Advanced glycation endproducts trigger autophagy in cadiomyocyte Via RAGE/PI3K/AKT/mTOR pathway

Hou, Xuwei; Hu, Zhaohui; Xu, Hanying; Xu, Jian; Shunrong, Zhang; Zhong, Yigang; He, Xiuying; Wang, Ningfu

doi:10.1186/1475-2840-13-78

Cited by 126 publications

(107 citation statements)

References 36 publications

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“…There is a strong link of rapidly altered metabolic activity induced by target inhibition of the IGF-1R signaling pathways in proliferating cells. Through direct interaction with IGF1Rβ, SM22α overexpression enhances tumor cell growth and activates the IGF1R/PI3K/Akt pathway [30,31]. Our results show that IGF2R also regulates cell proliferation, apoptosis, migration, and invasive ability.…”

Section: Discussionmentioning

confidence: 78%

IGF2R Expression is Associated with the Chemotherapy Response and Prognosis of Patients with Advanced NSCLC

Tian¹,

Yao²,

Song³

et al. 2014

Cell Physiol Biochem

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Background: Insulin-like growth factor (IGF) pathway has been suggested as a new molecular target for the treatment of cancer including Non-small cell lung cancer (NSCLC). We postulated that IGF-2 receptor (IGF2R) may be associated with treatment response and prognosis of NSCLC patients receiving chemotherapy. Methods: A total of 464 patients with inoperable advanced stage of NSCLC were enrolled. All patients received platinum-based chemotherapy. Meanwhile, the IGF2R expression in tumor samples was detected by Immunohistochemical analysis. The IGF2R expression was inhibited in several human NSCLC cell lines (H292, A549, NCI-H460, Calu-3 and NCI-H23) after small interfering RNA (siRNA) transfection and the cellular biology behavior were evaluated. Results: Of all NSCLC patients, 204 had high IGF2R expression and 260 had low IGF2R expression. The low IGF2R expression was significantly associated with the smoking status, higher tumor stage, and poorer differentiation status of these patients. Notably, we found that the low IGF2R expression was closely associated with the chemotherapy response in NSCLC patients. Patients with low IGF2R expressions had a poorer prognosis than those with high IGF2R expressions. IGF2R inhibition by si-RNA technique in NSCLC cell lines increased the proliferation, migration and invasion abilities, but reduced the apoptosis rate. IGF2R silencing significantly enhanced the chemo-resistance of NSCLC cell lines to cisplatin treatment. Conclusion: The IGF2R expression in tumor is associated with the chemotherapy response and prognosis of Patients with advanced NSCLC.

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Section: Discussionmentioning

confidence: 78%

IGF2R Expression is Associated with the Chemotherapy Response and Prognosis of Patients with Advanced NSCLC

Tian¹,

Yao²,

Song³

et al. 2014

Cell Physiol Biochem

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“…SIRT3 is overexpressed to a greater extent in several human oral cancer cells and tissues than in normal controls, and SIRT3 downregulation in these cells inhibited oral cancer cell growth and proliferation and enhanced radio- and chemo-therapeutic drug cytotoxicity [19]. High expression of SIRT3 is associated with a shorter survival time in esophageal cancer patients [20,21]. p53-induced growth arrest in human bladder cancer is regulated by the mitochondrial SIRT3 deacetylase [22,23].…”

Section: Discussionmentioning

confidence: 99%

The SIRT 3 Expression Profile is Associated with Pathological and Clinical Outcomes in Human Breast Cancer Patients

Yuan

et al. 2014

Cell Physiol Biochem

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Aims: To investigate the association of Sirtuin 3 (SIRT 3) expression between the clinical characteristics and prognosis in breast cancer patients. Methods: 308 female patients with histologically confirmed breast cancer were enrolled in this study. The SIRT 3 expressions in tumor samples were detected. All the patients were followed up overall survival time (OS) and disease-free survival (DFS) time. Results: SIRT 3 expression was significantly correlated with clinical characteristics including lymph node metastasis, pathological grade and tumor size of breast cancer. SIRT 3 expression status also affected the DFS and OS of breast cancer. Patients with high expression of SIRT 3 had shorter DFS and OS than those with low expression. Univariate and multivariate Cox analyses confirmed that high SIRT 3 expression predicted a poor prognosis in breast cancer patient. In vitro study revealed that the SIRT 3 knockdown by small interfering RNA technique dramatically reduced the proliferation, migration and invasion of breast cancer cell lines. Conclusion: Our results suggest that SIRT 3 may serve as a marker for clinical feature and prognosis for breast cancer.

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“…Hou et al reported that AGEs increase both the number of autophagosomes in endothelial cells and cell death (66). Inhibition of autophagy, however, enhanced AGE-mediated cell death in endothelial cells (155), suggesting that autophagy is functioning to protect against AGE-mediated cellular damage.…”

Section: Autophagy In Cell Types Beyond the Cardiomyocytementioning

confidence: 99%

Unbreak My Heart: Targeting Mitochondrial Autophagy in Diabetic Cardiomyopathy

Kubli

Gustafsson

2015

Antioxidants & Redox Signaling

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Significance: Diabetes is strongly associated with increased incidence of heart disease and mortality due to development of diabetic cardiomyopathy. Even in the absence of cardiovascular disease, cardiomyopathy frequently arises in diabetic patients. Current treatment options for cardiomyopathy in diabetic patients are the same as for nondiabetic patients and do not address the causes underlying the loss of contractility. Recent Advances: Although there are numerous distinctions between Type 1 and Type 2 diabetes, recent evidence suggests that the two disease states converge on mitochondria as an epicenter for cardiomyocyte damage. Critical Issues: Accumulation of dysfunctional mitochondria contributes to cardiac tissue injury in both acute and chronic conditions. Removal of damaged mitochondria by macroautophagy, termed ''mitophagy,'' is critical for maintaining cardiomyocyte health and contractility both under normal conditions and during stress. However, very little is known about the involvement of mitophagy in the pathogenesis of diabetic cardiomyopathy. A growing interest in this topic has given rise to a wave of publications that aim at deciphering the status of autophagy and mitophagy in Type 1 and Type 2 diabetes. Future Directions: This review summarizes these recent studies with the goal of drawing conclusions about the activation or suppression of autophagy and mitophagy in the diabetic heart. A better understanding of how autophagy and mitophagy are affected in the diabetic myocardium is still needed, as well as whether they can be targeted therapeutically. Antioxid. Redox Signal. 22, 1527Signal. 22, -1544

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Advanced glycation endproducts trigger autophagy in cadiomyocyte Via RAGE/PI3K/AKT/mTOR pathway

Cited by 126 publications

References 36 publications

IGF2R Expression is Associated with the Chemotherapy Response and Prognosis of Patients with Advanced NSCLC

IGF2R Expression is Associated with the Chemotherapy Response and Prognosis of Patients with Advanced NSCLC

The SIRT 3 Expression Profile is Associated with Pathological and Clinical Outcomes in Human Breast Cancer Patients

Unbreak My Heart: Targeting Mitochondrial Autophagy in Diabetic Cardiomyopathy

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