Cross-talk between EPAS-1/HIF-2α and PXR signaling pathway regulates multi-drug resistance of stomach cancer cell

Zhao, Jiuda; Bai, Zhenzhong; Feng, Fan; Song, Erlin; Du, Feng; Zhao, Jingbo; Shen, Guoshuang; Ji, Faxiang; Li, Guoyuan; Ma, Xinfu; Hang, Xingyi; Xu, Binghe

doi:10.1016/j.biocel.2016.01.006

Cited by 41 publications

(33 citation statements)

References 45 publications

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“…After 10-15 h (for invasion) or 4-6 h (for migration), chamber membrane was fixed with 4% paraformaldehyde and stained with crystal violet. The relative invading cells were measured according to the instructions provided [27, 28]. Values were presented as the mean ± SD of triplicated experiments.…”

Section: Methodsmentioning

confidence: 99%

MEIS1 inhibits clear cell renal cell carcinoma cells proliferation and in vitro invasion or migration

Zhu

Cui

et al. 2017

BMC Cancer

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BackgroundMyeloid ecotropic viral integration site 1 (MEIS1) protein plays a synergistic causative role in acute myeloid leukemia (AML). However, MEIS1 has also shown to be a potential tumor suppressor in some other cancers, such as non-small-cell lung cancer (NSCLC) and prostate cancer. Although multiple roles of MEIS1 in cancer development and progression have been identified, there is an urgent demand to discover more functions of this molecule for further therapeutic design.MethodsMEIS1 was overexpressed via adenovirus vector in clear cell renal cell carcinoma (ccRCC) cells. Western blot and real-time qPCR (quantitative Polymerase Chain Reaction) was performed to examine the protein and mRNA levels of MEIS1. Cell proliferation, survival, in vitro migration and invasion were tested by MTT, colony formation, soft-agar, transwell (in vitro invasion/migration) assays, and tumor in vivo growthwas measured on nude mice model. In addition, flow-cytometry analysis was used to detect cell cycle arrest or non-apoptotic cell death of ccRCC cells induced by MEIS1.ResultsMEIS1 exhibits a decreased expression in ccRCC cell lines than that in non-tumor cell lines. MEIS1 overexpression inhibits ccRCC cells proliferation and induces G1/S arrest concomitant with marked reduction of G1/S transition regulators, Cyclin D1 and Cyclin A. Moreover, MEIS1-1 overexpression also induces non-apoptotic cell death of ccRCC cells via decreasing the levels of pro-survival regulators Survivin and BCL-2. Transwell migration assay (TMA) shows that MEIS1 attenuates in vitro invasion and migration of ccRCC cells with down-regulated epithelial-mesenchymal transition (EMT) process. Further, in nude mice model, MEIS1 inhibits the in vivo growth of Caki-1 cells.ConclusionsBy investigating the role of MEIS1 in ccRCC cells’ survival, proliferation, anchorage-independent growth, cell cycle progress, apoptosis and metastasis, in the present work, we propose that MEIS1 may play an important role in clear cell renal cell carcinoma (ccRCC) development.

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Section: Methodsmentioning

confidence: 99%

MEIS1 inhibits clear cell renal cell carcinoma cells proliferation and in vitro invasion or migration

Zhu

Cui

et al. 2017

BMC Cancer

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“…Multidrug resistance can have many causes, including increased drug efflux, alterations in drug targets, DNA repair, cell cycle regulation and evasion of apoptosis .…”

Section: Discussionmentioning

confidence: 99%

miR‐495 sensitizes MDR cancer cells to the combination of doxorubicin and taxol by inhibiting MDR1 expression

Zou

Zong

et al. 2017

J Cellular Molecular Medi

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MDR1 is highly expressed in MDR A2780DX5 ovarian cancer cells, MDR SGC7901R gastric cancer cells and recurrent tumours. It pumps cytoplasmic agents out of cells, leading to decreased drug accumulation in cells and making cancer cells susceptible to multidrug resistance. Here, we identified that miR‐495 was predicted to target ABCB1, which encodes protein MDR1. To reduce the drug efflux and reverse MDR in cancer cells, we overexpressed a miR‐495 mimic in SGC7901R and A2780DX cells and in transplanted MDR ovarian tumours in vivo. The results indicated that the expression of MDR1 in the above cells or tumours was suppressed and that subsequently the drug accumulation in the MDR cells was decreased, cell death was increased, and tumour growth was inhibited after treatment with taxol‐doxorubicin, demonstrating increased drug sensitivity. This study suggests that pre‐treatment with miR‐495 before chemotherapy could improve the curative effect on MDR1‐based MDR cancer.

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“…Cells were analyzed by the inhibition-analysis experiments conducted according to methods described previously 13,14. Sorafenib concentrations were selected as: 10, 3, 1, 0.3, 0.1, 0.03, or 0.01 μmol/L.…”

Section: Methodsmentioning

confidence: 99%

Silencing the expression of copine-III enhances the sensitivity of hepatocellular carcinoma cells to the molecular targeted agent sorafenib

Chen

Jiang

Zhang

2018

CMAR

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BackgroundThe application of the oral targeted therapeutic agent sorafenib provides new hope for patients suffering from advanced stages of hepatocellular carcinoma (HCC), but the prognosis of such patients remains poor due to the rapid development of the multidrug resistance process in cancer pathogenesis. The present work evaluated whether copine-III, a novel cancer regulator encoded by the CPNE3 gene, would be a potential indicator of sorafenib resistance in HCC treatment.Materials and methodsThe endogenous expression of copine-III in clinical specimens was examined by quantitative polymerase chain reaction. Copine-III siRNA was transfected into HCC cells to downregulate copine-III expression. The effect of copine-III on sorafenib’s antitumor activation was identified by in vitro and in vivo experiments (MTT, Transwell, and flow cytometry as well as a nude mice model).ResultsHigh levels of copine-III in clinical specimens are related to poor prognosis of advanced HCC patients on sorafenib treatment. Infection of Ad-siCPNE3 significantly decreased the endogenous expression of copine-III and enhanced the susceptibility of MHCC97-H cells to sorafenib: the IC50 value decreased from 1.15±0.11 to 0.25±0.05 μmol/L. Moreover, silencing copine-III enhanced the effect of sorafenib on apoptosis, in vitro invasion/migration, and subcutaneous or intrahepatic growth of MHCC97-H cells in nude mice.ConclusionCopine-III is a novel potential indicator of prognosis for patients who received sorafenib for advanced HCC treatment.

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Cross-talk between EPAS-1/HIF-2α and PXR signaling pathway regulates multi-drug resistance of stomach cancer cell

Cited by 41 publications

References 45 publications

MEIS1 inhibits clear cell renal cell carcinoma cells proliferation and in vitro invasion or migration

MEIS1 inhibits clear cell renal cell carcinoma cells proliferation and in vitro invasion or migration

miR‐495 sensitizes MDR cancer cells to the combination of doxorubicin and taxol by inhibiting MDR1 expression

Silencing the expression of copine-III enhances the sensitivity of hepatocellular carcinoma cells to the molecular targeted agent sorafenib

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