Flavonoids of Rosa roxburghii Tratt exhibit radioprotection and anti-apoptosis properties via the Bcl-2(Ca2+)/Caspase-3/PARP-1 pathway

Xu, Ping; Cai, Xinhua; Zhang, Wenbo; Li, Yana; Qiu, Ping; Lu, Dandan; He, Xiaoyang

doi:10.1007/s10495-016-1270-1

Cited by 90 publications

(51 citation statements)

References 40 publications

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“…Caspase-3 activation subsequently leads to DNA breakage, nuclear chromatin condensation, and apoptosis. 6,[42][43][44] As our data show, CS has induced intrinsic mitochondria-mediated apoptosis in a caspase-3-dependent manner, accompanying collapse of mitochondrial membrane potential and ROS production from mitochondria into the cytoplasm. This indicates that mitochondrial dysfunction may have occurred during CS-induced MDA-MB-231 cells death.…”

Section: Discussionsupporting

confidence: 58%

Chitosan promotes ROS-mediated apoptosis and S phase cell cycle arrest in triple-negative breast cancer cells: evidence for intercalative interaction with genomic DNA

et al. 2017

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Section: Discussionsupporting

confidence: 58%

Chitosan promotes ROS-mediated apoptosis and S phase cell cycle arrest in triple-negative breast cancer cells: evidence for intercalative interaction with genomic DNA

et al. 2017

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“…Caspase-3 is a physiological enzymatic protease of Bcl-2 involved in the process of apoptosis (41). In the current study, overexpression of miR-140-5p in A549 cells markedly inhibited YES1 and Bcl-2 expression; however, the protein expression levels of Bax and caspase-3 were upregulated following transfection with miR-140-5p, compared with the NC group.…”

Section: Discussionmentioning

confidence: 43%

Effect of miR‑140‑5p on the regulation of proliferation and apoptosis in NSCLC and its underlying mechanism

et al. 2019

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Non-small cell lung cancer (NSCLC) is the most common type of lung cancer accounting for ~80% of lung cancer cases. According to novel research, numerous microRNAs (miRs) have been suggested to function as important regulators of cancer. In addition, the expression of miR-140-5p is decreased in patients with NSCLC. Therefore, it is important to further elucidate the role of miR-140-5p in NSCLC. Reverse transcription-quantitative polymerase chain reaction (RT-qPCR) was used in order to investigate the expression of miR-140-5p in NSCLC tissues and matched normal tissues and to determine miR-140-5p levels following transfection with mimics into A549 lung cancer cells. Targetscan software was used to predict the oncogene target of miR-140-5p. This analysis revealed that YES proto-oncogene 1 (YES1) includes a target site for miR-140-5p binding. The results revealed that YES1 is a potential target gene of miR-140-5p, and this was further confirmed by the results of luciferase reporter assays, which demonstrated that miR-140-5p directly targeted the predicted binding site in the 3'-untranslated region of YES1. Cell Counting Kit-8 (CCK-8) and flow cytometry assays were performed to determine the levels of cell viability and apoptosis. Western blot assays was performed to investigate the expression levels of YES1 and proteins associated with apoptosis in A549 cells following transfection. The results revealed that miR-140-5p expression was significantly downregulated in NSCLC tissues compared with matched normal tissues. The expression of miR-140-5p was significantly increased following transfection with miR-140-5p mimics. The results of CCK-8 and flow cytometry assays indicated that miR-140-5p inhibited proliferation and induced apoptosis of tumor cells. Western blot analysis and RT-qPCR revealed that YES1 and B-cell lymphoma 2 (Bcl-2) mRNA and protein expression levels were markedly decreased in A549 cells, while Bcl-2 associated X (Bax) and caspase-3 expression levels increased significantly following transfection with miR-140-5p mimics compared with the negative control group. In conclusion, miR-140-5p may induce apoptosis in A549 cells by targeting YES1 and regulating the expression of apoptosis-associated proteins Bcl-2, Bax and caspase-3.

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“…A variety of apoptosis-stimulating factors initiate different protease cutting of prokaryogen caspase3 and activate caspase3, and the activated caspase3 further cuts different substrates, leading to the amplification of protease cascade reaction cutting and finally leading to apoptosis of cells. Caspase3 is a necessary pathway for the cascade of apoptotic proteins [21]. In this study, our results demonstrated that the cleaved caspase3 and PARP were activated through up-regulating of Cav1.3 after PGE2 stimulation.…”

Section: Discussionsupporting

confidence: 56%

Ca2+ channel subunit a 1D inhibits endometriosis cell apoptosis and mediated by prostaglandin E2

Yang¹,

Yuan²,

Ma³

et al. 2019

Ginekol Pol

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Objectives: Endometriosis is considered as a chronic pelvic inflammatory disease and prostaglandin E2(PGE2) (a kind of the inflammatory cytokines) was increased in the endometriosis patient's peritoneal fluid . Ca2+ signal and Ca2+ channels play an important role in cell apoptosis. This study was to explore the L-type calcium channel (Cav1.3) expression and its biological function in endometriosis. Furthermore the molecular mechanism between Cav1.3 and PGE2 was also clarified. Material and methods:The real-time PCR and immunohistochemical were used to detect the expression of Cav1.3. Apoptosis was detected by Flow cytometry assay and Western blot assay.Results: Cav1.3 was high expression in endometriosis tissue and primary endometrial stromal cells (hEM15A). Treatment with PGE2 rapidly inhibited apoptosis and increased Cav1.3 expression in hEM15A . The silencing of Cav1.3 promoted apoptosis, which was unchanged after PGE2 treatment. Moreover, the inhibition of Cav1.3 by shRNA transfection activated cleaved PARP and cleaved caspase-3. Conclusions:These available evidences suggest that Cav1.3 is required for PGE2 induction apoptosis and relates to the pathophysiology of endometriosis. Interference with Cav1.3 may offer a neo-therapeutic window in endometriosis treatment.

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Flavonoids of Rosa roxburghii Tratt exhibit radioprotection and anti-apoptosis properties via the Bcl-2(Ca2+)/Caspase-3/PARP-1 pathway

Cited by 90 publications

References 40 publications

Chitosan promotes ROS-mediated apoptosis and S phase cell cycle arrest in triple-negative breast cancer cells: evidence for intercalative interaction with genomic DNA

Chitosan promotes ROS-mediated apoptosis and S phase cell cycle arrest in triple-negative breast cancer cells: evidence for intercalative interaction with genomic DNA

Effect of miR‑140‑5p on the regulation of proliferation and apoptosis in NSCLC and its underlying mechanism

Ca2+ channel subunit a 1D inhibits endometriosis cell apoptosis and mediated by prostaglandin E2

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