Myoepithelial Cells: Autocrine and Paracrine Suppressors of Breast Cancer Progression

Barsky, Sanford H.; Karlin, Nina J.

doi:10.1007/s10911-005-9585-5

Cited by 114 publications

(121 citation statements)

References 32 publications

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“…Myoepithelial cells, produce high levels of proteinase inhibitors and angiogenesis inhibitors and low amounts of proteinase angiogenic factors (Nguyen et al, 2000). With respect to this evidence, Barsky and Karlin stated that myoepithelial cells are angiogenesis inhibitors (Barsky and Karlin, 2005).…”

Section: Discussionmentioning

confidence: 99%

Expression of Ki67 and CD105 as Proliferation and Angiogenesis Markers in Salivary Gland Tumors

Andisheh-Tadbir¹,

Pardis²,

Ashkavandi³

et al. 2012

Asian Pacific Journal of Cancer Prevention

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Objective: To investigate the association between CD105 and tumor cell proliferation in salivary gland tumors. Methods: In this study, 59 samples of salivary tumors from Khalili Hospital archive, including 20 cases of pleomorphic adenoma (PA), 20 cases of mucoepidermoid carcinoma (MEC) and 19 cases of adenoid cystic carcinoma, as well as 10 cases of normal salivary gland tissue, were reviewed by immunohistochemistry (IHC) for CD105 and Ki67 staining. Results: CD105 positive vessels were absent in normal salivary gland tissue in the vicinity of tumors (51.6% of all tumors were positive). There was a statistically significant difference in frequency of CD105 staining between PA and malignant tumors and between four groups of different lesions (p<0.000) being highest in MEC. Intratumoral microvessel density was also elevated in malignant neoplasms (2.61±3.1) as compared to PA (0.46±0.6). Normal salivary glands did not express Ki67. There was a statistically significant difference in frequency and percentage of Ki67 immunoreactivity in malignant neoplasms (86.5% and 10.7±10.8 respectively) compared to PA (50% and 0.78±0.2) and among the four groups values were highest in MEC (p<0.000). Conclusion: n this study, it was observed a higher rate of angiogenesis and cellular proliferation was noted in malignant tumors compared to benign tumors, but no correlation was observed between these two markers.

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Section: Discussionmentioning

confidence: 99%

Expression of Ki67 and CD105 as Proliferation and Angiogenesis Markers in Salivary Gland Tumors

Andisheh-Tadbir¹,

Pardis²,

Ashkavandi³

et al. 2012

Asian Pacific Journal of Cancer Prevention

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“…Various reports, mainly in breast cancer, consider that myoepithelial cells act as a tumor suppressor, since they present a low matrix degrading enzyme expression, yet produce high levels of proteinase inhibitors, ) which makes the invasion process and angiogenesis more difficult (Nguyen et al 2000;Jones et al 2003;Barsky and Karlin 2005;Silva et al 2012). Myoepithelial cells have also been reported to exert an anti-proliferative effect on the tumor cells (Shao et al 1998).…”

Section: Introductionmentioning

confidence: 99%

Cellular senescence and autophagy of myoepithelial cells are involved in the progression of in situ areas of carcinoma ex-pleomorphic adenoma to invasive carcinoma. An in vitro model

Silva

Martinez

Demasi

et al. 2015

J. Cell Commun. Signal.

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During tumor invasion, benign myoepithelial cells of carcinoma ex-pleomorphic adenoma (CXPA) surround malignant epithelial cells and disappear. The mechanisms involved in the death and disappearance of these myoepithelial cells were investigated via analysis of the expression of regulatory proteins for apoptosis, autophagy and cellular senescence in an in situ in vitro model. Protein expression relating to apoptosis (Bax, Bcl-2, Survivin), autophagy (Beclin-1, LC3B) and cellular senescence (p21, p16) was evaluated using indirect immunofluorescence. β-galactosidase expression was assessed via histochemistry. Biopsies of CXPA (ex vivo) allowed immunhistochemical evaluation of p21 and p16, whilst LC3B, p21 and p16 protein expression was analyzed by western blotting. In the in vitro model, the myoepithelial cells were positive for LC3B (cytoplasm) and p21 (nucleus), whilst in vivo positivity for p21 and p16 was observed. In vitro, β-galactosidase activity increased in the myoepithelial cells over time. Western blotting analysis revealed an increased LC3B, p16 and p21 expression in the myoepithelial cells with previous contact with the malignant cells when compared with those without contact. The investigation of behavior of benign myoepithelial cells in ductal areas of CXAP revealed that the myoepithelial cells are involved in the autophagy-senescence phenotype that subsequently leads to their disappearance.

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“…8 A hallmark of progression from DCIS to invasive cancer is physical breach of the myoepithelial cell layer and underlying basement membrane. For tumor progression, studies suggest that myoepithelial cells play an active role in tumor suppression by secreting protease inhibitors, downregulating matrix metalloproteinases, 9,10 and producing tumor suppressive proteins such as maspin, p63, Wilms tumor 1, and laminin 1. 11e13 These data support the hypothesis that the tumor suppressive function of myoepithelium is lost with DCIS progression, resulting in the transition from preinvasive to invasive cancer.…”

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confidence: 99%

Myoepithelial Cell Differentiation Markers in Ductal Carcinoma in Situ Progression

Russell

Jindal

Agunbiade

et al. 2015

The American Journal of Pathology

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We describe a preclinical model that investigates progression of early-stage ductal carcinoma in situ (DCIS) and report that compromised myoepithelial cell differentiation occurs before transition to invasive disease. Human breast cancer MCF10DCIS.com cells were delivered into the mouse mammary teat by intraductal injection in the absence of surgical manipulations and accompanying wound-healing confounders. DCIS-like lesions developed throughout the mammary ducts with full representation of human DCIS histologic patterns. Tumor cells were incorporated into the normal mammary epithelium, developed ductal intraepithelial neoplasia and DCIS, and progressed to invasive carcinoma, suggesting the model provides a rigorous approach to study early stages of breast cancer progression. Mammary glands were evaluated for myoepithelium integrity with immunohistochemical assays. Progressive loss of the myoepithelial cell differentiation markers p63, calponin, and a-smooth muscle actin was observed in the mouse myoepithelium surrounding DCISinvolved ducts. p63 loss was an early indicator, calponin loss intermediate, and a-smooth muscle actin a later indicator of compromised myoepithelium. Loss of myoepithelial calponin was specifically associated with gain of the basal marker p63 in adjacent tumor cells. In single time point biopsies obtained from 16 women diagnosed with pure DCIS, a similar loss in myoepithelial cell markers was observed. These results suggest that further research is warranted into the role of myoepithelial cell p63 and calponin expression on DCIS progression to invasive disease. Clinical evidence is compelling for histologic progression of breast cancer through atypical hyperplasia, ductal carcinoma in situ (DCIS), invasive ductal carcinoma, and metastatic stages. 1 Such histopathologic progression studies and mutational profiling of epithelial cancers 2,3 suggest that acquisition of invasive potential is a relatively late event. However, genomic data analyses have revealed that most tumor cell gene expression changes occur at the transition from normal to DCIS, with few additional changes in expression occurring at the transition from DCIS to overt invasive disease. 4,5 These observations implicate key roles for nonepithelial cells in progression to invasive disease. 6,7 The lack of relevant model systems has hindered our understanding of the DCIS to invasive transition.The clinical definition of invasive breast cancer is spread of malignant tumor cells from the confines of the mammary duct into the adjacent tissue stroma. In the normal mammary gland, epithelial ductal and alveolar structures are

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Myoepithelial Cells: Autocrine and Paracrine Suppressors of Breast Cancer Progression

Cited by 114 publications

References 32 publications

Expression of Ki67 and CD105 as Proliferation and Angiogenesis Markers in Salivary Gland Tumors

Expression of Ki67 and CD105 as Proliferation and Angiogenesis Markers in Salivary Gland Tumors

Cellular senescence and autophagy of myoepithelial cells are involved in the progression of in situ areas of carcinoma ex-pleomorphic adenoma to invasive carcinoma. An in vitro model

Myoepithelial Cell Differentiation Markers in Ductal Carcinoma in Situ Progression

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