کد مقاله کد نشریه سال انتشار مقاله انگلیسی نسخه تمام متن
5556829 1560542 2017 10 صفحه PDF دانلود رایگان
عنوان انگلیسی مقاله ISI
Selenopheno quinolinones and coumarins promote cancer cell apoptosis by ROS depletion and caspase-7 activation
موضوعات مرتبط
علوم پزشکی و سلامت پزشکی و دندانپزشکی کاردیولوژی و پزشکی قلب و عروق
پیش نمایش صفحه اول مقاله
Selenopheno quinolinones and coumarins promote cancer cell apoptosis by ROS depletion and caspase-7 activation
چکیده انگلیسی

AimThis study was designed to investigate the mechanism underlying cancer cell apoptosis caused by selenophenoquinolinones and coumarins.Materials and methodsTwelve derivatives were studied according to their ability to suppress the proliferation of cancer cells in vitro (i.e., HepG2, MH-22A, MCF-7), induce cell apoptosis, modulate cellular antioxidant enzyme system activities (i.e., SOD, GPx, TrxR), influence the level of ROS, and modulate caspase activity.ResultsA plausible mechanism of apoptosis is presented. The lack of change in the activity of caspase-8 demonstrates that these compounds affect the intrinsic rather than the extrinsic pathway; moreover, the absence of caspase-9 activation suggests that the studied compounds are involved in the intrinsic pathway of apoptosis in a non-canonical manner. Provisionally, the increase in Smac/Diablo released from the mitochondria removes the inhibitory effect and activates caspase-7, leading to apoptosis. Additionally, the activation of caspase-1 activates effector caspase-7, thereby increasing the amount of cytochrome c and Smac/Diablo released from the mitochondria and ultimately leading to apoptosis.ConclusionThis present study provides scientific evidence that selenopheno quinolinones and coumarins promote cancer cell apoptosis by ROS depletion and caspase-7 activation in malignant cells.

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ناشر
Database: Elsevier - ScienceDirect (ساینس دایرکت)
Journal: Life Sciences - Volume 186, 1 October 2017, Pages 92-101
نویسندگان
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