Doxorubicin induced apoptosis was potentiated by neferine in human lung adenocarcima, A549 cells

Poornima, Paramasivan; Velmurugan, Bharath Kumar; Weng, Ching‐Feng; Padma, Viswanadha Vijaya

doi:10.1016/j.fct.2014.03.008

Cited by 60 publications

(53 citation statements)

References 44 publications

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“…Recent reports demonstrated that neferine synergized with some chemotherapeutic agents. Research findings from our research group also confirmed the chemosensitizing effect of neferine in lung cancer cells [Poornima et al, ]. The present study focuses on determining the ability of neferine on enhancing the sensitivity of human lung carcinoma cells to cisplatin.…”

Section: Discussionsupporting

confidence: 76%

“…Neferine reverses the multidrug resistance in human breast cancer cells (MCF-7/ADM) [Cao et al, 2004b], human hepatocarcinoma (HepG2/ADR) [Ai et al, 2007], and human gastric carcinoma cells (SGC7901/VCR) [Cao et al, 2004a]. Chemosensitization of anticancer drugs by neferine was reported earlier in MCF-7 cells by Tang and Cao [2001] and in A549 cells by Poornima et al [2014a]. Yoon et al [2013] have reported endoplasmic reticulum (ER) stress-induced apoptosis by neferine in Hep3B cells.…”

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confidence: 93%

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Neferine Potentiates the Antitumor Effect of Cisplatin in Human Lung Adenocarcinoma Cells Via a Mitochondria-Mediated Apoptosis Pathway

et al. 2017

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Cisplatin is one of the most potent chemotherapeutic agents for the treatment of many types of solid tumors but its efficacy is often limited by the development of resistance and dose limiting toxicity. Neferine is an alkaloid isolated from seed embryo of Nelumbo nucifera, it has recently been shown to have anticancer effects in various human cancer cell lines. The present investigation is designed to study the chemosensitizing ability of neferine with cisplatin in A549 cells. Neferine potentiates the cisplatin induced apoptosis through the exploration of characteristic apoptotic morphological changes, induced sub-G1 cell cycle arrest, ROS hypergeneration, significant loss of cellular antioxidant enzymes, as well as loss of mitochondrial membrane potential (ΔΨM). Furthermore our results revealed that neferine combined with cisplatin down regulate the expression of Bcl-2 and up regulate the expression of Bax, Bad, Bak, release of cytochrome c, p53 levels, then activated cleavage forms of caspase-9, caspase-3, and PARP. Moreover neferine and cisplatin combination significantly down regulated the protein levels of FAK and VEGF. In addition, we observed the activity of MMP-2 and MMP-9. Thus this study provides molecular evidence for the ROS mediated apoptosis of the combinatorial regimen of cisplatin and neferine in lung cancer cells. Thus these results suggest that using neferine with cisplatin combinatorial regimen could be potentiating the effect of cisplatin and neferine reduces the cisplatin dose requirement in cancer chemotherapy. J. Cell. Biochem. 118: 2865-2876, 2017. © 2017 Wiley Periodicals, Inc.

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Section: Discussionsupporting

confidence: 76%

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confidence: 93%

Neferine Potentiates the Antitumor Effect of Cisplatin in Human Lung Adenocarcinoma Cells Via a Mitochondria-Mediated Apoptosis Pathway

et al. 2017

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“…GSH could covalently bind to proteins by a process called glutathionylation, and acts as coenzyme for numerous enzymes involved in cell defense (Pompella et al, 2003). Previous reports demonstrate that the increase in the ROS generation can cause the alteration of antioxidant enzymes in several cancer cells (Poornima et al, 2014(Poornima et al, , 2013. The result of the present study reveals that HCD reduces the cellular antioxidant pool concomitantly with an increase in ROS level.…”

Section: Discussionmentioning

confidence: 58%

16-hydroxy-cleroda-3,13-dien-16,15-olide induced glioma cell autophagy via ROS generation and activation of p38 MAPK and ERK-1/2

Thiyagarajan

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Viswanadha

et al. 2016

Environmental Toxicology and Pharmacology

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“…Nef inhibited high glucose‐induced endothelial apoptosis via blocking ROS/Akt/NF‐κB pathway . Nef sensitize the A549 cells to low dosage of doxorubicin . Recently, anticancer potential of Nef in cancer cells and cardioprotective effect against isoproterenol‐induced myocardial ischemia has been reported from our laboratory .…”

Section: Introductionmentioning

confidence: 97%

Neferine prevents NF‐κB translocation and protects muscle cells from oxidative stress and apoptosis induced by hypoxia

et al. 2016

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Neferine (Nef), a bisbenzylisoquinoline alkaloid from lotus seed embryo has a wide range of pharmacological activities. Possible molecular mechanism for the cytoprotective action of Nef during hypoxic stress has not been explored till now. Hence, this is an attempt to elucidate the molecular mechanism involved in the Nef mediated cytoprotection on hypoxia-induced cell injury. Cytoprotective dose of Nef in muscle cells (Human rhabdomyosarcoma cells) exposed to hypoxia was determined by MTT assay. Nef at 500 nM offered better cytoprotection and was used for all the experiments. ROS, intracellular calcium accumulation and mitochondrial membrane (ΔψM) potential were measured using fluorescent probes. Further, we evaluated the effect Nef on hypoxia induced inflammatory and apoptotic responses by FACS and analyzing the expression patterns of NF-κB, COX-2, HIF-1α, caspase-3, caspase-9, Bcl2, and Bax. The results of this study revealed that pretreatment of the cells with Nef significantly decreased the ΔψM and ROS in the cells subjected to hypoxia. Further, Nef inhibited NF-κB there by inhibiting the expression of its downstream regulator COX-2, while it induced the functional HIF-1α expression. The results also indicate that Nef significantly inhibited the ROS dependent mitochondrial mediated apoptosis induced during hypoxia. The cytoprotection elicited by Nef in a model of hypoxia induced cell death involves both anti-inflammatory and anti-apoptotic response. These results suggest that Nef may be used as prophylactic agent against the hypoxic challenge. © 2016 BioFactors, 42(4):407-417, 2016.

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Doxorubicin induced apoptosis was potentiated by neferine in human lung adenocarcima, A549 cells

Cited by 60 publications

References 44 publications

Neferine Potentiates the Antitumor Effect of Cisplatin in Human Lung Adenocarcinoma Cells Via a Mitochondria-Mediated Apoptosis Pathway

Neferine Potentiates the Antitumor Effect of Cisplatin in Human Lung Adenocarcinoma Cells Via a Mitochondria-Mediated Apoptosis Pathway

16-hydroxy-cleroda-3,13-dien-16,15-olide induced glioma cell autophagy via ROS generation and activation of p38 MAPK and ERK-1/2

Neferine prevents NF‐κB translocation and protects muscle cells from oxidative stress and apoptosis induced by hypoxia

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