Src as a novel therapeutic target for endometriosis

Lawrenson, Kate; Lee, Nathan; Torres, Hugo A. M.; Lee, Janet M.; Brueggmann, Doerthe; Rao, Priya; Noushmehr, Houtan; Gayther, Simon A.

doi:10.1016/j.ygyno.2014.06.016

Cited by 8 publications

(11 citation statements)

References 39 publications

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“…IEEC16 was derived in-house from primary endometriosis sample and cultured in normal ovarian surface epithelial complete medium [17, 18]. Cell lines were characterized by STR-profiling and tested for mycoplasma at USC Norris Cancer Center.…”

Section: Methodsmentioning

confidence: 99%

“…Anchorage-independent colony formation and cell adhesion assays were performed as described in [18, 20]. Cell invasion assay performed using Cultrex® BME cell invasion assay (R&D Systems) according to manufacturer’s protocol.…”

Section: Methodsmentioning

confidence: 99%

“…Here, we investigate the potential functional role and the epigenetic impact of decreased ARID1A expression on oncogenesis by using an immortalized endometriosis cell line model, iEEC16 [17, 18], to evaluate for alterations of DNA methylation, nucleosome positioning, and histone modifications following ARID1A perturbation. Our studies reveal that the down-regulation of ARID1A expression in non-tumorigenic cells is sufficient to initiate tumorigenic transformation and dysregulation of gene expression through altered H3K27ac and targeted modulation of chromatin accessibility.…”

Section: Introductionmentioning

confidence: 99%

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Down-regulation of ARID1A is sufficient to initiate neoplastic transformation along with epigenetic reprogramming in non-tumorigenic endometriotic cells

et al. 2017

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The chromatin remodeler AT-Rich Interactive Domain 1A (ARID1A) is frequently mutated in ovarian clear cell carcinoma (OCCC) and endometriosis precursor lesions. Here, we show that knocking down ARID1A in an immortalized endometriosis cell line is sufficient to induce phenotypic changes indicative of neoplastic transformation as evidenced by higher efficiency of anchorage-independent growth, increased propensity to adhere to collagen, and greater capacity to invade basement membrane extract in vitro. ARID1A knockdown is associated with expression dysregulation of 99 target genes, and many of these expression changes are also observed in primary OCCC tissues. Further, pathway analysis indicates these genes fall within networks highly relevant to tumorigenesis including integrin and paxillin pathways. We demonstrate that the down-regulation of ARID1A does not markedly alter global chromatin accessibility or DNA methylation but unexpectedly, we find strong increases in the active H3K27ac mark in promoter regions and decreases of H3K27ac at potential enhancers. Taken together, these data provide evidence that ARID1A mutation can be an early stage event in the oncogenic transformation of endometriosis cells giving rise to OCCC.

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Section: Methodsmentioning

confidence: 99%

Section: Methodsmentioning

confidence: 99%

Section: Introductionmentioning

confidence: 99%

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Down-regulation of ARID1A is sufficient to initiate neoplastic transformation along with epigenetic reprogramming in non-tumorigenic endometriotic cells

et al. 2017

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“…EEC16 cells can be immortalized using TERT, but EEC16-TERT cells differentially express epithelial and mesenchymal markers, specifically, they do not express cytokeratin nor other epithelial markers, including BerEP4, but do express vimentin. EEC16 cells express keratin and vimentin but lack E-cadherin expression (65). The colony formation ability of the EEC16-TERT cell line has been indicated to be inhibited by the Src and Wnt signaling pathways, respectively, which may provide a novel strategy to manage endometriosis (65).…”

Section: Human Primary Endometrial Epithelial Cells (Eecs) and Endomementioning

confidence: 99%

“…EEC16 cells express keratin and vimentin but lack E-cadherin expression (65). The colony formation ability of the EEC16-TERT cell line has been indicated to be inhibited by the Src and Wnt signaling pathways, respectively, which may provide a novel strategy to manage endometriosis (65).…”

Section: Human Primary Endometrial Epithelial Cells (Eecs) and Endomementioning

confidence: 99%

In‑vitro models of human endometriosis (Review)

Fan

2019

Exp Ther Med

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Endometriosis is one of the most common benign gynecological diseases in women of reproductive age worldwide. In past decades, a number of in-vitro models have been used to investigate the pathology and therapeutic methods for the treatment of endometriosis. The current review summarized the majority of currently available in-vitro models, which utilize a variety of cell or tissues types, including endometriotic cell lines, primary endometrial stromal cells, endometrial stem cells, endometrial explants, peritoneal explants and immune cells. These cells or tissues are cultured individually, co-cultured in 2D or 3D systems with various matrices or cultured in chicken chorioallantotic membranes and amniotic membranes culture systems. These models are able to represent one or more aspects of the process of endometriosis. These models are helpful and can be used to investigate the development of endometriosis and the underlying mechanisms of this disorder in detail, and help investigators select appropriate models for their experiments. Recently, the new concept of endometriosis as a fibrotic condition will lead research to investigate the differentiation of myofibroblasts and the development of fibrosis in endometriotic lesions, which will increase the development of novel models that can be used to investigate endometriotic fibrosis. Contents 1. Introduction 2. In-vitro models 3. Discussion In-vitro models of human endometriosis (Review)

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In vitro modeling of endometriosis and endometriotic microenvironment – Challenges and recent advances

Gołąbek-Grenda

Olejnik

2022

Cellular Signalling

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Src as a novel therapeutic target for endometriosis

Cited by 8 publications

References 39 publications

Down-regulation of ARID1A is sufficient to initiate neoplastic transformation along with epigenetic reprogramming in non-tumorigenic endometriotic cells

Down-regulation of ARID1A is sufficient to initiate neoplastic transformation along with epigenetic reprogramming in non-tumorigenic endometriotic cells

In‑vitro models of human endometriosis (Review)

In vitro modeling of endometriosis and endometriotic microenvironment – Challenges and recent advances

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