Modulation of P-glycoprotein expression by triptolide in adriamycin-resistant K562/A02 cells

Li, Hao; Hui, Lulu; Xu, Wenlin; Shen, Huiling; Chen, Qiaoyun; Long, Lingliang; Zhu, Xiaolan

doi:10.3892/ol.2011.500

Cited by 23 publications

(10 citation statements)

References 26 publications

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“…Quercetin decreased cell number through the induction of apoptotic cell death in AGS cells that were measured by Annexin V/PI double staining and then were analyzed by flow cytometric assay. It is well documented that Annexin V/PI staining is a protocol for measuring and quantitating the percentage of apoptotic cell death . We also found that quercetin induces apoptotic cell death through ER stress in AGS cells based on ROS production and ATF‐6α, ATF‐6β, and GRP‐78 that were the hall markers of ER stress .…”

Section: Discussionsupporting

confidence: 51%

Quercetin induced cell apoptosis and altered gene expression in AGS human gastric cancer cells

Shang

Lee

et al. 2018

Environmental Toxicology

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Quercetin is one of the natural components from natural plant and it induces cell apoptosis in many human cancer cell lines. However, no available reports show that quercetin induces apoptosis and altered associated gene expressions in human gastric cancer cells, thus, we investigated the effect of quercetin on the apoptotic cell death and associated gene expression in human gastric cancer AGS cells. Results indicated that quercetin induced cell morphological changes and reduced total viability via apoptotic cell death in AGS cells. Furthermore, results from flow cytometric assay indicated that quercetin increased reactive oxygen species (ROS) production, decreased the levels of mitochondrial membrane potential (ΔΨ ), and increased the apoptotic cell number in AGS cells. Results from western blotting showed that quercetin decreased anti-apoptotic protein of Mcl-1, Bcl-2, and Bcl-x but increased pro-apoptotic protein of Bad, Bax, and Bid. Furthermore, quercetin increased the gene expressions of TNFRSF10D (Tumor necrosis factor receptor superfamily, member 10d, decoy with truncated death domain), TP53INP1 (tumor protein p53 inducible nuclear protein 1), and JUNB (jun B proto-oncogene) but decreased the gene expression of VEGFB (vascular endothelial growth factor B), CDK10 (cyclin-dependent kinase 10), and KDELC2 (KDEL [Lys-Asp-Glu-Leu] containing 2) that are associated with apoptosis pathways. Thus, those findings may offer more information regarding the molecular, gene expression, and signaling pathway for quercetin induced apoptotic cell death in human gastric cancer cells.

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Section: Discussionsupporting

confidence: 51%

Quercetin induced cell apoptosis and altered gene expression in AGS human gastric cancer cells

Shang

Lee

et al. 2018

Environmental Toxicology

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“…f. It possesses efficient antitumor activity against a range of cancer cells. TPL has been demonstrated to exert its reversal activity on various MDR cancer cells, mainly through the downregulation of MDR proteins, including P-glycoprotein (17)(18)(19). Our primary study revealed that TPL could notably inhibit the proliferation of a panel of MDR cancer cell lines, including A549/Taxol, MCF-7/ADR and Bel7402/5-Fu (20).…”

Section: Discussionmentioning

confidence: 99%

Triptolide exerts pro-apoptotic and cell cycle arrest activity on drug-resistant human lung cancer A549/Taxol cells via modulation of MAPK and PI3K/Akt signaling pathways

et al. 2016

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Abstract. Multidrug resistance (MDR) is a major obstacle in the effective chemotherapeutic treatment of cancers. Triptolide (TPL) is a diterpenoid isolated from Tripterygium wilfordii Hook. f., a traditional Chinese medicine. It was demonstrated in our previous study that TPL exerts anti-MDR cancers on various MDR cell lines (including A549/Taxol, MCF-7/ADR and Bel7402/5-Fu). The present study was designed to investigate its anti-proliferative activity on A549/Taxol cells, and explore the underlying mechanism of action. The anti-proliferative activity of TPL on A549/Taxol cells was assessed by 3-(4,5-dimethylthiazol-2-yl)-2,5-diphenyltetrazolium bromide (MTT) assay. Its pro-apoptosis and cell cycle arrest activities were analyzed by flow cytometry. Western blot assay was employed to investigate the levels of mitogen-activated protein kinases (MAPKs) and apoptosis-related proteins in cells. TPL efficiently suppressed the proliferation of A549/Taxol cells. Co-treatment with MAPK inhibitors in the MTT assay indicated that the extracellular signal-regulated kinase (ERK) and c-Jun N-terminal kinase (JNK) pathways were involved in the process. Upregulation of p-p38, p-ERK, p-GSK-3β, Bax and cleaved caspases-3 and -9, and downregulation of p-JNK, p-Akt and Bcl-2 were observed upon treatment with TPL in the A549/Taxol cells. The results from flow cytometry assay revealed that TPL induced apoptosis and S-phase arrest in A549/Taxol cells. This occurred as a result of the upregulation of p-ERK and p-GSK-3β, and the downregulation of p-JNK and p-Akt, and was responsible for the subsequent anti-proliferative activity.

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“…The efflux of anticancer drugs from tumor cells depends on P‐gp (Oga et al, 2012). Rhodamine‐123 is a well‐established P‐gp substrate to investigate the activity of the P‐gp by the detection of intracellular fluorescence by flow cytometry (Clark et al, 1996; Li et al, 2012). The results indicated that TFPI‐2 overexpression BEL‐7402/5‐FU cells enhanced the accumulation of rhodamine‐123 to 2.50‐fold and 2.85‐fold levels when compared with parent and negative control cells (Fig.…”

Section: Resultsmentioning

confidence: 99%

TFPI‐2 Downregulates Multidrug Resistance Protein in 5‐FU‐Resistant Human Hepatocellular Carcinoma BEL‐7402/5‐FU Cells

Lü

Hou

Song

et al. 2012

The Anatomical Record

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Tissue factor pathway inhibitor-2 (TFPI-2) is known to induce apoptosis and to suppress tumor metastasis in several types of cancer cells. However, there is little known about its reversal effect on chemoresistant tumor cells. This study investigated the effect of TFPI-2 in 5-fluorouracil (5-FU)-resistant human hepatocellular cancer BEL-7402/5-FU cells in vitro. We constructed TFPI-2 overexpression BEL-7402/5-FU cell lines and explored resistance index (RI) of 5-FU, function of the P-glycoprotein (P-gp) efflux pump, and the mRNA and protein expression of drug resistance gene, including multidrug resistance gene (MDR1), lung-resistance protein (LRP), multidrug resistance-associated protein (MRP1), glutathione-S-transferasep (GST-p), excision repair cross-complementing gene 1 (ERCC1), and p38 phosphorylation. We found that TFPI-2 improved the RI of 5-FU and inhibited P-gp function. Western blotting and real-time PCR revealed that TFPI-2 also decreased mRNA and protein expression of MDR1, LRP, MRP1, GSTp, and ERCC1, whereas p38 phosphorylation was increased. We considered that TFPI-2 reduces 5-FU resistance in BEL-7402/5-FU cells, and the mechanism appears to involve p38-mediated downregulation of drug resistance gene expression such as MDR1, LRP, MRP1, and ERCC1. Anat Rec,

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Modulation of P-glycoprotein expression by triptolide in adriamycin-resistant K562/A02 cells

Cited by 23 publications

References 26 publications

Quercetin induced cell apoptosis and altered gene expression in AGS human gastric cancer cells

Quercetin induced cell apoptosis and altered gene expression in AGS human gastric cancer cells

Triptolide exerts pro-apoptotic and cell cycle arrest activity on drug-resistant human lung cancer A549/Taxol cells via modulation of MAPK and PI3K/Akt signaling pathways

TFPI‐2 Downregulates Multidrug Resistance Protein in 5‐FU‐Resistant Human Hepatocellular Carcinoma BEL‐7402/5‐FU Cells

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