TBMS1 exerts its cytotoxicity in NCI-H460 lung cancer cells through nucleolar stress-induced p53/MDM2-dependent mechanism, a quantitative proteomics study

Lin, Yingying; Xie, Guobin; Xia, Jianguo; Su, Dan; Liu, Jie; Jiang, Fuquan; Xu, Yang

doi:10.1016/j.bbapap.2015.11.001

Cited by 17 publications

(18 citation statements)

References 34 publications

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“…TBMS1 has been shown to activate the caspase-dependent pathway (14), inhibit Wnt/β-catenin signaling pathway (11), and induce a p53/MDM2-dependent mechanism (13) to potentiate apoptosis and cytotoxic action. In our study, TBMS1 did not significantly influence the cellular viability and proliferation in MDA-MB-231 cells at lower concentration (5 µM).…”

Section: Discussionmentioning

confidence: 99%

Tubeimoside-1 suppresses breast cancer metastasis through downregulation of CXCR4 chemokine receptor expression

Peng¹,

Zhong²,

Gao³

2016

BMB Reports

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To examine the effect of TBMS1on breast cancer metastasis, and investigate the potential mechanism by which Tubeimoside-1 (TBMS1) inhibits the CXCR4 expression in breast cancer cells. The expression of CXCR4 in breast cancer cell lines was determined by immunoblotting and real-time PCR. The effect of TBMS1 on NF-κB binding activity was evaluated by EMSA assay and ChIP analysis. Cell proliferation and invasion were analyzed by MTT assay and transwell invasion assay, respectively. The effect of TBMS1 on breast cancer metastasis was further evaluated in a metastasis model of nude mice. TBMS1 suppressed the expression of CXCR4 through inhibition of NF-κB binding activity. TBMS1 inhibited CXCL12-induced invasion in breast cancer cells, while ectopic expression of CXCR4 abolished the inhibitive activity of TBMS1. TBMS1 suppressed breast cancer metastasis in the metastatic model of nude mice. TBMS1 suppressed the CXCR4-mediated metastasis of breast cancer by inhibiting NF-κB binding activity. [BMB Reports 2016; 49(9): 502-507]

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Section: Discussionmentioning

confidence: 99%

Tubeimoside-1 suppresses breast cancer metastasis through downregulation of CXCR4 chemokine receptor expression

Peng¹,

Zhong²,

Gao³

2016

BMB Reports

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“…Tubeimoside-1 down-modulated the expression of CXCR4 (a chemokine receptor which promotes tumor metastasis) in breast cancer cells by suppressing NF-κB binding activity to CXCR4 promoter as various transcriptional factors such as NF-κB, PPAR-γ, and HIF-1α mediate the up-regulation of CXCR4 in cancerous cells [67]. After exposure [68,69]. Though several studies have reported that tubeimoside-1 induces apoptosis via inhibition of NF-κB but whether, tubeimoside-1 has direct effect on NF-κB signaling pathway or via its up-stream signaling pathway JAK or STAT-3 still needs to be investigated by researchers.…”

Section: Figure 3: Regulation Of Cell Cycle In Different Cancers By Tmentioning

confidence: 99%

Tubeimoside-1, Triterpenoid Saponin, as a Potential Natural Cancer Killer

Zafar

Sarfraz

Rasul

et al. 2018

Natural Product Communications

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Nature, an expert craftsman of molecules, has generated extensive array of bioactive molecular entities. It persists as an inexhaustible resource for discovery of drugs and supplied enormous scaffold diversification for development into effectual drugs to treat multiple pathological conditions. This review provides an update on the sources, biological, and pharmacological effects of nature's gift, a triterpenoid saponin, tubeimoside-1 which is a major bioactive constituent of the bulb of Bolbostemma paniculatum. Tubeimoside-1 is known to possess various pharmacological properties such as anti-cancer, anti-HIV, and antiinflammatory. Recently, anti-proliferative potential of tubeimoside-1 has been widely studied. The present review article seeks to cover the recent developments of tubeimoside-1's pharmacological position in the arena of herbal drugs, providing an insight into its current status in therapeutic pursuits. This anti-cancer triterpenoid saponin fight cancer progression by induction of apoptosis, cell cycle arrest, and inhibiting metastasis by specifically targeting multiple signaling pathways those are usually deregulated in various cancers. The reported data recommend tubeimoside-1's mutitarget activity in preference to single effect that may perform an imperative role towards developing tubeimoside-1 into potential pharmacological drug.

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“…The protein level of p53 mainly depends on the mechanism of ubiquitination and degradation mediated by MDM2 . MDM2 inhibitors could increase the expression of p53 in some cancer cells, which promoted the apoptosis in those cells . Other studies have shown that GC‐1 cells had a low level of MDM2 protein, but the content of p53 protein increased after exposure to MC‐LR .…”

Section: Introductionmentioning

confidence: 99%

“…24 MDM2 inhibitors could increase the expression of p53 in some cancer cells, which promoted the apoptosis in those cells. 25,26 Other studies have shown that GC-1 cells had a low level of MDM2 protein, but the content of p53 protein increased after exposure to MC-LR. 27 Further studies are needed to determine whether MC-LR can decrease the expression of MDM2 and increase the level of p53.…”

mentioning

confidence: 99%

p53‐Dependent pathway and the opening of mPTP mediate the apoptosis of co‐cultured Sertoli‐germ cells induced by microcystin‐LR

Liu

Huang

et al. 2019

Environmental Toxicology

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Microcystin‐LR (MC‐LR), a potent endotoxin, can induce reproductive toxicity. In order to investigate the role and mechanisms of apoptosis (p53‐dependent and mitochondrial pathways) of germ cells induced by MC‐LR, the co‐cultured primary Sertoli‐germ cells from Sprague‐Dawley rats were used for the experiments. Expression levels of proteins, genes, and mitochondrial membrane potential (MMP) were obtained after exposing co‐cultured Sertoli‐germ cells to MC‐LR with or without the addition of the p53 inhibitor, pifithrin‐α (PFT‐α), and MMP inhibitor, cyclosporin A (CsA). Results indicated that MC‐LR could activate p53‐dependent pathway‐associated proteins in Sertoli‐germ cells, leading to a decrease in MMP (indicating the opening of mitochondrial permeability transition pore [mPTP] and the release of Cytochrome‐c [Cyt‐c]) from the mitochondria into the cytoplasm and eventually the induction of apoptosis. PFT‐α inhibited the expression ofp53, ameliorated the MMP of the co‐cultured Sertoli‐germ cells, and prevented the release of Cyt‐c from the mitochondria into the cytoplasm, which reduces the occurrence of apoptosis. Similarly, the decreased release of Cyt‐c from the mitochondria into the cytoplasm and the declined level of apoptosis in Sertoli‐germ cells induced by MC‐LR were observed after the addition of CsA. These results indicated that the apoptosis of the co‐cultured Sertoli‐germ cells induced by MC‐LR was mediated by the p53‐dependent pathway, with the involvement of the opening of mPTP.

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TBMS1 exerts its cytotoxicity in NCI-H460 lung cancer cells through nucleolar stress-induced p53/MDM2-dependent mechanism, a quantitative proteomics study

Cited by 17 publications

References 34 publications

Tubeimoside-1 suppresses breast cancer metastasis through downregulation of CXCR4 chemokine receptor expression

Tubeimoside-1 suppresses breast cancer metastasis through downregulation of CXCR4 chemokine receptor expression

Tubeimoside-1, Triterpenoid Saponin, as a Potential Natural Cancer Killer

p53‐Dependent pathway and the opening of mPTP mediate the apoptosis of co‐cultured Sertoli‐germ cells induced by microcystin‐LR

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