CacyBP/SIP enhances multidrug resistance of pancreatic cancer cells by regulation of P-gp and Bcl-2

Xiong, Chen; Zheng, Peichan; Xue, Zhe; Li, Jie; Wang, Wenwu; Chen, Xi; Xie, Fang; Yu, Zhen; Ouyang, Xin

doi:10.1007/s10495-013-0831-9

Cited by 18 publications

(12 citation statements)

References 25 publications

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“…Fluorescence intensity of intracellular ADR was detected by flow cytometry as described previously [14]. Briefly, cells were seeded into 6‐well plates (1 × 10 6 cells/per well) and cultured overnight at 37 °C.…”

Section: Methodsmentioning

confidence: 99%

MicroRNA‐106a induces multidrug resistance in gastric cancer by targeting RUNX3

Zhang

Cai

2013

FEBS Letters

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a b s t r a c tMultidrug resistance (MDR) is the main barrier to the success of chemotherapy for gastric cancer (GC). miR-106a, which is highly expressed in GC, influences a variety of aspects of GC. However, the function of miR-106a in MDR of GC still remains unclear. In the present study, we found that miR-106a is elevated in MDR cell lines. miR-106a promotes chemo-resistance of GC cells, accelerates ADR efflux, and suppresses drug-induced apoptosis. Finally, we show that runt-related trans factor 3 (RUNX3) is the functional target of miR-106a. Collectively, these findings demonstrate that miR106a may promote MDR in GC cells by targeting RUNX3.

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Section: Methodsmentioning

confidence: 99%

MicroRNA‐106a induces multidrug resistance in gastric cancer by targeting RUNX3

Zhang

Cai

2013

FEBS Letters

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“…Studies have reported that Cacybp is involved in colon cancer (11), glioma (12), gastric cancer (13), and pancreatic cancer (14). Studies have reported that Cacybp is involved in colon cancer (11), glioma (12), gastric cancer (13), and pancreatic cancer (14).…”

Section: Introductionmentioning

confidence: 99%

“…Studies have reported that Cacybp is involved in colon cancer (11), glioma (12), gastric cancer (13), and pancreatic cancer (14). Although there have been a large number of studies on the mechanisms of Cacybp in the early stage of tumorigenesis, these mainly focus on one or a few specific aspects (11)(12)(13)(14). To systematically study the mechanism of action of Cacybp in tumors, we selected human glioma data for analysis by bioinformatics.…”

Section: Introductionmentioning

confidence: 99%

Bioinformatic analysis of Cacybp‐associated proteins using human glioma databases

Xuan¹,

Gao²,

Jin³

et al. 2019

IUBMB Life

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The ubiquitin‐proteasome system is the primary cellular pathway for protein degradation, mediating 80% of intracellular protein degradation. Because of the widespread presence of ubiquitin‐modified protein substrates, ubiquitination can regulate a variety of cellular activities including cell proliferation, apoptosis, autophagy, endocytosis, DNA damage repair, and immune responses. With the continuous generation of genomics data in recent years it has become particularly important to analyze these data effectively and reasonably. Cacybp forms a complex with the E3 ubiquitinated ligase Siah1 to participate in ubiquitination. We analyzed Cacybp‐associated genes using the Gene Expression Omnibus (GEO) and CGGA (Chinese Glioma Genome Atlas) databases and identified 121 differentially expressed genes (DEGs), of which 46 were downregulated and 75 were upregulated. The biological processes, molecular functions, and protein–protein interaction (PPI) network of differential genes were analyzed by Cytoscape software and STRING software. We found no difference in Cacybp expression among different grades of gliomas and there was no significant association between the expression level of Cacybp and the prognosis of patients with glioma in LGG and GBM. © 2019 IUBMB Life, 1–8, 2019

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“…CacyBP/SIP is involved in protein de-phosphorylation, ubiquitination, cytoskeletal dynamics, and all of these functions have been implicated in a wide range of cellular processes, such as cell proliferation, tumorigenesis, cell differentiation and gene expression (Shi et al, 2014 ; Topolskawoś et al, 2016 ). In some tumor cells, CacyBP/SIP has been shown to be involved in cell apoptosis, but the promotion or suppression of cancer apoptosis by CacyBP/SIP may depend on cell type (Chen et al, 2013 ; Fu et al, 2016 ; Tang et al, 2016 ). The role of CacyBP/SIP in DF-1 cell apoptosis and the effects of CacyBP/SIP on NDV replication efficiency in these cells remains to be determined.…”

Section: Introductionmentioning

confidence: 99%

Newcastle Disease Virus V Protein Inhibits Cell Apoptosis and Promotes Viral Replication by Targeting CacyBP/SIP

Chu

Wang

Tang

et al. 2018

Front. Cell. Infect. Microbiol.

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Newcastle disease virus (NDV) has been classified by the World Organization for Animal Health (OIE) as a notable disease-causing virus, and this virus has the ability to infect a wide range of birds. V protein is a non-structural protein of NDV. V protein has been reported to inhibit cell apoptosis (Park et al., 2003a) and promote viral replication (Huang et al., 2003), however, the mechanisms of action of V protein have not been elucidated. In the present study, a yeast two-hybrid screen was performed, and V protein was found to interact with the CacyBP/SIP protein. The results of co-immunoprecipitation and immuno-colocalization assays confirmed the interaction between V protein and CacyBP/SIP. The results of quantitative-PCR and viral plaque assays showed that overexpression of CacyBP/SIP inhibited viral replication in DF-1 cells. Overexpression of CacyBP/SIP in DF-1 cells induced caspase3-dependent apoptosis. The effect of knocking down CacyBP/SIP by siRNA was the opposite of that observed upon overexpression. Moreover, it is known that NDV induces cell apoptosis via multiple caspase-dependent pathways. Furthermore, V protein inhibited cell apoptosis and downregulated CacyBP/SIP expression in DF-1 cells. Taken together, the findings of the current study indicate that V protein interacts with CacyBP/SIP, thereby regulating cell apoptosis and viral replication.

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CacyBP/SIP enhances multidrug resistance of pancreatic cancer cells by regulation of P-gp and Bcl-2

Cited by 18 publications

References 25 publications

MicroRNA‐106a induces multidrug resistance in gastric cancer by targeting RUNX3

MicroRNA‐106a induces multidrug resistance in gastric cancer by targeting RUNX3

Bioinformatic analysis of Cacybp‐associated proteins using human glioma databases

Newcastle Disease Virus V Protein Inhibits Cell Apoptosis and Promotes Viral Replication by Targeting CacyBP/SIP

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