Involvement of CD147 in regulation of multidrug resistance to P‐gp substrate drugs and <i>in vitro</i> invasion in breast cancer cells

Li, Qing Quan; Wang, Wen Juan; Xu, Jing; Cao, Xi; Chen, Qi; Yang, Jin Ming; Xu, Zhenshan

doi:10.1111/j.1349-7006.2007.00487.x

Cited by 56 publications

(49 citation statements)

References 27 publications

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“…Previous reports demonstrated that continued activation of AKT was related to the resistance to conventional chemotherapeutic agents (55)(56)(57)(58). To determine whether the MDR reversal activity of lapatinib was related to the change of AKT (D) Grayscale ratios of MRP1/GAPDH were analyzed with ImageJ.…”

Section: Discussionmentioning

confidence: 99%

Lapatinib Antagonizes Multidrug Resistance-Associated Protein 1-Mediated Multidrug Resistance by Inhibiting Its Transport Function

Lin

Wang

et al. 2014

Mol Med

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Lapatinib, a tyrosine kinase inhibitor, is used in the treatment of advanced or metastatic breast cancer overexpressing human epidermal receptor 2 (HER2). Lapatinib can modulate the function of ATP-binding cassette (ABC) transporters (ABCB1 and ABCG2), which are the major mechanism responsible for multidrug resistance (MDR) in cancer. In this study, we investigated the effect of lapatinib on multidrug resistance-associated protein 1 (MRP1 [ABCC1]), MRP2 (ABCC2), MRP4 (ABCC4) and lung relative resistance protein (LRP) drug efflux pumps. We demonstrated that lapatinib could enhance the efficacy of conventional chemotherapeutic agents in MRP1-overexpressing cells in vitro and in vivo, but no effect in MRP2-, MPR4-and LRP-overexpressing cells. Furthermore, lapatinib significantly increased the accumulation of rhodamine 123 (Rho123) and doxorubicin (DOX) in MRP1-overexpressing cells. However, lapatinib did not alter the protein or mRNA expression levels of MRP1. Further studies showed that the level of phosphorylation of AKT and extracellular signal-regulated protein kinases 1 and 2 (ERK1/2) were not altered at the indicated concentrations of lapatinib. In conclusion, lapatinib enhanced the efficacy of conventional chemotherapeutic agents in MRP1-overexpressing cells by inhibiting MRP1 transport function without altering the level of AKT or ERK1/2 phosphorylation. These findings will encourage the clinical research of lapatinib combined with conventional chemotherapeutic drugs in MRP1-overexpressing cancer patients.

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Section: Discussionmentioning

confidence: 99%

Lapatinib Antagonizes Multidrug Resistance-Associated Protein 1-Mediated Multidrug Resistance by Inhibiting Its Transport Function

Lin

Wang

et al. 2014

Mol Med

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“…The sensitivity of cells to VCR was evaluated using 3-(4,5-dimethylthiazol-2-yl)-2, 5-diphenyltetrazolium bromide (MTT) assay as described previously (17). Briefly, cells in the logarithmic phase were seeded in 96-well plates at a density of 1x10 4 cells/well.…”

Section: Methodsmentioning

confidence: 99%

Special AT-rich sequence binding protein 1 regulates the multidrug resistance and invasion of human gastric cancer cells

Sun

et al. 2012

Oncology Letters

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Abstract. Special AT-rich sequence binding protein 1 (SATB1) is a nuclear factor that functions as a global chromatin organizer to regulate gene expression. Recent studies have suggested an oncogenic role of SATB1 in breast cancer. However, the role of SATB1 in gastric cancer, especially in regulating the malignant phenotypes, including multidrug resistance (MDR) and metastasis, remains poorly understood. In this study, the aggressive human gastric cancer cell line SGC7901 and its corresponding MDR variant SGC7901/VCR cells were used as a model. SATB1 expression was examined by RT-PCR and western blot analysis. Results showed that SATB1 was upregulated in SGC7901/VCR cells. An in vitro drug sensitivity assay demonstrated a positive correlation between SATB1 expression levels and drug resistance. Gain and loss of SATB1 function experiments further demonstrated that SATB1 contributes to MDR by inhibiting the accumulation of vincristine (VCR) in gastric cancer cells and protecting the cells from VCR-induced apoptosis. In addition, SATB1 may promote the invasion of gastric cancer cells. The present study provides a novel insight into the oncogenic role of SATB1 in gastric cancer, suggesting that SATB1 is a promising target for the therapy of drug-resistant and invasive gastric cancer.

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“…The multidrug chemosensitivity of cells under investigation and their corresponding controls was assessed as described previously. (13) The relative inhibitory rate of cell growth by different concentrations of ADM was calculated according to the following formula:…”

Section: Methodsmentioning

confidence: 99%

Overexpression and involvement of special AT‐rich sequence binding protein 1 in multidrug resistance in human breast carcinoma cells

Chen

et al. 2009

Cancer Science

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Special AT-rich sequence binding protein (SATB) 1 has been proposed to act as a determinant for the acquisition of metastatic activity by controlling expression of a specific set of genes that promote metastatic activity. Here we found that SATB1 expression is upregulated in multidrug-resistant breast cancer cells that exhibit higher invasive potential than the parental cells. Apart from accelerating metastasis and inducing epithelial-mesenchymal transition, SATB1 was demonstrated to confer resistance to both P-glycoprotein-related and P-glycoprotein-non-related drugs on MCF7 cells, which was accompanied by decreasing accumulation of adriamycin in SATB1-overexpressing transfectants. SATB1 depletion could partially reverse the multidrug resistance (MDR) phenotype of MCF7 ⁄ ADR in vitro and in vivo. The SATB1-induced P-glycoprotein-mediated MDR could be reversed by treatment with anti-Pglycoprotein mAb. Moreover, SATB1 plays an important role in anti-apoptotic activity in MCF7 ⁄ ADR cells in response to adriamycin treatment, which suggests another mechanism contributing to SATB1-related MDR of breast cancers. These data provide new insights into the mode by which breast tumors acquire the MDR phenotype and also imply a role for SATB1 in this process. (Cancer Sci 2010; 101: 80-86) S pecial AT-rich sequence binding protein (SATB) 1, the global chromatin organizer and transcription factor, has emerged as a key factor in regulating gene expression during the differentiation and activation of T cells, making it a key player in the immune system.(1) Previous studies have unraveled the role of SATB1 in the organization of the chromatin ''loopscape'' and its dynamic nature in response to physiological stimuli. At the genome-wide level, SATB1 seems to play a role in the organization of the transcriptionally poised chromatin. (2,3) SATB1 organizes the MHC class I locus into distinct chromatin loops by tethering matrix association regions to the nuclear matrix at fixed distances.(4-6) Silencing of SATB1 mimics the effects of interferon (IFN)-c treatment on the chromatin loop architecture of the MHC class I locus and alters the expression of genes within the locus. Besides the immune system, SATB1 is also expressed in many cancer cells, such as colorectal cancer cells,lymphoma cells, (8) and breast cancer cells. (9) SATB1 has now revealed a darker side. Rygiel et al. found that SATB1 expression in colorectal cancer seems to be associated with an aggressive phenotype.(7) SATB1 correlates with high expression of tumor necrosis factor (TNF)-a, which mediates the inflammatory processes in tumor invasion, angiogenesis, and metastasis. On the other hand, SATB1 influences the expression of anti-inflammatory interleukin (IL)-4 and IL-10, which in turn are known to lead to escape from cancer immune surveillance. In addition, SATB1 is also an essential contributing factor in the most aggressive forms of breast cancer.(9) By introducing SATB1 into otherwise non-metastatic breast cancer cells, invasive tumors can be induced in mice; ...

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Involvement of CD147 in regulation of multidrug resistance to P‐gp substrate drugs and in vitro invasion in breast cancer cells

Cited by 56 publications

References 27 publications

Lapatinib Antagonizes Multidrug Resistance-Associated Protein 1-Mediated Multidrug Resistance by Inhibiting Its Transport Function

Lapatinib Antagonizes Multidrug Resistance-Associated Protein 1-Mediated Multidrug Resistance by Inhibiting Its Transport Function

Special AT-rich sequence binding protein 1 regulates the multidrug resistance and invasion of human gastric cancer cells

Overexpression and involvement of special AT‐rich sequence binding protein 1 in multidrug resistance in human breast carcinoma cells

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