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GSE174741 LINC01133 inhibits invasion and promotes proliferation in an endometriosis epithelial cell line
Contributors : Quanah J Hudson ; Iveta Yotova ; Florian M Pauler ; Rene WenzlSeries Type : Expression profiling by high throughput sequencingOrganism : Homo sapiensEndometriosis is a common gynecological disorder characterized by ectopic growth of endometrium outside the uterus and associated with chronic pain and infertility. We investigated the role of LINC01133 in endometriosis, an lncRNA that has been implicated in several types of cancer. We found that LINC01133 is upregulated in ectopic endometriosis lesions. As expression appeared higher in the epithelial endometrial layer, we performed an siRNA knockdown of LINC011...
Source: GEO: Gene Expression Omnibus - August 23, 2021 Category: Genetics & Stem Cells Tags: Expression profiling by high throughput sequencing Homo sapiens Source Type: research

Interleukin-6 (IL-6) activates the NOTCH1 signaling pathway through E-proteins in endometriotic lesions.
CONCLUSIONS: IL-6 induced NOTCH1 expression is mediated by E-proteins in the ectopic GE cells, which may promote endometriotic lesion development. PMID: 32119078 [PubMed - as supplied by publisher]
Source: The Journal of Clinical Endocrinology and Metabolism - March 1, 2020 Category: Endocrinology Authors: Song Y, Su RW, Joshi NR, Kim TH, Lessey BA, Jeong JW, Fazleabas AT Tags: J Clin Endocrinol Metab Source Type: research

Elevated phosphatase of regenerating liver 3 (PRL-3) promotes cytoskeleton reorganization, cell migration and invasion in endometrial stromal cells from endometrioma
STUDY QUESTION Is phosphatase of regenerating liver-3 (PRL-3) associated with increased motility of endometriotic cells from endometrioma? SUMMARY ANSWER Elevated PRL-3 promotes cytoskeleton reorganization, cell migration and invasion of endometrial stromal cells (ESCs) from endometrioma. WHAT IS KNOWN ALREADY Overexpression of PRL-3 is associated with cancer cell migration, invasion and metastatic phenotype. STUDY DESIGN, SIZE, DURATION Primary human ESCs were isolated from eutopic endometrium of women without endometriosis (EuCo, n = 10), with histologically proven endometrioma (EuEM, n = 19) and from the cyst wall of...
Source: Human Reproduction - March 15, 2016 Category: Reproduction Medicine Authors: Zhan, H., Ma, J., Ruan, F., Bedaiwy, M. A., Peng, B., Wu, R., Lin, J. Tags: Gynaecology Source Type: research

Deletion of Arid1a in Reproductive Tract Mesenchymal Cells Reduces Fertility in Female Mice.
Abstract Women with endometriosis can suffer from decreased fecundity or complete infertility via abnormal oocyte function or impaired placental-uterine interactions required for normal pregnancy establishment and maintenance. Although AT-rich interactive domain 1A (SWI-like) (ARID1A) is a putative tumor suppressor in human endometrial cancers and endometriosis-associated ovarian cancers, little is known about its role in normal uterine function. To study the potential function of ARID1A in the female reproductive tract, we generated mice with a conditional knockout of Arid1a using anti-Müllerian hormone receptor...
Source: Biology of Reproduction - March 9, 2016 Category: Reproduction Medicine Authors: Wang X, Khatri S, Broaddus R, Wang Z, Hawkins SM Tags: Biol Reprod Source Type: research

151pd * arid1a role in cell cycle regulation and proliferation in mouse and human gynaecological tissues reveals potential therapeutic targets
Conclusions: A core ARID1A-driven transcriptional programme, conserved accross normal tissues and species appears to exist, centred around regulation of genes involved in the G2/M checkpoint. ARID1A loss promotes proliferation in normal tissues, providing important clues as to the mechanisms of ARID1A-driven carcinogenesis. Mitotic kinases emerge as potential therapeutic targets in ARID1A mutant tumours, an observation that is not evident from studies in cancer cell lines.Disclosure: All authors have declared no conflicts of interest.
Source: Annals of Oncology - September 24, 2014 Category: Cancer & Oncology Authors: Gounaris, I., Brenton, J. Tags: basic science Source Type: research