Estrogen and Progesterone Receptors in Endometrial Cancer: Where Are We Today?

Swasti,

doi:10.4172/2161-0932.1000e127

Cited by 6 publications

(5 citation statements)

References 22 publications

(25 reference statements)

Supporting

Mentioning

Contrasting

Order By: Relevance

“…2F) displayed a reduced expression of ezrin, confirming a critical regulatory role of E2 on ezrin via ERα. These results in thyroid cancer cells were compatible with the previous reports showing that estrogen enhanced the growth and metastatic phenotype of ovarian, breast and endometrial carcinoma cells 20,21 . The ex vivo analysis also revealed that majority of patients from which thyroid lesions obtained were females of reproductive age (Table 2).…”

Section: Discussionsupporting

confidence: 93%

See 1 more Smart Citation

Role of phospho–ezrin in differentiating thyroid carcinoma

Lathika

Nair

Saritha

et al. 2019

Sci Rep

View full text Add to dashboard Cite

Comprehensive theory explaining the relationship between estrogen (E2) and ezrin in metastasis of thyroid cancer remains non-elicited. In vitro results revealed that E2 could stimulate the expression and phosphorylation of ezrin in a time and dose dependent manner. Our data clearly showed that E2 enhanced the migration and invasion of cells, which was reversed by the transfection of cells with ezrin specific siRNA. Further, we observed that Phosphoinositide 3-kinase (PI3K) ROCK-2 are among the kinases responsible for E2 induced phosphorylation of ezrin. Clinical validation of ezrin/phospho-ezrin revealed that phospho-ezrin was intensely expressed in follicular thyroid carcinoma (FTC) and follicular variant of papillary thyroid carcinoma (FVPTC), while it was completely absent in follicular adenoma (FA) lesions in which the differentiation of the follicular neoplasms remains subtle. When histology of different carcinomas is correlated with benign FA with respect to phospho-ezrin, we observed that the marker was highly significant (p = 0.0001). 100% sensitivity, specificity and diagnostic accuracy of the above marker in the histological association of FTC, FVPTC with FA, enables us to suggest phospho-ezrin as a diagnostic marker to differentiate the follicular neoplasms. These data are the first to suggest the dynamic regulation of ezrin phosphorylation during metastasis in FTC.

show abstract

Section: Discussionsupporting

confidence: 93%

“…The regulatory role of E2 on ezrin is established in several estrogen-responsive tissues like breast and ovary 20,21 . To study the effect of E2 on ezrin, ERα positive FTC-133 and normal thyroid cells (Nthy) were treated with 10 nM E2 for different time intervals 6 h, 12 h, 24 h, 48 h respectively.…”

Section: Resultsmentioning

confidence: 99%

Role of phospho–ezrin in differentiating thyroid carcinoma

Lathika

Nair

Saritha

et al. 2019

Sci Rep

View full text Add to dashboard Cite

show abstract

“…They also emphasize that gonadotropins and estrogens are involved in the control of angiogenesis and the metastatic potential of ovarian cancer with SEMA [27]. This is also important for our research because endometrial cancer is estrogen-dependent [28,29].…”

Section: Discussionmentioning

confidence: 99%

Expression of Semaphorin 3B (SEMA3B) in Various Grades of Endometrial Cancer

Dziobek

Opławski²,

Grabarek

et al. 2019

Med Sci Monit

View full text Add to dashboard Cite

Background SEMA3B is known as an inhibitor of angiogenesis and cell proliferation. During carcinogenesis, the loss of SEMA3B function is observed, which results in the progression of neoplastic changes. The aim of this study was to evaluate the expression profile of SEMA3B in endometrial cancer (G1–G3) in comparison to the control group and to assess whether the observed changes in expression could become a molecular marker in endometrial cancer. Material/Methods The study group consisted of 45 patients diagnosed with endometrial cancer (G1, 17; G2, 15; G3, 13). The control group included 15 patients. SEMA3B expression was assessed using the immunohistochemical method. Statistical analysis was carried out using the Statistica 12 PL program (StatSoft, USA). It included the Kruskal-Wallis test and post hoc Dunn’s test (p<0.05). Results Statistically significant differences in the level of SEMA3B expression were observed between all analyzed groups. The expression pattern of SEMA3B was as follows: cancer cells G1>G2>G3; endothelial cells: G3>G1>G2; stromal cells: G2>G1>G3. Conclusions Analysis of the SEMA3B expression profile shows the complexity of neoplastic transformation, which confirms the different expression of SEMA3B in endometrial cancer cells and endothelial cells. The present results and data in the literature data suggest that SEMA3B expression indicates the progression of carcinogenesis in the context of endometrial cancer.

show abstract

“…For these RL95-2 and KLE EC cell lines compared to the model HIEEC cell line, there was no difference in expression of ESR1. This is surprising, as differences in ERα have previously been associated with histology, response to therapy, and metastatic potential of EC (Swasti, 2018). Previously, we showed lower GPER expression in HEC-1A vs HIEEC cells (v2), and vs Ishikawa cells (v3, v4) (Hevir-Kene and Rižner, 2015).…”

Section: Discussionmentioning

confidence: 74%

In the Model Cell Lines of Moderately and Poorly Differentiated Endometrial Carcinoma, Estrogens Can Be Formed via the Sulfatase Pathway

Pavlič

Gjorgoska

Hafner

et al. 2021

Front. Mol. Biosci.

View full text Add to dashboard Cite

Endometrial cancer (EC) is the most common gynecological malignancy in resource-abundant countries. The majority of EC cases are estrogen dependent but the mechanisms of estrogen biosynthesis and oxidative metabolism and estrogen action are not completely understood. Here, we evaluated formation of estrogens in models of moderately and poorly differentiated EC: RL95-2 and KLE cells, respectively. Results revealed high expression of estrone-sulfate (E1-S) transporters (SLCO1A2, SLCO1B3, SLCO1C1, SLCO3A1, SLC10A6, SLC22A9), and increased E1-S uptake in KLE vs RL95-2 cells. In RL95-2 cells, higher levels of sulfatase and better metabolism of E1-S to E1 were confirmed compared to KLE cells. In KLE cells, disturbed balance in expression of HSD17B genes led to enhanced activation of E1 to E2, compared to RL95-2 cells. Additionally, increased CYP1B1 expression and down-regulation of genes encoding phase II metabolic enzymes: COMT, NQO1, NQO2, and GSTP1 suggested decreased detoxification of carcinogenic metabolites in KLE cells. Results indicate that in model cell lines of moderately and poorly differentiated EC, estrogens can be formed via the sulfatase pathway.

show abstract

Estrogen and Progesterone Receptors in Endometrial Cancer: Where Are We Today?

Cited by 6 publications

References 22 publications

Role of phospho–ezrin in differentiating thyroid carcinoma

Role of phospho–ezrin in differentiating thyroid carcinoma

Expression of Semaphorin 3B (SEMA3B) in Various Grades of Endometrial Cancer

In the Model Cell Lines of Moderately and Poorly Differentiated Endometrial Carcinoma, Estrogens Can Be Formed via the Sulfatase Pathway

Contact Info

Product

Resources

About