Iodine-131 induces apoptosis in human cardiac muscle cells through the p53/Bax/caspase-3 and PIDD/caspase-2/t-BID/cytochrome c/caspase-3 signaling pathway

Wang, Yansheng; Liu, Changqing; Wang, Jianchun; Zhang, Yang; Chen, Linlin

doi:10.3892/or.2017.5813

Cited by 16 publications

(10 citation statements)

References 26 publications

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“…Caspase 2 (CASP2) may function in stress-induced cell death pathways, cell cycle maintenance and tumor suppression (13). CASP2 can induce apoptosis, and overexpression of CASP2 was previously demonstrated in several types of cells (14,15). CASP2 is regulated by several miRNAs, such as miR-183 in ovarian cancer (16).…”

Section: Introductionmentioning

confidence: 91%

Upregulated miRNA‑182‑5p expression in tumor tissue and peripheral blood samples from patients with non‑small cell lung cancer is associated with downregulated Caspase 2 expression

Yang¹,

Dou²,

Sui³

et al. 2019

Exp Ther Med

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Lung cancer has the highest morbidity and mortality rates among all malignant tumors worldwide. Previous studies demonstrated that microRNA (miR)-182-5p may serve different roles in different types of cancer, including renal cell carcinoma and liver cancer. However, the functional role of miR-182-5p in non-small cell lung cancer (NSCLC) remains unknown. In the current study, the expression level of miR-182-5p in tumor tissue and peripheral blood samples obtained from patients with NSCLC was examined. The biological function of miR-182-5p on NSCLC cell proliferation was also investigated. Tissue and adjacent normal tissue samples were collected from 33 patients with NSCLC. In addition, peripheral blood samples were obtained from patients with NSCLC and 26 healthy control patients. The NSCLC cell line H1299 was used for all functional assays. Reverse transcription-quantitative polymerase chain reaction was used to determine the miR-182-5p or Caspase 2 (CASP2) mRNA expression levels in NSCLC tissue and peripheral blood samples, as well as in the NSCLC cell line. Western blotting was used to examine the protein expression level of CASP2 in tissue samples and cells, and ELISA was performed to measure the protein level of CASP2 in peripheral blood samples. MTT assay was performed to examine NSCLC cell proliferation. Flow cytometry was used to detect apoptosis. Dual-luciferase reporter assay was used to examine whether miRN182-5p directly interacts with CASP2. The current study demonstrated that miR-182-5p expression was upregulated in NSCLC tissue and peripheral blood samples from patients with NSCLC, which suggests that miR-182-5p, may serve a functional role in NSCLC. In addition, inhibition of miR-182-5p expression suppressed cell proliferation and enhanced cell apoptosis in NSCLC cells. CASP2 expression was downregulated in NSCLC tissue and peripheral blood samples from patients with NSCLC. The current study demonstrated that miR-182-5p may regulate NSCLC cell proliferation and apoptosis by regulating CASP2 expression as miR-182-5p directly binds with the 3′-untranslated region of CASP2, thereby regulating CASP2 expression.

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Section: Introductionmentioning

confidence: 91%

Upregulated miRNA‑182‑5p expression in tumor tissue and peripheral blood samples from patients with non‑small cell lung cancer is associated with downregulated Caspase 2 expression

Yang¹,

Dou²,

Sui³

et al. 2019

Exp Ther Med

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“…Cyclin D was expressed at the G1 Cyclin. Researchers had previously demonstrated that Bax/Bad mitochondrial translocation, up-regulation of p53, caspase-3 activation, PARP cleavage and DNA fragmentation were associated with apoptotic cell death in cardiomyocytes (Wang, Liu, Wang, Zhang and Chen, 2017). Punicalagin reduced H 2 O 2 -induced apoptosis by modulating the levels of reactive oxygen in PC12 cells (Clementi et al, 2017).…”

Section: Discussionmentioning

confidence: 99%

Protective effects of blueberry against hydrogen peroxide-induced oxidative stress in HEPG2 cells

Wang

Liu

et al. 2019

BFJ

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Purpose Blueberry contains bioactive compounds which are beneficial to organisms, such as phenolics and flavonoids. The purpose of this paper is to evaluate the potential protective effects of blueberry extracts (BE) on H2O2-induced HepG2 cells. Design/methodology/approach Cell protection was evaluated via the survivals of the cell. Reactive oxygen species (ROS) level, antioxidant enzyme and malondialdehyde (MDA) were detected. Western blot was carried out to analysis protein which was related to the cell apoptosis pathway. Changes in morphology including: cell total apoptosis/necrosis and G0/G1 cycle arresting were also concomitant. Findings The levels of ROS and malondialdehyde (MDA) reduced after the BE treatment while the contents of superoxide dismutase, and glutathione peroxidase (GSH-Px) increased in HepG2 cells induced by H2O2. Furthermore, mechanistic studies indicated that BE regulated the activation of mitochondrial apoptosis signal-regulating (Bcl-2, Bax). Qu was used as a positive control group. All these results demonstrated that the BE have a potential against oxidative stress in vitro. Originality/value Few studies have focused on the bioactivities of blueberry on oxidative stress. Taken together, the results confirm that polyphenol-enriched BE have the ability to protect against oxidative stress in cells. It has a great potential as a functional food ingredient to health benefits. Furthermore, this work showed the value of using simple biological models to screen for compounds that are of interest for food and pharmacological industry.

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“…Puma is a powerful proapoptotic protein that is able to inhibit the expression of the antiapoptotic protein Bcl-2 (32). If the balance between proapoptotic factors and antiapoptotic factors is altered, the permeability of the mitochondrial membrane increases and cytochrome c is released into the cytoplasm, thus activating the caspase cascade, which results in caspase-mediated breakdown of the mitochondrial membrane (33)(34)(35). Puma is transcriptionally activated by p53 (36,37).…”

Section: Discussionmentioning

confidence: 99%

Hirsutanol A inhibits T‑acute lymphocytic leukemia Jurkat cell viability through cell cycle arrest and p53‑dependent induction of apoptosis

et al. 2021

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Acute lymphocytic leukemia (ALL) is a type of childhood leukemia with the highest incidence; T-acute lymphocytic leukemia (T-ALL) is far more difficult to treat than B-acute lymphocytic leukemia (B-ALL) and has a poor long-term prognosis. Therefore, there is an urgent requirement to develop effective drugs for the treatment of T-ALL. Hirsutanol A is a natural sesquiterpenoid compound. The aim of the present study was to evaluate the in vitro anticancer activity of hirsutanol A against T-acute lymphocytic leukemia Jurkat cells and investigate the mechanism of action. A Cell Counting Kit-8 assay demonstrated that hirsutanol A inhibited the viability of Jurkat cells in a dose-and time-dependent manner. In addition, hirsutanol A induced cell cycle arrest at the G 2 phase as determined via flow cytometry. Furthermore, Hoechst staining, Annexin V-FITC/propidium iodide double staining, mitochondrial membrane potential detection using JC-1 and western blot analysis of apoptotic proteins indicated that the inhibitory effect of hirsutanol A on Jurkat cells was associated with the induction of apoptosis. Of note, hirsutanol A induced the expression of the tumor suppressor p53, whereas simultaneous treatment with pifithrin-α, an inhibitor of p53, significantly reduced Jurkat cell apoptosis induced by hirsutanol A. In summary, the present study suggested that hirsutanol A inhibited Jurkat cell viability through induction of cell cycle arrest and p53-dependent initiation of apoptosis, thus hirsutanol may serve as a promising compound for the treatment of T-ALL. By screening a natural compound library owned by State Key Laboratory of Quality Research in Chinese Medicine (Macau, China), it was revealed that hirsutanol A exerted a clear inhibitory effect on the viability of the T-ALL cell line Jurkat. Hirsutanol A is a sesquiterpenoid compound initially

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Iodine-131 induces apoptosis in human cardiac muscle cells through the p53/Bax/caspase-3 and PIDD/caspase-2/t-BID/cytochrome c/caspase-3 signaling pathway

Cited by 16 publications

References 26 publications

Upregulated miRNA‑182‑5p expression in tumor tissue and peripheral blood samples from patients with non‑small cell lung cancer is associated with downregulated Caspase 2 expression

Upregulated miRNA‑182‑5p expression in tumor tissue and peripheral blood samples from patients with non‑small cell lung cancer is associated with downregulated Caspase 2 expression

Protective effects of blueberry against hydrogen peroxide-induced oxidative stress in HEPG2 cells

Hirsutanol A inhibits T‑acute lymphocytic leukemia Jurkat cell viability through cell cycle arrest and p53‑dependent induction of apoptosis

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