این سایت در حال حاضر پشتیبانی نمی شود و امکان دارد داده های نشریات بروز نباشند
Iranian Journal of Basic Medical Sciences، جلد ۱۹، شماره ۷، صفحات ۷۷۹-۷۸۶
عنوان فارسی
چکیده فارسی مقاله
کلیدواژه‌های فارسی مقاله
عنوان انگلیسی Effects of valproic acid and pioglitazone on cell cycle progression and proliferation of T-cell acute lymphoblastic leukemia Jurkat cells
چکیده انگلیسی مقاله Objective(s): T-cell acute lymphoblastic leukemia (T-ALL) is an aggressive hematologic malignant tumor. Administration of chemical compounds influencing apoptosis and T cell development has been discussed as promising novel therapeutic strategies. Valproic acid (VPA) as a recently emerged anti-neoplastic histone deacetylase (HDAC) inhibitor and pioglitazone (PGZ) as a high-affinity peroxisome proliferator-activated receptor-gamma (PPARγ) agonist have been shown to induce apoptosis and cell cycle arrest in different studies. Here, we aimed to investigate the underlying molecular mechanisms involved in anti-proliferative effects of these compounds on human Jurkat cells. Materials and Methods: Treated cells were evaluated for cell cycle progression and apoptosis using flowcytometry and MTT viability assay. Real-time RT-PCR was carried out to measure the alterations in key genes associated with cell death and cell cycle arrest. Results: Our findings illustrated that both VPA and PGZ can inhibit Jurkat E6.1 cells in vitro after 24 hr; however, PGZ 400 μM presents the most anti-proliferative effect. Interestingly, treated cells have been arrested in G2/M with deregulated cell division cycle 25A (Cdc25A) phosphatase and cyclin-dependent kinase inhibitor 1B (CDKN1B or p27) expression. Expression of cyclin D1 gene was inhibited when DNA synthesis entry was declined. Cell cycle deregulation in PGZ and VPA-exposed cells generated an increase in the proportion of aneuploid cell population, which has not reported before. Conclusion: These findings define that anti-proliferative effects of PGZ and VPA on Jurkat cell line are mediated by cell cycle deregulation. Thus, we suggest PGZ and VPA may relieve potential therapeutic application against apoptosis-resistant malignancies.
کلیدواژه‌های انگلیسی مقاله Pioglitazone, Proliferation, T-cell leukemia, Valproic acid
نویسندگان مقاله ماریه سقاییان جزی | marie saghaeian jazi
student research committee, golestan university of medical sciences, gorgan, iran|department of molecular medicine, school of advanced technologies in medicine, golestan university of medical sciences, gorgan, iran

سازمان اصلی تایید شده: دانشگاه علوم پزشکی گلستان (Golestan university of medical sciences)

سعید محمدی | saeed mohammadi
student research committee, golestan university of medical sciences, gorgan, iran|department of molecular medicine, school of advanced technologies in medicine, golestan university of medical sciences, gorgan, iran

سازمان اصلی تایید شده: دانشگاه علوم پزشکی گلستان (Golestan university of medical sciences)

یعقوب یزدانی | yaghoub yazdani
infectious diseases research center and laboratory science research center, golestan university of medical sciences, gorgan, iran

سازمان اصلی تایید شده: دانشگاه علوم پزشکی گلستان (Golestan university of medical sciences)

سیما صدیقی | sima sedighi
joint, bone, and connective tissue research center jbcrc , golestan university of medical sciences, gorgan, iran

سازمان اصلی تایید شده: دانشگاه علوم پزشکی گلستان (Golestan university of medical sciences)

علی معماریان | ali memarian
stem cell research center, golestan university of medical sciences, gorgan, iran

سازمان اصلی تایید شده: دانشگاه علوم پزشکی گلستان (Golestan university of medical sciences)

مهرداد آقایی | mehrdad aghaei
joint, bone, and connective tissue research center jbcrc , golestan university of medical sciences, gorgan, iran

سازمان اصلی تایید شده: دانشگاه علوم پزشکی گلستان (Golestan university of medical sciences)

نشانی اینترنتی http://ijbms.mums.ac.ir/article_7364.html
فایل مقاله فایلی برای مقاله ذخیره نشده است
کد مقاله (doi)
زبان مقاله منتشر شده en
موضوعات مقاله منتشر شده
نوع مقاله منتشر شده Original Article
برگشت به: صفحه اول پایگاه   |   نسخه مرتبط   |   نشریه مرتبط   |   فهرست نشریات