The effect of combined miR‐200c replacement and cisplatin on apoptosis induction and inhibition of gastric cancer cell line migration

The effect of combined miR‐200c replacement and cisplatin on apoptosis induction and inhibition of gastric cancer cell line migration


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نویسندگان: مهری قصبی بناب , جعفر مجیدی ذوالبین , بهزاد منصوری , علی محمدی , نوید شمالی , نغمه شیرافکن , الهام باغبانی , توحید کاظمی , بهزاد برادران

کلمات کلیدی: apoptosis, gastric cancer, metastasis, miR‐200c

نشریه: 19614 , 1097-4652 , 234 , 2019

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نویسنده ثبت کننده مقاله بهزاد برادران
مرحله جاری مقاله تایید نهایی
دانشکده/مرکز مربوطه مرکز تحقیقات ایمونولوژی
کد مقاله 68991
عنوان فارسی مقاله The effect of combined miR‐200c replacement and cisplatin on apoptosis induction and inhibition of gastric cancer cell line migration
عنوان لاتین مقاله The effect of combined miR‐200c replacement and cisplatin on apoptosis induction and inhibition of gastric cancer cell line migration
ناشر 9
آیا مقاله از طرح تحقیقاتی و یا منتورشیپ استخراج شده است؟ بلی
عنوان نشریه (خارج از لیست فوق)
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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One of the major obstacles in the treatment of cancer is resistance to standard chemotherapeutic drugs. According to the numerous reports, miR‐200c is involved in many cancers, especially gastric cancer, and also miR‐200c has been known as an effective factor in the elimination of chemotherapy resistance. The purpose of this study was to explore the potential function and mechanism of miR‐200c and cisplatin in the inhibition of migration and induction of apoptosis in gastric cancer cells. In this study, first, miR‐200c mimics and LNA‐anti‐miR‐200c were transfected into KATOIII cells. Moreover, 3‐(4,5‐dimethylthiazol‐2‐yl)‐2,5‐diphenyltetrazolium bromide assay results revealed that increased miR‐200c expression and cisplatin can more inhibited the proliferation of KATOIII cells. MiR‐200c overexpression inhibited the movement of KATOIII cells in wound healing assay. Subsequently, miR‐200c/cisplatin could suppress colony formation in KATOIII cells. To identify a potential miR‐200c target, we investigated the effect of miR‐200c modulation on RhoE, PTEN, VEGFR, and MMP9 expression levels. Increased miR‐200c expression caused a reduction in VEGFR and MMP9 mRNA and protein, suggesting that VEGFR and MMP9 are targets of miR‐200c. In addition, reverse‐transcription polymerase chain reaction assays showed that RhoE is target gene of miR‐200c and LNA‐anti‐miR‐200c suppressed the expression of PTEN. Flow cytometry and 4′,6‐diamidino‐2‐phenylindole staining analysis indicated that miR‐200c increased the cisplatin‐induced apoptosis which may be associated with suppression of RhoE expression in KATOIII cells, also cell‐cycle analysis showed the arrest of cell‐cycle progression at the G2 phase. These data demonstrated that miR‐200c functioned as a suppressor gene in KATOIII cells. Also, miR‐200c can be a potential therapeutic approach to overcome chemoresistance during cisplatin chemotherapy.

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نویسنده نفر چندم مقاله
مهری قصبی بناباول
جعفر مجیدی ذوالبیندوم
بهزاد منصوریسوم
علی محمدیچهارم
نوید شمالیپنجم
نغمه شیرافکنششم
الهام باغبانیهفتم
توحید کاظمیهشتم
بهزاد برادراننهم

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The effect of combined.pdf1398/08/152139255دانلود