Interruption of Hepatocyte Growth Factor Signaling Augmented Oridonin-Induced Death in Human Non-small Cell Lung Cancer A549 Cells &lt;i&gt;via&lt;/i&gt; c-Met-Nuclear Factor-κB-Cyclooxygenase-2 and c-Met-Bcl-2-Caspase-3 Pathways

Liu, Ying; Shi, Qi-Feng; Qi, Min; Tashiro, Shin‐ichi; Onodera, Satoshi; Ikejima, Takashi

doi:10.1248/bpb.b12-00197

Cited by 25 publications

(13 citation statements)

References 51 publications

(54 reference statements)

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“…Given the close relationship between vascular density and cell survival, the VEGF-mediated angiogenesis might contribute towards improved engraftment of HGF-transfected cells in failing heart, which could ameliorate the heart function post-MI. Moreover, HGF-induced cell survival was associated with the c-Met-Bcl-2-caspase-3 signaling pathways [39]. We found that the levels of Bcl-2 significantly increased in the myocardial tissue after cell transplantation.…”

Section: Discussionmentioning

confidence: 97%

Transplantation of HGF gene-engineered skeletal myoblasts improve infarction recovery in a rat myocardial ischemia model

et al. 2017

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BackgroundSkeletal myoblast transplantation seems a promising approach for the repair of myocardial infarction (MI). However, the low engraftment efficacy and impaired angiogenic ability limit the clinical efficiency of the myoblasts. Gene engineering with angiogenic growth factors promotes angiogenesis and enhances engraftment of transplanted skeletal myoblasts, leading to improved infarction recovery in myocardial ischemia. The present study evaluated the therapeutic effects of hepatocyte growth factor (HGF) gene-engineered skeletal myoblasts on tissue regeneration and restoration of heart function in a rat MI model.Methods and resultsThe skeletal myoblasts were isolated, expanded, and transduced with adenovirus carrying the HGF gene (Ad-HGF). Male SD rats underwent ligation of the left anterior descending coronary artery. After 2 weeks, the surviving rats were randomized into four groups and treated with skeletal myoblasts by direct injection into the myocardium. The survival and engraftment of skeletal myoblasts were determined by real-time PCR and in situ hybridization. The cardiac function with hemodynamic index and left ventricular architecture were monitored; The adenovirus-mediated-HGF gene transfection increases the HGF expression and promotes the proliferation of skeletal myoblasts in vitro. Transplantation of HGF-engineered skeletal myoblasts results in reduced infarct size and collagen deposition, increased vessel density, and improved cardiac function in a rat MI model. HGF gene modification also increases the myocardial levels of HGF, VEGF, and Bcl-2 and enhances the survival and engraftment of skeletal myoblasts.ConclusionsHGF engineering improves the regenerative effect of skeletal myoblasts on MI by enhancing their survival and engraftment ability.

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Section: Discussionmentioning

confidence: 97%

Transplantation of HGF gene-engineered skeletal myoblasts improve infarction recovery in a rat myocardial ischemia model

et al. 2017

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“…During apoptosis, the permeability of the mitochondrial membrane increased, leading to a loss of membrane potential and release of cytochrome c into the cytosol, which binds to apoptotic protease activating factor-1 (Apaf-1). 17 The Bcl-2 and Bcl-xL proteins have been identified as antiapoptotic proteins, which bind to the outer membrane of the mitochondrion and prevent the release of cytochrome c . 18 The proapoptotic members of this family, Bax and Bak, are responsible for permeabilizing the membrane under stress and promoting the release of cytochrome c from the mitochondria.…”

Section: Resultsmentioning

confidence: 99%

MicroRNA-29c-5p suppresses gallbladder carcinoma progression by directly targeting CPEB4 and inhibiting the MAPK pathway

et al. 2017

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Gallbladder cancer (GBC) is a leading cause of cancer-related deaths worldwide, and its prognosis remains poor, with a 5-year survival rate of ~5%. Given the crucial role of microRNAs (miRNAs) in cancer metastasis, we aimed to analyze the expression and function of the metastasis-associated miRNA miR-29c-5p in GBC.We validated that expression of miR-29c-5p was significantly downregulated in GBC and was closely associated with lymph node metastasis, overall survival and disease-free survival in 40 GBC patients who were followed clinically. Ectopic overexpression of miR-29c-5p dramatically repressed proliferation, metastasis, and colony formation and induced apoptosis in vitro, and it suppressed tumorigenicity in vivo through the MAPK pathway. Cytoplasmic polyadenylation element binding protein 4 (CPEB4) was identified as a critical effector target of miR-29c-5p. Enforced expression of miR-29c-5p significantly inhibited the expression of CPEB4, and restoration of CPEB4 expression reversed the inhibitory effects of miR-29c-5p on GBC cell proliferation and metastasis. Transforming growth factor-β (TGF-β) upregulated CPEB4 by downregulating miR-29c-5p, leading to MAPK pathway activation. In conclusion, the TGF-β/miR-29c-5p/CPEB4 axis has a pivotal role in the pathogenesis and poor prognosis of GBC, suggesting that miR-29c-5p is a tumor-suppressive miRNA that may serve as potential prognostic biomarker or therapeutic target for GBC.

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“…A number of previous studies have also demonstrated that HGF exerted an anti-apoptotic effect through the proapoptotic caspase-3 signaling pathway in various cells. 34,35) It has been reported that PTX can significantly decrease caspase-3 activities and reduce apoptosis to a significant extent in rat pups with hypoxic-ischemic encephalopathy. 36) Collectively, our data suggest that PTX prevents the activation of myocardial apoptosis induced by ADR, and the anti-apoptotic effect of PTX is probably mediated through cellular signaling of the HGF pathways.…”

Section: Discussionmentioning

confidence: 99%

Pentoxifylline Prevents Driamycin-Induced Myocardial Fibrosis and Apoptosis in Rats

Zang¹,

Lin

et al. 2015

Int. Heart J.

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SummaryAdriamycin (ADR) is a potent antineoplastic agent, but long-term treatment is limited by its cumulative, life-threatening cardiomyopathy. Recently, a few reports have shown that pentoxifylline (PTX) might produce cardioprotection in cardiac dysfunction. Here, we investigated the protective effects of PTX on ADR-induced cardiomyopathy in rats. Male rats were randomly assigned either to saline, ADR (adriamycin, 5 mg/kg/week), or A (adriamycin, 5 mg/kg/week) + PTX (pentoxifylline, 50 mg/kg/day) groups. After 3 weeks, these animals were sacrificed and the heart tissue was harvested for histological analysis and assessment of hepatocyte growth factor (HGF) and caspase-3 expression. Histopathological findings showed that PTX can alleviate myocardial damage caused by ADR. Cardiac fibrosis was significantly suppressed in the A+PTX group compared to that in the ADR group. The HGF gene expression was decreased significantly in the ADR group compared with the control group, but was increased in the A+PTX group. Caspase-3 was up-regulated in the ADR group, and down-regulated in the A+PTX group. These results show that treatment with PTX exerts a protective effect against ADR-induced myocardial fibrosis via regulation of HGF and caspase-3 gene expression. PTX may thus represent a useful new clinical tool for the treatment of ADR-induced cardiomyopathy. (Int Heart J 2015; 56: 651-655)

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Interruption of Hepatocyte Growth Factor Signaling Augmented Oridonin-Induced Death in Human Non-small Cell Lung Cancer A549 Cells <i>via</i> c-Met-Nuclear Factor-κB-Cyclooxygenase-2 and c-Met-Bcl-2-Caspase-3 Pathways

Cited by 25 publications

References 51 publications

Transplantation of HGF gene-engineered skeletal myoblasts improve infarction recovery in a rat myocardial ischemia model

Transplantation of HGF gene-engineered skeletal myoblasts improve infarction recovery in a rat myocardial ischemia model

MicroRNA-29c-5p suppresses gallbladder carcinoma progression by directly targeting CPEB4 and inhibiting the MAPK pathway

Pentoxifylline Prevents Driamycin-Induced Myocardial Fibrosis and Apoptosis in Rats

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