Expression of Glypican-3 (GPC3) in Malignant and Non-malignant Human Breast Tissues

Castillo, Luciana Andrea; Huvelle, María Amparo Lago; Fujita, André; Lobba, Aline Ramos Maia; Tascon, Rocio; Garcia, Tatiene Romera; Armanasco, Eduardo; Bagnoli, Fábio; Oliveira, Vilmar Marques de; Galvão, Maria Antonieta Longo; Montor, Wagner Ricardo; Sogayar, Maria Cleide; Joffé, Elisa Bal de Kier; Puricelli, Lydia; Labriola, Letícia; Peters, María Giselle

doi:10.2174/1874079001508010012

Cited by 8 publications

(15 citation statements)

References 18 publications

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“…25 In a study conducted by Castillo et al on human breast tissues, no association was found between the GPC3 expression and clinicopathologic parameters. 26 The present study detected no association between the GPC3 expression and clinicopathologic parameters, suggesting that GPC3 might be an independent marker. Yet, further studies with larger sample size are recommended.…”

Section: Discussioncontrasting

confidence: 76%

Evaluation of Glypican-3 expression in benign and malignant salivary gland tumors

Andisheh-Tadbir

Ashraf

Gudarzi

et al. 2019

Journal of Oral Biology and Craniofacial Research

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Introduction: Glypican-3 (GPC3) is involved in regulation of cell proliferation and morphogenesis. It is abundant in embryonic tissue, but limited in most adult tissues. GPC3 deletion or mutation can disturb the balance between cell apoptosis and proliferation, which may result in tumorigenesis. This study aimed to investigate the GPC3 expression in salivary gland tumors (SGTs) and the adjacent non-neoplastic tissues. Methods: This study reviewed 50 samples of salivary tumors from the archive of Khalili Hospital, Shiraz, Iran, including 17 cases of pleomorphic adenoma (PA), 16 cases of mucoepidermoid carcinoma (MEC), and 17 cases of adenoid cystic carcinoma (ACC); as well as a control group of 23 cases of normal salivary gland tissues. GPC3 expression was investigated through immunohistochemistry. Results: GPC3 expression was significantly higher in malignant tumors (MEC and ACC) than in PA, and higher in PA than in the normal salivary glands (P < 0.001). The expression intensity was moderate to strong in malignant tumors and weak to moderate in benign tumors. No strong positivity was observed in normal salivary gland tissues (P < 0.001). Nor was any association detected between the GPC3 expression and intensity with the clinicopathologic parameters. Conclusion: Although GPC3 overexpression was observed at the protein level in SGTs, and its expression was not related with the clinicopathologic factors, the potential use of GPC3 for diagnostic, therapeutic, and prognostic purposes requires further investigations.

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Section: Discussioncontrasting

confidence: 76%

Evaluation of Glypican-3 expression in benign and malignant salivary gland tumors

Andisheh-Tadbir

Ashraf

Gudarzi

et al. 2019

Journal of Oral Biology and Craniofacial Research

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“…As is shown in Table II, the current literature has some contradictions which must be further evaluated to better understand the expression of GPC-3 in tissue types. The tissues represented as having two or more sources contradicting one another in normal tissue (expressed/not expressed) are: gastric glands, kidney tubules, testicular germ cells, breast tissue, gall bladder, and ovary (19)(20)(21)(22)(23)(24)(25)(26)(27). In addition, there are also sources reporting no expression, trace amounts, or scarce expression in normal tissue.…”

Section: Expression Pattern Of Gpc-3 In Human and Mousementioning

confidence: 99%

“…It was observed that high serum AfP corresponded with a high sGPC-3N level. The study states that sGPC-3N may serve as an independent prognostic biomarker in HCC patients (24).…”

Section: Gpc-3 As a Serum Marker For Early Detection Of Hccmentioning

confidence: 99%

Biology and function of glypican-3 as a candidate for early cancerous transformation of hepatocytes in hepatocellular carcinoma

et al. 2017

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Glypican-3 (GPC-3), a transmembrane heparan sulfate proteoglycan (HSPG), has recently been investigated as a player in tissue-dependent cellular signaling, specifically as a regulator of growth. Noteworthy, the regulatory protein has been implicated in both stimulatory and inhibitory pathways involving cell growth. Initially, GPC-3 was thought to act as a cell cycle regulator, as a loss-of-function mutation in the gene caused a hyper-proliferative state known as Simpson-Golabi-Behmel (SGB) overgrowth syndrome. Additionally, certain cancer types have displayed a downregulation of GPC-3 expression. More recently, the protein has been evaluated as a useful marker for hepatocellular carcinoma (HCC) due to its increased expression in the liver during times of growth. In contrast, the GPC-3 marker is not detectable in normal adult liver. Immunotherapy that targets GPC-3 and its affiliated proteins is under investigation as these new biomarkers may hold potential for the detection and treatment of HCC and other diseases in which GPC-3 may be overexpressed. Studies have reported that an overexpression of GPC-3 in HCC predicts a poorer prognosis. This prognostic value further pushes the question regarding GPC-3's role in the regulation and progression of HCC. This review will summarize the current knowledge regarding the clinical aspects of GPC-3, while also synthesizing the current literature with the aim to better understand this molecule's biological interactions at a molecular level, not only in the liver, but in the rest of the body as well. Due to the existing gap in the literature surrounding GPC-3, we believe further investigation of function, structure and domains, cellular localization, and other subfields is warranted to evaluate the protein as a whole, as well as its part in the study of HCC.

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“…In contrast, GPC3 expression is downregulated in lung adenocarcinoma [ 22 ], cell clear renal carcinoma [ 23 ], mesothelioma, ovarian [ 24 , 25 ] and gastric cancer [ 26 ]. Regarding breast cancer, we have recently performed comparative studies of GPC3 expression, indicating lower GPC3 levels in tumors as compared to peritumor tissues [ 27 ]. In summary, depending on the tissue, GPC3 displays a very different pattern of expression during tumor progression.…”

Section: Introductionmentioning

confidence: 99%

Glypican-3 induces a mesenchymal to epithelial transition in human breast cancer cells

et al. 2016

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Breast cancer is the disease with the highest impact on global health, being metastasis the main cause of death. To metastasize, carcinoma cells must reactivate a latent program called epithelial-mesenchymal transition (EMT), through which epithelial cancer cells acquire mesenchymal-like traits.Glypican-3 (GPC3), a proteoglycan involved in the regulation of proliferation and survival, has been associated with cancer. In this study we observed that the expression of GPC3 is opposite to the invasive/metastatic ability of Hs578T, MDA-MB231, ZR-75-1 and MCF-7 human breast cancer cell lines. GPC3 silencing activated growth, cell death resistance, migration, and invasive/metastatic capacity of MCF-7 cancer cells, while GPC3 overexpression inhibited these properties in MDA-MB231 tumor cell line. Moreover, silencing of GPC3 deepened the MCF-7 breast cancer cells mesenchymal characteristics, decreasing the expression of the epithelial marker E-Cadherin. On the other side, GPC3 overexpression induced the mesenchymal-epithelial transition (MET) of MDA-MB231 breast cancer cells, which re-expressed E-Cadherin and reduced the expression of vimentin and N-Cadherin. While GPC3 inhibited the canonical Wnt/β-Catenin pathway in the breast cancer cells, this inhibition did not have effect on E-Cadherin expression. We demonstrated that the transcriptional repressor of E-Cadherin - ZEB1 - is upregulated in GPC3 silenced MCF-7 cells, while it is downregulated when GPC3 was overexpressed in MDA-MB231 cells. We presented experimental evidences showing that GPC3 induces the E-Cadherin re-expression in MDA-MB231 cells through the downregulation of ZEB1.Our data indicate that GPC3 is an important regulator of EMT in breast cancer, and a potential target for procedures against breast cancer metastasis.

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Expression of Glypican-3 (GPC3) in Malignant and Non-malignant Human Breast Tissues

Cited by 8 publications

References 18 publications

Evaluation of Glypican-3 expression in benign and malignant salivary gland tumors

Evaluation of Glypican-3 expression in benign and malignant salivary gland tumors

Biology and function of glypican-3 as a candidate for early cancerous transformation of hepatocytes in hepatocellular carcinoma

Glypican-3 induces a mesenchymal to epithelial transition in human breast cancer cells

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