt;M. Carvacrol led to a significant reduction (&lt;/span&gt;&lt;span class="fontstyle3"&gt;P &lt;/span&gt;&lt;span class="fontstyle2"&gt;&amp;lt; 0.05) for &lt;/span&gt;&lt;span class="fontstyle3"&gt;IL‑6 &lt;/span&gt;&lt;span class="fontstyle2"&gt;gene expression in a dose‑dependent manner compared to control. IL‑6 protein reduced 41.5% and 52.7% when compared with control cells at 360 and 420 &lt;/span&gt;&lt;span class="fontstyle4"&gt;µ&lt;/span&gt;&lt;span class="fontstyle2"&gt;M of carvacrol, respectively.&lt;br /&gt;Carvacrol led to a decline in pSTAT3, pAKT, and pERK1/2 above 360 &lt;/span&gt;&lt;span class="fontstyle4"&gt;µ&lt;/span&gt;&lt;span class="fontstyle2"&gt;M compared to control. PC3 potential invasion was significantly reduced after treatment with carvacrol in a dose‑dependent manner. &lt;/span&gt;&lt;/p&gt;&lt;p&gt;&lt;span class="fontstyle0"&gt;&lt;strong&gt;Conclusions&lt;/strong&gt;: &lt;/span&gt;&lt;span class="fontstyle2"&gt;Decreased IL‑6 protein level by carvacrol resulted in diminishing of pSTAT3, pERK1/2, and pAKT signaling proteins, which leads to the reduction of the cell survival, proliferation, and invasion in PC3 cells.&lt;br /&gt;&lt;/span&gt;&lt;/p&gt;&lt;p&gt;&lt;span class="fontstyle0" style="color: #00652e;"&gt;&lt;strong&gt;Keywords&lt;/strong&gt;: &lt;/span&gt;&lt;span class="fontstyle3"&gt;Cell survival, interleukin‑6, prostatic neoplasms, STAT3 protein, terpenes&lt;/span&gt;&lt;/p&gt;</abstract><web_url>http://ijpm.mui.ac.ir/index.php/ijpm/article/view/2147</web_url><pdf_url>http://ijpm.mui.ac.ir/index.php/ijpm/article/download/2147/717717943</pdf_url></Article></Articles>
