Vitexin protects isoproterenol induced post myocardial injury by modulating hipposignaling and ER stress responses

Ashokkumar, Rathinavel; Jamuna, Sankar; Sadullah, Mohammed Sadullah Sakeena; Devaraj, S. Niranjali

doi:10.1016/j.bbrc.2018.01.104

Cited by 25 publications

(13 citation statements)

References 24 publications

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“…Furthermore, Mst1 downregulation has been identified as a potential early detection biomarker for numerous types of cancer, including colorectal cancer ( 47 ), breast cancer ( 48 ), pancreatic cancer ( 49 ), lung cancer ( 50 ) and liver cancer. At the molecular level, Mst1 has been reported to be associated with the ER stress response ( 51 ), cellular oxidative stress ( 52 ), epithelial-to-mesenchymal transition ( 53 ), transforming growth factor β-mediated tissue fibrosis ( 54 ) and mitophagy ( 7 ). The present study reported that Mst1 was downregulated in A549 cells, which was similar to previous conclusions ( 55 ).…”

Section: Discussionmentioning

confidence: 99%

Mst1 regulates non-small cell lung cancer A549 cell apoptosis by inducing mitochondrial damage via ROCK1/F‑actin pathways

et al. 2018

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Mammalian STE20-like kinase 1 (Mst1) is well recognized as a major tumor suppressor in cancer development, growth, metabolic reprogramming, metastasis, cell death and recurrence. However, the roles of Mst1 in non-small cell lung cancer (NSCLC) A549 cell phenotypic alterations remain to be elucidated. The present study aimed to explore the functional role and underlying mechanisms of Mst1 with regards to A549 cell proliferation, migration and apoptosis; this study focused on mitochondrial homeostasis and Rho-associated coiled-coil containing protein kinase 1 (ROCK1)/F-actin pathways. The results demonstrated that Mst1 was downregulated in A549 cells compared with in a normal pulmonary epithelial cell line. Subsequently, overexpression of Mst1 in A549 cells reduced cell viability and promoted cell apoptosis. Furthermore, overexpression of Mst1 suppressed A549 cell proliferation and migration. At the molecular level, the reintroduction of Mst1 in A549 cells led to activation of mitochondrial apoptosis, as evidenced by a reduction in mitochondrial potential, overproduction of ROS, cytochrome c release from the mitochondria into the nucleus, and upregulation of pro-apoptotic protein expression. In addition, Mst1 overexpression was closely associated with impaired mitochondrial respiratory function and suppressed cellular energy metabolism. Functional studies illustrated that Mst1 overexpression activated ROCK1/F-actin pathways, which highly regulate mitochondrial function. Inhibition of ROCK1/F-actin pathways in A549 cells sustained mitochondrial homeostasis, alleviated caspase-9-dependent mitochondrial apoptosis, enhanced cancer cell migration and increased cell proliferation. In conclusion, these data firmly established the regulatory role of Mst1 in NSCLC A549 cell survival via the modulation of ROCK1/F-actin pathways, which may provide opportunities for novel treatment modalities in clinical practice.

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Section: Discussionmentioning

confidence: 99%

Mst1 regulates non-small cell lung cancer A549 cell apoptosis by inducing mitochondrial damage via ROCK1/F‑actin pathways

et al. 2018

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“…It has been reported that a number of components of CHM can inhibit the growth of tumor cells both in vitro and in vivo, such as polysaccharides, flavones, terpenoids, and phenols [21,22,23,24,25,26]. The components of polysaccharides, flavones, and triterpenes in AAEE, AAEE-Pe, and AAEE-Ea were quantified.…”

Section: Discussionmentioning

confidence: 99%

The Extracts of Artemisia absinthium L. Suppress the Growth of Hepatocellular Carcinoma Cells through Induction of Apoptosis via Endoplasmic Reticulum Stress and Mitochondrial-Dependent Pathway

Wei

Ziyayiding

et al. 2019

Molecules

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Artemisia absinthium L. has pharmaceutical and medicinal effects such as antimicrobial, antiparasitic, hepatoprotective, and antioxidant activities. Here, we prepared A. absinthium ethanol extract (AAEE) and its subfractions including petroleum ether (AAEE-Pe) and ethyl acetate (AAEE-Ea) and investigated their antitumor effect on human hepatoma BEL-7404 cells and mouse hepatoma H22 cells. The cell viability of hepatoma cells was measured by 3-(4,5-dimethylthiazol-2-yl)-2,5-diphenyltetrazolium bromide (MTT) assay. The apoptosis, cell cycle, mitochondrial membrane potential (Δψm), and reactive oxygen species (ROS) were analyzed by flow cytometry. The levels of proteins in the cell cycle and apoptotic pathways were detected by Western blot. AAEE, AAEE-Pe, and AAEE-Ea exhibited potent cytotoxicity for both BEL-7404 cells and H22 cells through the induction of cell apoptosis and cell cycle arrest. Moreover, AAEE, AAEE-Pe, and AAEE-Ea significantly reduced Δψm, increased the release of cytochrome c, and promoted the cleavage of caspase-3, caspase-9, and poly(ADP-ribose) polymerase (PARP) in BEL-7404 and H22 cells. AAEE, AAEE-Pe, and AAEE-Ea significantly upregulated the levels of ROS and C/EBP-homologous protein (CHOP). Further, AAEE, AAEE-Pe, and AAEE-Ea significantly inhibited tumor growth in the H22 tumor mouse model and improved the survival of tumor mice without side effects. These results suggest that AAEE, AAEE-Pe, and AAEE-Ea inhibited the growth of hepatoma cells through induction of apoptosis, which might be mediated by the endoplasmic reticulum stress and mitochondrial-dependent pathway.

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“…The activated Hippo-YAP signaling pathway promoted neuron survival in the TNFα-induced microenvironment by inhibiting ER stress (52). In addition, downregulation of YAP evoked ER stress and contributed to myocyte death in isoproterenol-induced myocardial infarction (53). The results of the present study are consistent with previous studies.…”

Section: Discussionmentioning

confidence: 99%

YAP promotes gastric cancer cell survival and migration/invasion via the ERK/endoplasmic reticulum stress pathway

Liu

Mei

et al. 2019

Oncol Lett

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Yes-associated protein (YAP) has been reported to serve an important role in gastric cancer cell survival and migration. However, the underlying mechanism remains unclear. The aim of present study was to identify the underlying mechanism through which Yap sustains gastric cancer viability and migration. The results of the present study demonstrated that YAP expression was upregulated in gastric cancer MKN-28/74 cells compared with normal gastric GES-1 cells. Functional studies revealed that silencing of YAP inhibited gastric cancer MKN-28/74 cell viability and invasion. Mechanistically, YAP may promote gastric cancer cell survival and migration/invasion by inhibiting the endoplasmic reticulum (ER) stress pathway. In addition, YAP may regulate ER stress by activating the ERK signaling pathway. The results of the present study suggested that YAP may be a tumor promoter in gastric cancer and act through the ERK/ER stress pathway; therefore, YAP may have potential implications for new approaches to gastric cancer therapy.

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Vitexin protects isoproterenol induced post myocardial injury by modulating hipposignaling and ER stress responses

Cited by 25 publications

References 24 publications

Mst1 regulates non-small cell lung cancer A549 cell apoptosis by inducing mitochondrial damage via ROCK1/F‑actin pathways

Mst1 regulates non-small cell lung cancer A549 cell apoptosis by inducing mitochondrial damage via ROCK1/F‑actin pathways

The Extracts of Artemisia absinthium L. Suppress the Growth of Hepatocellular Carcinoma Cells through Induction of Apoptosis via Endoplasmic Reticulum Stress and Mitochondrial-Dependent Pathway

YAP promotes gastric cancer cell survival and migration/invasion via the ERK/endoplasmic reticulum stress pathway

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