Methylation of PLCD1 and adenovirus-mediated PLCD1 overexpression elicits a gene therapy effect on human breast cancer

Mu, Haixi; Wang, Na; Zhao, Luo; Li, Shuman; Li, Qianqian; Chen, Ling; Luo, Xinrong; Qiu, Zhu; Li, Lili; Ren, Guosheng; Xu, Yongzhu; Zhou, Xiangyang; Xiang, Tingxiu

doi:10.1016/j.yexcr.2015.01.017

Cited by 38 publications

(36 citation statements)

References 32 publications

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“…As demonstrated previously, cell migration is suppressed in breast cancer cells expressing PLCD1 [9, 10]. In the present study, PLCD1 was expressed in MDA-MB-231 and MCF-7 cells, and knocked down in BT-549 cells, to evaluate its function in cell migration and invasion.…”

Section: Resultsmentioning

confidence: 51%

“…Expression of PLCD1 is downregulated in breast cancer cell lines and primary breast cancers following aberrant hypermethylation of its promoter [9, 10]. In this study, expression of PLCD1 was detected in a panel of breast cancer tissues that were matched with non-cancerous adjacent breast tissue samples, but PLCD1 was markedly downregulated in breast cancer tissue (Figure 1A).…”

Section: Resultsmentioning

confidence: 72%

“…PLCD1 inhibits MMP7 expression, resulting in anti-tumour effects in gastric and breast cancers [5, 10], but the underlying mechanism remains elusive. In this study, immunoblotting was used to evaluate the effect of PLCD1 expression on ERK1/2, GSK-3β, β-catenin and MMP7 protein levels.…”

Section: Resultsmentioning

confidence: 99%

“…Several candidate TSGs implicated in aerodigestive tumours have been identified through extensive expression profiling and epigenetic characterization, including BLU , DLEC1 and PLCD1 [5]. PLCD1 has also been identified as a TSG in gastric cancer [5], oesophageal squamous cell carcinoma [6], KRAS-mutated colorectal cancer [7], chronic myeloid leukaemia [8], and breast cancer in our previous work [9, 10]. …”

Section: Introductionmentioning

confidence: 99%

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Phospholipase Cδ1 suppresses cell migration and invasion of breast cancer cells by modulating KIF3A-mediated ERK1/2/β- catenin/MMP7 signalling

et al. 2017

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Phospholipase C δ1 (PLCD1) encodes an enzyme involved in energy metabolism, calcium homeostasis and intracellular movement. It is located at 3p22 in a region that is frequently deleted in multiple cancers, and the PLCD1 enzyme is a potential tumour suppressor in breast cancer that inhibits matrix metalloprotease (MMP) 7, but the detailed mechanism remains elusive. In this study, we found that PLCD1 was downregulated in breast cancers, and the gain-or-loss functional assay revealed that PLCD1 inhibited cell migration and invasion in vitro via the ERK1/2/β-catenin/MMP7 signalling pathway. Furthermore, KIF3A was identified as a downstream mediator of PLCD1, and there was an inverse correlation between the expression of PLCD1 and KIF3A. Knockdown of KIF3A expression alone suppressed cell migration and invasion, and attenuated ERK1/2/β-catenin/MMP7 signalling that was reactivated by knocking down PLCD1 in vitro. Collectively, our findings suggest that PLCD1 acts as a tumour suppressor, by KIF3A-mediated suppression of ERK1/2/β-catenin/MMP7 signalling, at least in part, in breast cancer.

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Section: Resultsmentioning

confidence: 51%

Section: Resultsmentioning

confidence: 72%

Section: Resultsmentioning

confidence: 99%

Section: Introductionmentioning

confidence: 99%

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Phospholipase Cδ1 suppresses cell migration and invasion of breast cancer cells by modulating KIF3A-mediated ERK1/2/β- catenin/MMP7 signalling

et al. 2017

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“…HCT116 and HT29 were kindly provided by Prof. Qian Tao (the Chinese University of Hongkong, China). Cells were maintained at 37 °C, in a humidified atmosphere containing 5 % CO 2 , in RPMI 1640 (Gibco-BRL, USA) medium supplemented with 10% fetal bovine serum (Gibco, USA), 100 U/ml of penicillin, and 100 mg/ml streptomycin [18]. For DNA demethylation, cells were treated with 10 µM 5-aza-2’-deoxy cytidine (Aza; Sigma-Aldrich) for 3 days and then treated with 100 nM histone deacetylase inhibitor trichostatin A (TSA; Cayman Chemical Co.) for 1 day.…”

Section: Methodsmentioning

confidence: 99%

ADAMTS9 is Silenced by Epigenetic Disruption in Colorectal Cancer and Inhibits Cell Growth and Metastasis by Regulating Akt/p53 Signaling

Chen

Tang

Feng

et al. 2017

Cell Physiol Biochem

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Background/Aims: ADAMTS (disintegrin-like and metalloproteinase with thrombospondin motifs) proteins are extracellular zinc metalloproteinases that play an important role in extracellular matrix assembly and degradation, connective tissue structuring, angiogenesis, and cell migration. Multiple studies suggest that ADAMTS proteins (e.g. ADAMTS9) can act as tumor suppressors. In gastric, esophageal, and nasopharyngeal carcinomas ADAMTS9 is frequently down-regulated by promoter methylation. Whether ADAMTS9 can function as a tumor suppressor gene (TSG) in colorectal cancer is still unclear. Methods: We performed immunohistochemistry, RT-PCR, and qRT-PCR, to examine the expression of ADAMTS9 in colorectal cancer cell lines and primary colorectal cancer tissues. Methylation-specific PCR was also carried out to investigate the promoter methylation status of ADAMTS9. We also explored the functions of ADAMTS9 in colorectal cancer cell lines through in vitro experiments. Results: ADAMTS9 expression was down-requlated or silenced in 83.3% (5/6) of colorectal cancer cell lines, and frequently repressed in 65.6% (21/32) of colorectal cancer tissues. Down-regulation of ADAMTS9 was partially due to promoter methylation. Exogenous expression of ADAMTS9 in colorectal cancer cell lines inhibited cell proliferation and migration through the regulation of cell cycle and apoptosis. In addition, ADAMTS9 prevented the activation of Akt, and its downstream targets in colorectal cancer cell lines. Conclusion: Our findings suggest ADAMTS9 is a TSG in colorectal cancer.

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Noteworthy prognostic value of phospholipase C delta genes in early stage pancreatic ductal adenocarcinoma patients after pancreaticoduodenectomy and potential molecular mechanisms

et al. 2019

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The purpose of this investigation was to explore the prognostic value of phospholipase C delta (PLCD) genes in early stage pancreatic ductal adenocarcinoma (PDAC) and its potential molecular mechanisms. The prognostic value of PLCD genes in early stage PDAC was assessed using the Kaplan-Meier method and multivariate Cox proportional hazards regression model. Genome-wide correlation analysis was performed on PLCD3 to identify the highly correlated genes in the transcriptome. Then, PLCD3 and these correlated genes together underwent a bioinformatics analysis to elucidate the potential molecular biological functions of PLCD3 in PDAC. PLCD1 and PLCD3 are significantly overexpressed in PDAC. In PDAC patients, PLCD3 is

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Methylation of PLCD1 and adenovirus-mediated PLCD1 overexpression elicits a gene therapy effect on human breast cancer

Cited by 38 publications

References 32 publications

Phospholipase Cδ1 suppresses cell migration and invasion of breast cancer cells by modulating KIF3A-mediated ERK1/2/β- catenin/MMP7 signalling

Phospholipase Cδ1 suppresses cell migration and invasion of breast cancer cells by modulating KIF3A-mediated ERK1/2/β- catenin/MMP7 signalling

ADAMTS9 is Silenced by Epigenetic Disruption in Colorectal Cancer and Inhibits Cell Growth and Metastasis by Regulating Akt/p53 Signaling

Noteworthy prognostic value of phospholipase C delta genes in early stage pancreatic ductal adenocarcinoma patients after pancreaticoduodenectomy and potential molecular mechanisms

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