چاپ صفحه |  صفحه نخست سامانه |  نویسندگان |  اطلاعات تفضیلی |  دانلود مقاله | دانشگاه علوم پزشکی تبریز |
| نویسنده ثبت کننده مقاله | خلیل حاجی اصغرزاده |
| مرحله جاری مقاله | تایید نهایی |
| دانشکده/مرکز مربوطه | مرکز سلولهای بنیادی |
| کد مقاله | 86312 |
| عنوان فارسی مقاله | Cross-talk between nicotinic acetylcholine receptors and miRNAs: A novel mechanism in nicotine-mediated tumor progression |
| عنوان لاتین مقاله | Cross-talk between nicotinic acetylcholine receptors and miRNAs: A novel mechanism in nicotine-mediated tumor progression |
| نوع ارائه | سخنرانی |
| عنوان کنگره / همایش | The 8th International Congress on BioMedicine (ICB) |
| نوع کنگره / همایش | بین المللی |
| کشور محل برگزاری کنگره/ همایش | Iran (Islamic Republic) |
| شهر محل برگزاری کنگره/ همایش | Tehran |
| سال انتشار/ ارائه شمسی | 1403 |
| سال انتشار/ارائه میلادی | 2024 |
| تاریخ شمسی شروع و خاتمه کنگره/همایش | 1403/08/19 الی 1403/08/24 |
| آدرس لینک مقاله/ همایش در شبکه اینترنت | https://www.icbcongress.com/?lang=en |
| آدرس علمی (Affiliation) نویسنده متقاضی | Stem Cell Research Center, Tabriz University of Medical Sciences, Tabriz, Iran |
| نویسنده | نفر چندم مقاله |
|---|---|
| خلیل حاجی اصغرزاده | اول |
| عنوان | متن |
|---|---|
| کلمات کلیدی | Alpha-7 nicotinic acetylcholine receptor; Nicotine; miRNA; HepG2; Hepatocellular carcinoma |
| خلاصه مقاله | Acetylcholine (ACh) is the first discovered neurotransmitter. Its significance was highlighted in the 1900s when cholinergic system components involved in ACh's production, degradation, and action were found in various cancer types, including liver cancer, marking a new era in oncology research. Understanding the molecular mechanisms by which ACh regulates cancer cell functions, proliferation, regeneration, and differentiation is crucial. To explore the link between alpha 7 nicotinic receptor activation and microRNAs, we conducted experiments with HepG2 cell cultures. We confirmed that these cells express alpha 7 receptors, and nicotine treatment enhances this expression. Numerous studies have documented the harmful effects of nicotine on liver cancer patients. Our analysis showed that nicotine treatment reduces the expression of microRNA-124. We aimed to determine if nicotine influences the STAT-3 gene's expression via microRNA-124 in HepG2 cells. Our results demonstrated that nicotine treatment increases STAT-3 expression. We also observed similar effects in an animal model of liver disease, where nicotine administration led to increased STAT-3 levels, confirmed by immunofluorescence. Nicotine appears to downregulate microRNA-124 by upregulating alpha-7 nicotinic receptors. Since microRNA-124 is a vital tumor suppressor, its reduction may explain nicotine's role in cancer progression. Additionally, nicotine boosts STAT-3 expression, which could worsen cancer progression by increasing cytokines like interleukin-6 and TNF-alpha. The expression levels of alpha 7 nicotinic receptors may also serve as a vital cancer biomarker. Given the rise of electronic cigarette use and nicotine's effects on microRNAs and inflammation, it is advisable to minimize nicotine exposure. |
| نام فایل | تاریخ درج فایل | اندازه فایل | دانلود |
|---|---|---|---|
| Abstract.pdf | 1403/09/21 | 121819 | دانلود |
| Certificate.pdf | 1403/09/21 | 634628 | دانلود |
