Galectin‑7 is elevated in endometrioid (type I) endometrial cancer and promotes cell migration

Menkhorst, Ellen; Griffiths, Meaghan; Sinderen, Michelle Van; Rainczuk, Kate; Niven, Keith; Dimitriadis, Evdokia

doi:10.3892/ol.2018.9193

Cited by 15 publications

(15 citation statements)

References 40 publications

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“…VIM expression is upregulated in epithelial tumors of uterine corpus origin, but not epithelial tumors of ovarian origin 52 . ICAM-1 is expressed in migratory EC 53 , and is linked to increased peritoneal adhesion in endometriosis 54 . VIM and ICAM-1 may serve as markers of ARID1A-negative tumors of endometrial origin.…”

Section: Discussionmentioning

confidence: 99%

ARID1A and PI3-kinase pathway mutations in the endometrium drive epithelial transdifferentiation and collective invasion

et al. 2019

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ARID1A and PI3-Kinase (PI3K) pathway alterations are common in neoplasms originating from the uterine endometrium. Here we show that monoallelic loss of ARID1A in the mouse endometrial epithelium is sufficient for vaginal bleeding when combined with PI3K activation. Sorted mutant epithelial cells display gene expression and promoter chromatin signatures associated with epithelial-to-mesenchymal transition (EMT). We further show that ARID1A is bound to promoters with open chromatin, but ARID1A loss leads to increased promoter chromatin accessibility and the expression of EMT genes. PI3K activation partially rescues the mesenchymal phenotypes driven by ARID1A loss through antagonism of ARID1A target gene expression, resulting in partial EMT and invasion. We propose that ARID1A normally maintains endometrial epithelial cell identity by repressing mesenchymal cell fates, and that coexistent ARID1A and PI3K mutations promote epithelial transdifferentiation and collective invasion. Broadly, our findings support a role for collective epithelial invasion in the spread of abnormal endometrial tissue.

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Section: Discussionmentioning

confidence: 99%

ARID1A and PI3-kinase pathway mutations in the endometrium drive epithelial transdifferentiation and collective invasion

et al. 2019

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“…The xCELLigence assay was conducted to examine the real-time adhesive capacity of JAG1 knockdown compared to scrambled control Ishikawa cells, as we previously described. 29 This assay works by measuring the electrical flow transmission between gold microelectrodes embedded on each well of 96-well plate. Adhering cells disrupt the electrical transmission between electrodes and the impedance in flow is expressed as cell index and is positively correlated with cell adhesive capacity.…”

Section: Xcelligence Assaymentioning

confidence: 99%

Jagged1 regulates endometrial receptivity in both humans and mice

2021

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The human endometrium undergoes cycle-dependent changes and is only receptive to an implanting blastocyst within a narrow window of 2-4 days in the mid-secretory phase. Such functional changes require delicate interplay between a diversity of factors including cytokines and signaling pathways. The Notch signaling pathway members are expressed in human endometrium. We have previously demonstrated that Notch ligand Jagged1 (JAG1) localizes in the endometrial luminal epithelium (LE) and is abnormally reduced in infertile women during receptivity. However, the functional consequences of reduced JAG1 production on endometrial receptivity to implantation of the blastocyst are unknown. This study aimed to determine the role of JAG1 in regulating endometrial receptivity in humans and mice. Knockdown of JAG1 in both primary human endometrial epithelial cells and Ishikawa cells significantly reduced their adhesive capacity to HTR8/SVneo (trophoblast cell line) spheroids. We confirmed that in human endometrial epithelial cells, JAG1 interacted with Notch Receptor 3 (NOTCH3) and knockdown of JAG1 significantly reduced the expression of Notch signaling downstream target HEY1 and classical receptivity markers. Knockdown of Jag1 in mouse LE significantly impaired blastocyst implantation.We identified ten genes (related to tight junction, infertility, and cell adhesion) that were differentially expressed by Jag1 knockdown in LE in mice. Further analysis of the tight junction family members in both species revealed that JAG1 altered the expression of tight junction components only in mice. Together, our data demonstrated that JAG1 altered endometrial epithelial cell adhesive capacity and regulated endometrial receptivity in both humans and mice likely via different mechanisms.

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“…Cell migration and proliferation was significantly greater with the G3 grading than with the G1 grading. The conclusions drawn by the authors are that galectin 7 have possible influence on the formation of distant metastases in endometrial cancer [ 23 ].…”

Section: Discussionmentioning

confidence: 99%

Could Galectin 3 Be a Good Prognostic Factor in Endometrial Cancer?

et al. 2020

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Galectin 3 is a modulator of several basic biological functions. It may be involved in the development of obesity and type 2 diabetes—risk factors of endometrial cancer. The study involved 144 patients, after abrasion due to postmenopausal bleeding. Galectin 3 concentrations were quantified in serum by multiplex fluorescent bead-based immunoassays. Median serum galectin 3 concentrations revealed significant differences between FIGO III and IV vs. FIGO I and II patients. Statistically higher concentrations were reported for patients with lymph node metastases compared to patients without it (p = 0.001) as well as in patients with lymphovascular space invasion compared to patients without LVSI (p = 0.02). No statistically significant differences were observed for median of galectin 3 levels depending on the surgical procedure (laparoscopy vs. laparotomy, p = 0.0608). Patients with galectin 3 levels exceeding the median value were characterized by overall survival being shorter by 11.9 months. High levels of galectin 3 were correlated with shorter disease-free survival, the difference is up to 14.8 months. Galectin 3 can be an independent prognostic factor in patients with endometrial cancer. Among the recognized prognostic factors and the concentrations of the galectin 3 marker at the adopted time points, the univariate analysis showed a significant effect of staging, grading, and cutoff galectin 3 on the OS. For multivariate analysis, the galectin 3 cutoff point had the greatest significant impact on OS.

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Galectin‑7 is elevated in endometrioid (type I) endometrial cancer and promotes cell migration

Cited by 15 publications

References 40 publications

ARID1A and PI3-kinase pathway mutations in the endometrium drive epithelial transdifferentiation and collective invasion

ARID1A and PI3-kinase pathway mutations in the endometrium drive epithelial transdifferentiation and collective invasion

Jagged1 regulates endometrial receptivity in both humans and mice

Could Galectin 3 Be a Good Prognostic Factor in Endometrial Cancer?

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