Tumour suppressor PTEN enhanced enzyme activity of GPx, SOD and catalase by suppression of PI3K/AKT pathway in non-small cell lung cancer cell lines

Akça, Hakan; Demiray, Aydın; Aslan, Mutay; Açıkbaş, İbrahim; Tokgün, Onur

doi:10.3109/14756366.2011.654114

Cited by 34 publications

(24 citation statements)

References 20 publications

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“…GPx enzymes have been shown to be induced by several different pathways, including PI3K/AKT/mTOR and p53 28 36. The latter two pathways are known to be also modified by direct interaction with NS5A,29 37 and thus may play a functional role in GPx induction in HCV-infected cells.…”

Section: Discussionmentioning

confidence: 99%

Glutathione peroxidase 4 is reversibly induced by HCV to control lipid peroxidation and to increase virion infectivity

Brault

Lévy

Duponchel

et al. 2014

Gut

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Section: Discussionmentioning

confidence: 99%

Glutathione peroxidase 4 is reversibly induced by HCV to control lipid peroxidation and to increase virion infectivity

Brault

Lévy

Duponchel

et al. 2014

Gut

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“…This is further consolidated as constitutive activation of PI3K averted the anticipated ROS response to alcohol. Other groups have shown that Akt inhibition may elicit an induction of SOD expression (Akca et al, 2013; Lijnen et al, 2010). However, we have shown a reduction in SOD-3 expression with MA and HA in Akt knockout hearts.…”

Section: Discussionmentioning

confidence: 99%

Acute Alcohol Modulates Cardiac Function as PI3K/Akt Regulates Oxidative Stress

Umoh

Walker

AlRubaiee

et al. 2014

Alcohol Clin Exp Res

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Background Clinical manifestations of alcohol abuse on the cardiac muscle include defective contractility with the development of heart failure. Interestingly, low alcohol consumption has been associated with reduced risk of cardiovascular disease. Although several hypotheses have been postulated for alcoholic cardiomyopathy and for the low-dose beneficial cardiovascular effects, the precise mechanisms and mediators remain largely undefined. We hypothesize that modulation of oxidative stress by PI3K/Akt plays a key role in the cardiac functional outcome to acute alcohol exposure. Methods Thus, acutely exposed rat cardiac tissue and cardiocytes to low (LA: 5 mM), moderate (MA: 25 mM), and high (HA: 100 mM) alcohol were assessed for markers of oxidative stress in the presence and absence of PI3K/Akt activators (IGF-1 0.1 μM or constitutively active PI3K: Ad.BD110 transfection) or inhibitor (LY294002 1 μMor Akt-negative construct Ad.Akt(K179M) transfection). Results Acute LA reduced Akt, superoxide dismutase (SOD-3) and NFκB, ERK1, and p38 MAPK gene expression. Acute HA only increased that of SOD-3 and NFκB. These effects were generally inhibited by Ad.Akt(K179M) and enhanced with Ad.BD110 transfection. In parallel, LA reduced but HA enhanced Akt activity, which was reversed by IGF-1 and inhibited by Ad.Akt(K179M), respectively. Also, LA reduced caspase 3/7 activity and oxidative stress, while HA increased both. The former was blocked, while the latter effect was enhanced by Ad.Akt(K179M). The reverse was true with PI3K/Akt activation. This translated into reduced viability with HA, with no effect with LA. On the functional level, acute LA improved cardiac output and ejection fraction, mainly through increased stroke volume. This was accompanied with enhanced end-systolic pressure–volume relationship and preload recruitable stroke work. Opposite effect was recorded for HA. LA and HA in vivo functional effects were alleviated by LY and enhanced by IGF-1 treatment. Conclusions Acute LA and HA seem to oppositely affect cardiac function through modulation of oxidative stress where PI3K/Akt plays a pivotal role.

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“…The serine-threonine kinase Akt (also known as PKB) is a centrally important downstream effector of PIP3, which regulates proliferation, growth and survival (20,21). Previous studies have shown that PTEN plays an important role in the pathogenesis of diabetes and numerous cancer diseases, and further study has indicated that induction of PTEN by activation of PPARγ inhibits the PI3K/Akt signaling pathway-mediated proliferation of tumor cells (22)(23)(24)(25). The present study showed that the expression of PTEN was significantly decreased in the MCT-induced group, along with the activation of PI3K/Akt pathway, and the accelerated process of PASMCs proliferation and pulmonary vascular remodeling.…”

Section: Discussionmentioning

confidence: 99%

Activation of peroxisome proliferator-activated receptor γ ameliorates monocrotaline-induced pulmonary arterial hypertension in rats

et al. 2015

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Abstract. Activation of peroxisome proliferator-activated receptor γ (PPARγ) suppresses the proliferation of pulmonary artery smooth muscle cells (PASMCs) and vascular remodeling in rats and humans, and therefore improves the development of pulmonary arterial hypertension (PAH). However, molecular mechanisms underlying these effects have not been completely understood. In the present study, the effects of PPARγ activation in monocrotaline (MCT)-induced pulmonary artery remodeling in rats were investigated. Eighteen Sprague-Dawley (SD) rats were randomly assigned into three groups (n=6): Control (Con), PAH and PAH treated with rosiglitazone (MCT + Rosi). The right ventricular systolic pressure (RVSP), the ratio of the right to left ventricle plus septum weight [RV/(LV + S)], the percentage of medial wall thickness (%MT) and wall area (%WA) were used to evaluate the development of PAH. Tissue morphology was measured using hematoxylin and eosin staining. The protein levels of the phosphatase and tensin homologue deleted on chromosome ten (PTEN), Akt (ser473) phosphorylation (p-Akt) and total Akt in intrapulmonary arteries were determined by western blot analysis. MCT treatment significantly increased the RVSP, which was reduced by rosiglitazone treatment. The ratio of RV/(LV + S), %MT and %WA induced by MCT were similarly inhibited, which was associated with the increase of PTEN expression and the inhibition of Akt phosphorylation levels by rosiglitazone. In conclusion, activation of PPARγ ameliorates the proliferation of PASMCs and vascular remodeling by regulating the PTEN/PI3K/Akt pathway, suggesting that the activation of PPARγ has potential benefits for PAH.

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Tumour suppressor PTEN enhanced enzyme activity of GPx, SOD and catalase by suppression of PI3K/AKT pathway in non-small cell lung cancer cell lines

Cited by 34 publications

References 20 publications

Glutathione peroxidase 4 is reversibly induced by HCV to control lipid peroxidation and to increase virion infectivity

Glutathione peroxidase 4 is reversibly induced by HCV to control lipid peroxidation and to increase virion infectivity

Acute Alcohol Modulates Cardiac Function as PI3K/Akt Regulates Oxidative Stress

Activation of peroxisome proliferator-activated receptor γ ameliorates monocrotaline-induced pulmonary arterial hypertension in rats

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