Mahanine induces apoptosis, cell cycle arrest, inhibition of cell migration, invasion and PI3K/AKT/mTOR signalling pathway in glioma cells and inhibits tumor growth in vivo

Chen, Maohua; Yin, Xiang; Lü, Chuan; Chen, Xiandong; Ba, Hua-Jun; Cai, Jianping; Sun, Jun

doi:10.1016/j.cbi.2018.11.009

Cited by 23 publications

(10 citation statements)

References 25 publications

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“…Matrix metalloproteins (MMPs) are involved in degrading the extracellular matrix in various pathophysiological processes, promoting tumor metastasis (Conlon and Murray, 2019). It has been demonstrated that MMP2, an important member of MMP family, can be targeted by Akt to promote glioblastoma metastasis (M. Chen et al, 2019). It has been shown that inhibition of PI3K and Akt led to suppression of MMP-2/-9 activity and protein levels in cancer cells (G. Chen et al, 2017).…”

Section: Discussionmentioning

confidence: 99%

“…To understand the molecular mechanisms by which ANXA1 controlled glioma cell proliferation, migration and invasion, we explored the effect of ANXA1 on expression levels of cell cycle-related proteins and several key signal pathways, which are closely related to the above mentioned biological function of glioma cells (M. Chen et al, 2019;Wei et al, 2019). Western blot analysis showed that ANXA1 had a prominent effect on cdc25C, cdc2 and cyclin B1 protein levels and PI3K/Akt signaling cascades but had no effect on cyclin D1, GSK-3b or b-catenin signaling in U87 cells (Figure 5A to D).…”

Section: Inhibition Of Anxa1 Induces G2/m Cell Cycle Arrest and By Inhibiting The Pi3k/akt Signaling Pathwaymentioning

confidence: 99%

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Knockdown of Annexin-A1 Inhibits Growth, Migration and Invasion of Glioma Cells by Suppressing the PI3K/Akt Signaling Pathway

Wei

Liu

et al. 2021

ASN Neuro

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ANXA1, which can bind phospholipid in a calcium dependent manner, is reported to play a pivotal role in tumor progression. However, the role and mechanism of ANXA1 involved in the occurrence and development of malignant glioma are still not well studied. Therefore, we explored the effects of ANXA1 on normal astrocytes and glioma cell proliferation, apoptosis, migration and invasion and the underlying mechanisms. We found that ANXA1 was markedly up-regulated in glioma cell lines and glioma tissues. Down-regulation of ANXA1 inhibited normal astrocytes and glioma cell proliferation and induced the cell apoptosis, which suggested that the consequences of loss of Annexin 1 are not specific to the tumor cells. Furthermore, the siRNA-ANXA1 treatment significantly reduced tumor growth rate and tumor weight. Moreover, decreasing ANXA1 expression caused G2/M phase arrest by repressing expression levels of cdc25C, cdc2 and cyclin B1. Interestingly, ANXA1 did not affect the expressions of β-catenin, GSK-3β and NF-κB, the key signaling molecules associated with cancer progression. However, siRNA-ANXA1 was found to negatively regulate phosphorylation of AKT and the expression and activity of MMP2/-9. Finally, the decrease of cell proliferation and invasiveness induced by ANXA1 down-regulation was partially reversed by combined treatment with AKT agonist insulin-like growth factor-1 (IGF-1). Meanwhile, the inhibition of glioma cell proliferation and invasiveness induced by ANXA1 down-regulation was further enhanced by combined treatment with AKT inhibitor LY294002. In summary, these findings demonstrate that ANXA1 regulates proliferation, migration and invasion of glioma cells via PI3K/AKT signaling pathway.

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Section: Discussionmentioning

confidence: 99%

Section: Inhibition Of Anxa1 Induces G2/m Cell Cycle Arrest and By Inhibiting The Pi3k/akt Signaling Pathwaymentioning

confidence: 99%

Knockdown of Annexin-A1 Inhibits Growth, Migration and Invasion of Glioma Cells by Suppressing the PI3K/Akt Signaling Pathway

Wei

Liu

et al. 2021

ASN Neuro

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“…Previous findings have demonstrated that MK LE and its primary active compounds regulate multiple signaling pathways, including phosphatidylinositol 3 kinase (PI3K)/protein kinase B (AKT), mammalian target of rapamycin (mTOR) and mitogen-activated protein kinase (MAPK). M. koenigii and its primary active compounds exert complementary effects on oxidative stress and the alteration of proteins [94,95].…”

Section: Discussionmentioning

confidence: 99%

Repeatedly heated mix vegetable oils-induced atherosclerosis and effects of Murraya koenigii

Gul

Siddiq

Hussain

et al. 2020

BMC Complement Med Ther

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Background: Statins are considered as standard drugs to control cholesterol levels, but their use is also associated with renal hypertrophy, hemorrhagic stroke, hepatomegaly, and myopathy. Murraya koenigii is an herb that is used in traditional cuisine and as a medicine in South Asia. Here we assessed the antidyslipidemic and antiatherosclerotic effects of this spice in repeated heated mix vegetable oils (RHMVO)-induced atherosclerotic models. Methods: Aqueous extract of M. koenigii leaves (Mk LE) was prepared and its phytoconstituents were determined. Rabbits were divided into 5 groups (n = 10). Except for the control group, all the other four groups were treated with RHMVO for 16 weeks (dose = 2 ml/kg/day) to induce dyslipidemia and atherosclerosis. These groups were further treated for 10 weeks either with 300 and 500 mg/kg/day Mk LE, lovastatin, RHMVO, or left untreated. Body and organ weights were measured along with oxidative stress and tissue damage parameters. Lipid profile and hepatic function markers were studied. Atheroma measurement and histopathological examination were also performed in control and treated groups. Results: Mk LE significantly (p < 0.05) attenuated RHMVO-induced dyslipidemia and atheroma formation. Furthermore, fat accumulation and lipid peroxidation in hepatic tissues were reduced by Mk LE in a dosedependent manner. Our results indicated that the antidyslipidemic effects of Mk LE in 500 mg/kg/day dose were comparable to lovastatin. Additionally, oxidative stress markers were reduced much more significantly in Mk LE-500 than in the statin group (p < 0.05). Conclusions: This study recommends Mk LE as a potent antioxidant and lipid-lowering natural medicine that can attenuate the RHMVO-induced atherosclerotic in optimal doses and duration. Therefore, Mk LE can be accessible, cheap, and free of adverse effects alternate to statins.

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“…Previous findings have demonstrated that an M. koenigii extract and its primary active compounds regulate multiple signaling pathways, including phosphatidylinositol 3 kinase (PI3K)/protein kinase B (AKT), mammalian target of rapamycin (mTOR) and mitogen-activated protein kinase (MAPK). M. koenigii and its primary active compounds exert complementary effects on oxidative stress and the alteration of proteins [94,95]. They are associated with mitochondrial-mediated apoptotic pathways.…”

Section: Apoptosismentioning

confidence: 99%

Medicinal Profile, Phytochemistry, and Pharmacological Activities of Murraya koenigii and its Primary Bioactive Compounds

Balakrishnan

Vijayraja²,

et al. 2020

Antioxidants

120

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The discovery of several revitalizing molecules that can stop or reduce the pathology of a wide range of diseases will be considered a major breakthrough of the present time. Available synthetic compounds may provoke side effects and health issues, which heightens the need for molecules from plants and other natural resources under discovery as potential methods of replacing synthetic compounds. In traditional medicinal therapies, several plant extracts and phytochemicals have been reported to impart remedial effects as better alternatives. Murraya koenigii (M. koenigii) belongs to the Rutaceae family, which is commonly used as a medicinally important herb of Indian origin in the Ayurvedic system of medicine. Previous reports have demonstrated that the leaves, roots, and bark of this plant are rich sources of carbazole alkaloids, which produce potent biological activities and pharmacological effects. These include antioxidant, antidiabetic, anti-inflammatory, antitumor, and neuroprotective activities. The present review provides insight into the major components of M. koenigii and their pharmacological activities against different pathological conditions. The review also emphasizes the need for more research on the molecular basis of such activity in various cellular and animal models to validate the efficacy of M. koenigii and its derivatives as potent therapeutic agents.

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Mahanine induces apoptosis, cell cycle arrest, inhibition of cell migration, invasion and PI3K/AKT/mTOR signalling pathway in glioma cells and inhibits tumor growth in vivo

Cited by 23 publications

References 25 publications

Knockdown of Annexin-A1 Inhibits Growth, Migration and Invasion of Glioma Cells by Suppressing the PI3K/Akt Signaling Pathway

Knockdown of Annexin-A1 Inhibits Growth, Migration and Invasion of Glioma Cells by Suppressing the PI3K/Akt Signaling Pathway

Repeatedly heated mix vegetable oils-induced atherosclerosis and effects of Murraya koenigii

Medicinal Profile, Phytochemistry, and Pharmacological Activities of Murraya koenigii and its Primary Bioactive Compounds

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