Alpha7 Nicotinic Acetylcholine Receptor Mediates Nicotine-induced Apoptosis and Cell Cycle Arrest of Hepatocellular Carcinoma HepG2 Cells
Alpha7 Nicotinic Acetylcholine Receptor Mediates Nicotine-induced Apoptosis and Cell Cycle Arrest of Hepatocellular Carcinoma HepG2 Cells
نویسندگان: خلیل حاجی اصغرزاده , محمد حسین صومی , بهزاد منصوری , محمد امین دوستوندی , فاطمه وحیدیان , امیر علی مختارزاده , داریوش شانه بندی , بهزاد برادران , محسن علیزاده
کلمات کلیدی: Alpha7 nicotinic acetylcholine receptor; Small interfering RNA; Nicotine; HepG2; Apoptosis
نشریه: 952 , 1 , 10 , 2020
| نویسنده ثبت کننده مقاله |
بهزاد برادران |
| مرحله جاری مقاله |
تایید نهایی |
| دانشکده/مرکز مربوطه |
مرکز تحقیقات ایمونولوژی |
| کد مقاله |
69192 |
| عنوان فارسی مقاله |
Alpha7 Nicotinic Acetylcholine Receptor Mediates Nicotine-induced Apoptosis and Cell Cycle Arrest of Hepatocellular Carcinoma HepG2 Cells |
| عنوان لاتین مقاله |
Alpha7 Nicotinic Acetylcholine Receptor Mediates Nicotine-induced Apoptosis and Cell Cycle Arrest of Hepatocellular Carcinoma HepG2 Cells |
| ناشر |
9 |
| آیا مقاله از طرح تحقیقاتی و یا منتورشیپ استخراج شده است؟ |
بلی |
| عنوان نشریه (خارج از لیست فوق) |
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| نوع مقاله |
Original Article |
| نحوه ایندکس شدن مقاله |
ایندکس شده سطح یک – ISI - Web of Science |
| آدرس لینک مقاله/ همایش در شبکه اینترنت |
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| Purpose: The cytotoxic properties upon treatment with nicotine have been reported in several studies, but the underlying mechanisms remain not fully defined. The alpha7 nicotinic acetylcholine receptor (α7nAChR) is one of the important nicotinic receptors, which nicotine partly by binding to this receptor exerts its effects. The current study aimed to investigates the
influences of nicotine on cellular proliferative and apoptotic activities and tried to determine the involvement of α7nAChR in these functions.
Methods: Human hepatocellular carcinoma (HepG2) cell line was used to determine the
individual or combined effects of treatments with nicotine (10 μM) and specific siRNA (100
nM) targeting α7nAChR expression. The MTT assay, DAPI staining assay, and flow cytometry
assay were applied to measure the cell viability, apoptosis and cell cycle progression of the
cells, respectively. In addition, the changes in the mRNA level of the genes were assessed by
qRT-PCR.
Results: Compared to control groups, the cells treated with nicotine exhibited significant dosedependent decreases in cell viability (log IC50 = -5.12±0.15). Furthermore, nicotine induced apoptosis and cell cycle arrest especially at G2/M Phase. The qRT-PCR revealed that nicotine increased the mRNA levels of α7nAChR as well as caspase-3 and suppressed the expression
of cyclin B1. Treatment with α7-siRNA abolished these effects of nicotine.
Conclusion: These experiments determined that upregulation of α7nAChR by nicotine inhibits HepG2 cells proliferation and induces their apoptosis. These effects blocked by treatment with α7-siRNA, which indicates the involvement of α7nAChR pathways in these processes. |
| نام فایل |
تاریخ درج فایل |
اندازه فایل |
دانلود |
| 331-Alpha7 Nicotinic Acetylcholine Receptor Mediates Nicotine-induced.pdf | 1399/03/03 | 1449851 | دانلود |