Effects of VBMDMP on the reversal of cisplatin resistance in human lung cancer A549/DDP cells

Wang, Cheng-Kun; Zhang, Yang; Zhang, Zhijie; Qiu, Qinwei; Cao, Ji; He, Zhiwei

doi:10.3892/or.2014.3607

Cited by 5 publications

(5 citation statements)

References 36 publications

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“…FAK plays a pivotal role in integrin-mediated signal transduction, including the regulation of cell survival[40]. Activated FAK could bind multiple intracellular proteins to invoke several downstream signaling pathways such as the PI3K/AKT and MAPK pathways, thus stimulating tumor cell proliferation and inhibiting apoptosis, which is a major mechanism of tumor drug resistance[39]. In our study, BIRC2 , BIRC3 , and MLCK were found to be significantly deregulated.…”

Section: Discussionmentioning

confidence: 64%

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Transcriptome Sequencing Reveals Key Pathways and Genes Associated with Cisplatin Resistance in Lung Adenocarcinoma A549 Cells

Fang

Zhang

et al. 2017

PLoS ONE

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Acquired resistance to cisplatin-based chemotherapy frequently occurs in patients with non-small cell lung cancer, and the underlying molecular mechanisms are not well understood. The aim of this study was to investigate whether a distinct gene expression pattern is associated with acquired resistance to cisplatin in human lung adenocarcinoma. Whole-transcriptome sequencing was performed to compare the genome-wide gene expression patterns of the human lung adenocarcinoma A549 cisplatin-resistant cell line A549/DDP with those of its progenitor cell line A549. A total of 1214 differentially expressed genes (DEGs) were identified, 656 of which were upregulated and 558 were downregulated. Functional annotation of the DEGs in the Kyoto Encyclopedia of Genes and Genomes database revealed that most of the identified genes were enriched in the PI3K/AKT, mitogen-activated protein kinase, actin cytoskeleton regulation, and focal adhesion pathways in A549/DDP cells. These results support previous studies demonstrating that the pathways regulating cell proliferation and invasion confer resistance to chemotherapy. Furthermore, the results proved that cell adhesion and cytoskeleton regulation is associated with cisplatin resistance in human lung cancer. Our study provides new promising biomarkers for lung cancer prognosis and potential therapeutic targets for lung cancer treatment.

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Section: Discussionmentioning

confidence: 64%

“…FAK is a cytoplasmic non-receptor tyrosine kinase, and its activation is accompanied by the accumulation of focal adhesion molecules[39]. FAK plays a pivotal role in integrin-mediated signal transduction, including the regulation of cell survival[40].…”

Section: Discussionmentioning

confidence: 99%

Transcriptome Sequencing Reveals Key Pathways and Genes Associated with Cisplatin Resistance in Lung Adenocarcinoma A549 Cells

Fang

Zhang

et al. 2017

PLoS ONE

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“…Inhibition of miR-196a reversed DDP resistance of A549/DDP cell lines, which may be linked to inhibition of drug efflux, downregulation of drug-resistant protein expression, cell apoptosis, and suppression of cell proliferation (30). Moreover, a fusion protein based on two tumstatin-derived sequences named recombinant VBMDMP (rVBMDMP) decreased cancer cell resistance to DDP in A549/DDP cell xenograft model of nude mice (31). Epigallocatechin-3-gallate (EGCG), the major polyphenol in green tea, was also shown to resensitize non-small cell lung cancer cells to DDP via demethylation of candidate genes.…”

Section: Discussionmentioning

confidence: 99%

Baicalin attenuates DDP (cisplatin) resistance in lung cancer by downregulating MARK2 and p-Akt

Xu¹,

Mei²,

Tan³

2016

International Journal of Oncology

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DDP (cisplatin) resistance in lung cancer has been widely reported. Baicalin is a flavone glycoside found in genus Scutellaria. However, the effects of baicalin on DDP resistance in lung cancer are unclear. The aim of present study was to investigate effects of combination of baicalin and DDP on proliferation and invasion of human lung cancer cells, and explore possible mechanisms. MTT assay was utilized to evaluate effects of baicalin and DDP on the proliferation of A549 and A549/DPP (DPP-resistant) human lung cancer cells. The probability sum method was used to determine effects of the drug combination. Transwell invasion assay was utilized to detect tumor cell invasion. The mRNA expression of MARK2 in A549 and A549/DPP cells was detected by qPCR. Protein expression of MARK2, p-Akt and Akt was detected by western blot analysis. Baicalin and DPP when used alone inhibited the proliferation of A549 and A549/DDP cells in a dose-dependent manner at 24 and 48 h. For A549 cells, baicalin (8 µg/ml) antagonized DDP (1, 2, 4 and 8 µg/ml) at 24 h. For A549/DDP cells, baicalin and DDP were additive when the concentration of DDP was 4 µg/ml at 24 h. Effects of baicalin and DDP on proliferation inhibition were additive and synergistic when concentrations of DDP were 8 and 4 µg/ml, respectively, at 48 h for both A549 and A549/DDP cells. When baicalin (8 µg/ml) and DDP (4 µg/ml) were combined, the inhibitory rate of tumor cell invasion increased markedly compared to DPP or baicalin alone groups in both A549 and A549/DDP cells. A549/DDP cells had significantly higher MARK2 mRNA levels and protein expression of MARK2 and p-Akt. Baicalin decreased MARK2 mRNA and protein expression of MARK2 and p-Akt in A549/DDP cells dose-dependently. In conclusion, baicalin and DDP were synergistic at inhibiting proliferation and invasion of human lung cancer cells at appropriate dosages and incubation time in the presence or absence of DDP resistance. The attenuation of DDP resistance was associated with downregulation of MARK2 and p-Akt.

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“…35 – 38 Several studies have shown that reducing cisplatin-resistant protein could reverse cisplatin resistance or enhance tumor sensitivity to cisplatin. 39 – 41 A host of cisplatin-resistant proteins have been reported, for instance, LRP, MRP2, and breast cancer resistance protein. 36 , 42 , 43 LRP is overexpressed in several non-P-glycoprotein cancer cell lines with performance of MDR.…”

Section: Discussionmentioning

confidence: 99%

Combination of gambogic acid with cisplatin enhances the antitumor effects on cisplatin-resistant lung cancer cells by downregulating MRP2 and LRP expression

Zhang¹,

Zhou²,

Yu³

et al. 2016

OTT

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Cisplatin resistance is a main clinical problem of lung cancer therapy. Gambogic acid (GA) could prohibit the proliferation of a variety of human cancer cells. However, the effects of GA on cisplatin-resistant lung cancer are still unclear. The objective of the present study was to find out the antitumor effects of GA on cisplatin-resistant human lung cancer A549/DDP cells and further explore its underlying mechanisms. Cell Counting Kit-8 assay was used to observe the impacts of GA and/or cisplatin on the proliferation of lung cancer cells; flow cytometry was used to detect the effects of GA on cell cycle and apoptosis; Western blot was used to examine the effects of GA on the expression of lung resistance protein (LRP) and multidrug resistance-associated protein 2 (MRP2) protein in A549/DDP cells. Our results showed that GA dose- and time-dependently prohibited the proliferation and induced significant cell apoptosis in A549 and A549/DDP cells. GA also induced G0/G1 arrest in both A549/DDP and A549 cells. Moreover, GA upregulated protein expression level of cleaved caspase-3 and Bax and downregulated protein expression level of pro-caspase-9 and Bcl-2 in time- and dose-dependent way in A549/DDP cells. GA combined with cisplatin enhanced the cells apoptotic rate and reduced the cisplatin resistance index in A549/DDP cells. In addition, GA reduced the MRP2 and LRP protein expression level in A549/DDP cells. GA inhibits the proliferation, induces cell cycle arrest and apoptosis in A549/DDP cells. Combination of GA with cisplatin enhances the antitumor effects on cisplatin-resistant lung cancer cells by downregulating MRP2 and LRP expression.

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Effects of VBMDMP on the reversal of cisplatin resistance in human lung cancer A549/DDP cells

Cited by 5 publications

References 36 publications

Transcriptome Sequencing Reveals Key Pathways and Genes Associated with Cisplatin Resistance in Lung Adenocarcinoma A549 Cells

Transcriptome Sequencing Reveals Key Pathways and Genes Associated with Cisplatin Resistance in Lung Adenocarcinoma A549 Cells

Baicalin attenuates DDP (cisplatin) resistance in lung cancer by downregulating MARK2 and p-Akt

Combination of gambogic acid with cisplatin enhances the antitumor effects on cisplatin-resistant lung cancer cells by downregulating MRP2 and LRP expression

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