چاپ صفحه |  صفحه نخست سامانه |  چکیده مقاله |  نویسندگان |  دانلود مقاله | دانشگاه علوم پزشکی تبریز |
| نویسنده ثبت کننده مقاله | امیر مهدی زاده حقیقی |
| مرحله جاری مقاله | تایید نهایی |
| دانشکده/مرکز مربوطه | مرکز تحقیقات غدد درون ریز |
| کد مقاله | 61661 |
| عنوان فارسی مقاله | انتقال RNAi بواسطه لیپوزوم بر علیه ژن های Erk1 و Erk2 حساسیت به شیمی درمانی را در سلول های هپاتوسلولار کارسینومایی HepG2 به یک میزان افزایش نمی دهد. |
| عنوان لاتین مقاله | Liposome-mediated RNA interference delivery against Erk1 and Erk2 does not equally promote chemosensitivity in human hepatocellular carcinoma cell line HepG2. |
| ناشر | 8 |
| آیا مقاله از طرح تحقیقاتی و یا منتورشیپ استخراج شده است؟ | خیر |
| عنوان نشریه (خارج از لیست فوق) | artificial cells, nanomedicine and biotechnology |
| نوع مقاله | Original Article |
| نحوه ایندکس شدن مقاله | ایندکس شده سطح یک – ISI - Web of Science |
| آدرس لینک مقاله/ همایش در شبکه اینترنت | https://www.ncbi.nlm.nih.gov/pubmed/28058860 |
| BACKGROUND: Extracellular signal-regulated kinase (Erk)1 and Erk2 are central mediators of mitogen-activated protein kinase signaling pathway, which plays a key role in proliferation and chemoresistance of cancer cells. However, the effect of Erk1 and Erk2 in these processes may not be the same. The aim of this study was to investigate differential effect of Erk1 and Erk2 down-regulation on chemoresistance in human hepatocellular carcinoma (HCC) cells. Expression level and relative expression analysis in HepG2 cells were performed using RT-PCR and qRT-PCR, respectively. Phosphorylated-Erk1/2 and apoptosis analysis was performed by flow-cytometry (FCM) technique. RESULTS: The results showed a higher expression level of Erk2 relative to Erk1 in HepG2 cells (P < 0.01). A significant decrease in phosphorylated-Erk1/2 and a compensational response was observed after Erk1 and/or Erk2 silencing using specific small interfering ribonucleic acids (siRNAs) (P < 0.01). Furthermore, 5-fluorouracil (5-FU) chemotherapy following siRNA-mediated knockdown lead to a significant enhancement of chemosensitivity with a higher rate of early apoptosis in Erk2 silencing relative to that of Erk1) + 9%, P < 0.01). 5-FU treatment after dual knockdown of Erk1/2 showed higher rate of early apoptosis relative to single Erk1 silencing (+9.25%, P < 0.01) and also higher rate of late apoptosis compared to single Erk1 and Erk2 silencing (+4.96% and +4.66%, P < 0.01). CONCLUSION: Our data show that liposomal siRNA-mediated down-regulation of Erk1/2 can lead to potent chemosensitizing effects in HepG2 cells. Moreover, a higher chemosensitivity following Erk2 down-regulation than Erk1 down-regulation may be associated with the higher expression of Erk2 in human HCC. |
| نویسنده | نفر چندم مقاله |
|---|---|
| امیر مهدی زاده حقیقی | اول |
| محمد حسین صومی | دوم |
| مسعود دارابی امین | سوم |
| صفر فرج نیا | چهارم |
| ابوالفضل اکبرزاده | پنجم |
| سهیلا منتظرصاحب | ششم |
| مهدی یوسفی | هفتم |
| مرتضی جبارپور بنیادی | هشتم |
| نام فایل | تاریخ درج فایل | اندازه فایل | دانلود |
|---|---|---|---|
| mehdizadeh.pdf | 1396/08/10 | 1204053 | دانلود |
