Leptin receptor expression during the progression of endometrial carcinoma is correlated with estrogen and progesterone receptors

Méndez-López, Luis Fernando; Zavala-Pompa, Ángel; Cortés‐Gutiérrez, Elva I.; Cerda‐Flores, Ricardo M.; Dávila-Rodríguez, Martha I.

doi:10.5114/aoms.2017.64721

Cited by 16 publications

(16 citation statements)

References 35 publications

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“…Thus, leptin/OB-R and estrogen/ER signaling pathways may work together to accelerate the progression of type I EmCa. However, in contrast to a previous report [ 34 ], we found that type II EmCa expresses higher levels of OB-R. Remarkably, type II EmCa shares genomic features with basal-like breast cancer [ 8 ], which shows low levels or absence of ER, progesterone, and EGFR2 (Her2) receptors.…”

Section: Discussioncontrasting

confidence: 99%

“…Moreover, OB-R and estrogen receptor (ER) are coexpressed in cancer indicating a possible interaction between leptin and estrogen systems to promote carcinogenesis. It was recently reported that OB-R was downregulated during the progression of EmCa, which correlated with ER and progesterone receptor expression patterns [ 34 ]. Thus, leptin/OB-R and estrogen/ER signaling pathways may work together to accelerate the progression of type I EmCa.…”

Section: Discussionmentioning

confidence: 99%

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Type II Endometrial Cancer Overexpresses NILCO: A Preliminary Evaluation

et al. 2017

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Objective The expression of NILCO molecules (Notch, IL-1, and leptin crosstalk outcome) and the association with obesity were investigated in types I and II endometrial cancer (EmCa). Additionally, the involvement of NILCO in leptin-induced invasiveness of EmCa cells was investigated. Methods The expression of NILCO mRNAs and proteins were analyzed in EmCa from African-American (n = 29) and Chinese patients (tissue array, n = 120 cases). The role of NILCO in leptin-induced invasion of Ishikawa and An3ca EmCa cells was investigated using Notch, IL-1, and leptin signaling inhibitors. Results NILCO molecules were expressed higher in type II EmCa, regardless of ethnic background or obesity status of patients. NILCO proteins were mainly localized in the cellular membrane and cytoplasm of type II EmCa. Additionally, EmCa from obese African-American patients showed higher levels of NILCO molecules than EmCa from lean patients. Notably, leptin-induced EmCa cell invasion was abrogated by NILCO inhibitors. Conclusion Type II EmCa expressed higher NILCO molecules, which may suggest it is involved in the progression of the more aggressive EmCa phenotype. Obesity was associated with higher expression of NILCO molecules in EmCa. Leptin-induced cell invasion was dependent on NILCO. Hence, NILCO might be involved in tumor progression and could represent a new target/biomarker for type II EmCa.

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Section: Discussioncontrasting

confidence: 99%

Section: Discussionmentioning

confidence: 99%

Type II Endometrial Cancer Overexpresses NILCO: A Preliminary Evaluation

et al. 2017

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“…ESRα and ESRβ are encoded by separate genes, ESR1 and ESR2 , respectively, found on different chromosomes [17]. ESRs play important roles in the pathophysiology of various gynaecological diseases, including cancers [19, 20].…”

Section: Introductionmentioning

confidence: 99%

Oestrogen receptor alpha PvuII polymorphism and uterine fibroid incidence in Caucasian women

Ciebiera

Wrzosek

Wojtyła

et al. 2018

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IntroductionUterine fibroids (UFs) are benign, monoclonal tumours of the female genital tract that originate from the myometrium. They may be diagnosed in as many as 80% of women depending on the selected population. UFs depend mostly on steroid hormones. Elevated levels of oestrogens and progesterone are believed to be among the most important factors inducing their formation and growth. These facts suggest that oestrogen (ESR) and progesterone receptors are crucial in UF pathophysiology as well. Previous studies have shown that, in some populations, polymorphisms in ESR genes (e.g. PvuII) constitute an important risk factor for UFs.Material and methodsThe aim of our study was to investigate whether ESRα PvuII polymorphism is associated with an increased risk of UFs in Caucasian women of Polish origin. A total of 197 patients (114 UF-positive and 83 controls) were included in this retrospective cohort study. ESRα gene polymorphism PvuII (rs2234693) was assayed with PCR and restriction fragment length polymorphism (RFLP).ResultsOur study found no significant difference in the occurrence of ESR PvuII polymorphism between women with UFs and UF-free controls in the selected population.ConclusionsOur results did not indicate a significant association between ESRα gene PvuII polymorphism and the risk of UFs in Caucasian women of Polish origin. More studies and comparisons between races are necessary to clarify the role of ESRα in the development and progression of UFs.

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“…The use of complementary techniques provides a deeper insight into the molecular events that are taking place in the tissue by the identification of biomarkers. In this regard, current histological data support the progressive nature of carcinomas [35][36][37] . From this perspective, carcinomas are preceded by atypical hyperplasia that in turn progress from typical hyperplasia.…”

Section: The Carcinogenesis Of Epithelial Tissuesmentioning

confidence: 59%

On the Origin of Carcinoma

Méndez¹

2021

Preprint

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The origin of cancer remains one of the most important enigmas in modern biology. The prevailing paradigm has failed to grasp a comprehensive view of the disease. Naturally, therapies developed under the current assumptions are inadequate and cancer is practically an incurable disease. Meanwhile, descriptive studies continuously extend the molecular complexity of cancer without an equivalent advancement in its understanding. Furthermore, they tend to accumulate inconsistencies inexplicable under the classical view. This paper presents a compelling theory of the origin of carcinomas. By hypothesis, a series of generic events in epithelial tissues promoted by cellular aging and inflammation enables the reactivation of developmental programs. The origin of carcinomas in vivo is described as the time-ordered cell state transitions undergone by epithelial cells in the hyperplasia due to replicative senescence and inflammation towards a mesenchymal undifferentiated endogenous cell state with cancerous behavior. In support of the theory, the molecular, cellular, and histopathological evidence is critically reviewed. A plausible model for the origin of carcinomas is presented to explain the mechanism underlying carcinogenesis from an evolutive and developmental perspective. The implications of the hypothesis in the current strategies for cancer prevention and treatment are discussed along with rational alternatives and some predictions for possible experimental validation.

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Leptin receptor expression during the progression of endometrial carcinoma is correlated with estrogen and progesterone receptors

Cited by 16 publications

References 35 publications

Type II Endometrial Cancer Overexpresses NILCO: A Preliminary Evaluation

Type II Endometrial Cancer Overexpresses NILCO: A Preliminary Evaluation

Oestrogen receptor alpha PvuII polymorphism and uterine fibroid incidence in Caucasian women

On the Origin of Carcinoma

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