shRNA Targeting PLCε Inhibits Bladder Cancer Cell Growth In Vitro and In Vivo

Cheng, Horng‐Long; Luo, Chunli; Wu, Xiaohou; Zhang, Yao; He, Yong; Wu, QiSi; Xia, Yuguo; Zhang, Jia-Mo

doi:10.1016/j.urology.2011.03.014

Cited by 29 publications

(21 citation statements)

References 20 publications

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“…However, the mechanism of action is not completely understood, and controversial data were reported. A number of evidences indicate that PI-PLC ε might favour cancer initiation and/or progression, as in bladder (Cheng et al 2011;Ou et al 2010), murine skin (Bai et al 2004, Oka 2010, Li et al 2009), head and neck cancers (Bourguignon et al 2006). The rs 2274223 polymorphism was significantly associated to increased risk of squamous cell carcinoma and gastric cancer (Hao 2013 By contrast, tumour suppressive role for PI-PLC ε was recently suggested in Ras-triggered cancers (Martins et al 2014).…”

Section: Discussionmentioning

confidence: 99%

Ezrin silencing remodulates the expression of Phosphoinositide‐specific Phospholipase C enzymes in human osteosarcoma cell lines

Vasco

Leopizzi²,

Puggioni³

et al. 2014

Journal of Cell Communication and Signaling

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Ezrin, a protein belonging to the Ezrin, radixin and moesin (ERM) family, was engaged in the metastatic spread of osteosarcoma. The Protein 4.1, Ezrin, radixin, moesin (FERM) domain of Ezrin binds the membrane Phosphatydil inositol (4,5) bisphosphate (PIP2), a crucial molecule belonging to the Phosphoinositide (PI) signal transduction pathway. The cytoskeleton cross-linker function of Ezrin largely depends on membrane PIP2 levels, and thus upon the activity of related enzymes belonging to the PI-specific phospholipase C (PI-PLC) family. Based on the role of Ezrin in tumour progression and metastasis, we silenced the expression of Vil2 (OMIM *123900), the gene which codifies for Ezrin, in cultured human osteosarcoma 143B and Hs888 cell lines. After Ezrin silencing, the growth rate of both cell lines was significantly reduced and morphogical changes were observed. We also observed moderate variations both of selected PI-PLC enzymes within the cell and of expression of the corresponding PLC genes. In 143B cell line the transcription of PLCB1 decreased, of PLCG2 increased and of PLCE differed in a time-dependent manner. In Hs888, the expression of PLCB1 and of PLCD4 significantly increased, of PLCE moderately increased in a time dependent manner; the expression of PLCG2 was up-regulated. These observations indicate that Ezrin silencing affects the transcription of selected PLC genes, suggesting that Ezrin might influence the expression regulation of PI-PLC enzymes.

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Section: Discussionmentioning

confidence: 99%

Ezrin silencing remodulates the expression of Phosphoinositide‐specific Phospholipase C enzymes in human osteosarcoma cell lines

Vasco

Leopizzi²,

Puggioni³

et al. 2014

Journal of Cell Communication and Signaling

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“…13 Cells were cultured in RPMI 1640 supplemented with 10% newborn calf serum (GIBCO®) in 5% carbon dioxide in a humid incubator at 37C.…”

Section: Cell Culturementioning

confidence: 99%

Exploration of the Correlations Between Interferon-γ in Patient Serum and HEPACAM in Bladder Transitional Cell Carcinoma, and the Interferon-γ Mechanism Inhibiting BIU-87 Proliferation

Xu¹,

He²,

Wu³

et al. 2012

Journal of Urology

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“…Silencing PLCE1 has been shown to inhibit bladder tumor growth in vitro and in vivo (28). PLCE1 stimulation has been shown to induce pro-inflammatory cytokine expression and augment inflammation in response to chemical carcinogens or UV irradiation (17,29-30), which could promote skin cancer development.…”

Section: Discussionmentioning

confidence: 99%

PLCE1 mRNA and Protein Expression and Survival of Patients with Esophageal Squamous Cell Carcinoma and Gastric Adenocarcinoma

Burton

et al. 2014

Cancer Epidemiology, Biomarkers &Amp; Prevention

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Background Germline genetic variants in PLCE1 (10q23) have demonstrated consistent associations with risk of esophageal squamous cell carcinoma (ESCC) and gastric cancer among Chinese. We evaluated PLCE1 mRNA and protein expression in paired tumor-normal tissues, and their relationship with survival. Methods PLCE1 mRNA was profiled using three probes in the Affymetrix GeneChip U133 for paired tumor-normal tissues of ESCC (n=132), gastric cardia adenocarcinoma (GCA, n=62) and gastric noncardia adenocarcinoma (GNCA, n=72). We used immunohistochemistry to detect PLCE1 protein on slides from tissue microarrays in paired tumor-normal tissues of ESCC (n=303), and tumors of GCA (n=298) and GNCA (n=124). Results Compared with normal tissues, PLCE1 mRNA expression was significantly reduced in ESCC tumors (P=0.03, probe_205112_at), as well as in GCA and GNCA tumors (P<0.0001, each probe). Protein expression was non-significantly reduced in ESCC tumors (P=0.51). Increased tumor-normal mRNA fold change (probe_205112_at) was associated with longer survival in ESCC (9.6 months for highest vs lowest quartile; P-trend=0.02). Increased mRNA tumor-normal fold change (probe_205111_at) was associated with longer survival for GCA (10.7 months for highest quartile; P-trend=0.04), but not for GNCA cases (P=0.72). Similar to mRNA, elevated tumor-normal fold change for protein in ESCC was also associated with improved survival (8.1 months for highest quartile; P-trend=0.04). Conclusions Dysregulated PLCE1 mRNA expression was observed for both ESCC (one probe only) and GCA tumors, and the altered PLCE1 expression appears to be associated with cancer prognosis. Impact A potential role for PLCE1 in the early detection and/or therapy of ESCC and GCA warrants further investigation.

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shRNA Targeting PLCε Inhibits Bladder Cancer Cell Growth In Vitro and In Vivo

Cited by 29 publications

References 20 publications

Ezrin silencing remodulates the expression of Phosphoinositide‐specific Phospholipase C enzymes in human osteosarcoma cell lines

Ezrin silencing remodulates the expression of Phosphoinositide‐specific Phospholipase C enzymes in human osteosarcoma cell lines

Exploration of the Correlations Between Interferon-γ in Patient Serum and HEPACAM in Bladder Transitional Cell Carcinoma, and the Interferon-γ Mechanism Inhibiting BIU-87 Proliferation

PLCE1 mRNA and Protein Expression and Survival of Patients with Esophageal Squamous Cell Carcinoma and Gastric Adenocarcinoma

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