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| http://dx.doi.org/10.1102/1470-7330.2008.0001 | DOI Listing |
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Elevated LINC00115 expression correlates with aggressive endometrial cancer phenotypes via JAK/STAT pathway modulation.
Hum Mol Genet
January 2025
Department of Reproductive Medicine, The First Affiliated Hospital of Henan University of CM, No. 19, Renmin Road, Jinshui District, Zhengzhou City, Henan Province, China.
This study systematically explores the oncogenic role of the long non-coding RNA (lncRNA) LINC00115 in endometrial cancer (EC) and reveals its unique mechanism in promoting proliferation, invasion, and metastasis via the JAK/STAT signaling pathway. LINC00115 is significantly upregulated in EC tissues and closely associated with advanced TNM staging and lymph node metastasis. Functional assays showed that knockdown of LINC00115 suppressed EC cell proliferation, invasion, and metastasis, while overexpression enhanced these malignant behaviors.
View Article and Find Full Text PDFUterus didelphys: the first case report on molecular profiling of endometrial tissue from both uterine cavities.
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January 2025
Department of Gynecology and Reproductive Medicine, Karolinska University Hospital, Huddinge, Stockholm, 14183, Sweden.
Background: A didelphic uterus represents a unique and infrequent congenital condition in which a woman possesses two distinct uteri, each with its own cervix. This anomaly arises due to partial or incomplete merging of the Müllerian ducts during the developmental stages in the womb. Accounting for uterine malformations, a didelphic uterus is a relatively rare condition, affecting approximately 0.
View Article and Find Full Text PDFTime-series single-cell transcriptomic profiling of luteal-phase endometrium uncovers dynamic characteristics and its dysregulation in recurrent implantation failures.
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Shenzhen Key Laboratory of Fertility Regulation, Reproductive Medicine Center, the University of Hong Kong-Shenzhen Hospital, Shenzhen, China.
Understanding human endometrial dynamics in the establishment of endometrial receptivity remains a challenge, which limits early diagnosis and treatment of endometrial-factor infertility. Here, we decode the endometrial dynamics of fertile women across the window of implantation and characterize the endometrial deficiency in women with recurrent implantation failure. A computational model capable of both temporal prediction and pattern discovery is used to analyze single-cell transcriptomic data from over 220,000 endometrial cells.
View Article and Find Full Text PDFOvarian steroids modulate mRNA expression of ECM associated genes and collagen deposition induced by TGF β1 in equine endometrium in vitro.
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Institute of Animal Reproduction and Food Research, Polish Academy of Sciences, Olsztyn, 10-748, Poland.
Equine endometrosis is a major cause of infertility in mares and is characterized by degenerative, functional and fibrotic changes in the endometrium with increased collagen (COL) deposition. Transforming growth factor (TGF)-β1 is one of the major pro-fibrotic factors involved in the excessive deposition of extracellular matrix (ECM) components in the equine endometrium. It has been demonstrated that ovarian steroids, specifically 17β-estradiol (E2) and progesterone (P4), not only regulate the cyclicity of the estrous cycle, but also have been implicated as anti- or pro-fibrotic factors.
View Article and Find Full Text PDFNCAPG promotes the malignant progression of endometrioid cancer through LEF1/SEMA7A/PI3K-AKT.
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January 2025
Department of Obstetrics and Gynecology, The Second Xiangya Hospital of Central South University, Changsha, Hunan, 410011, China.
Article Synopsis
- NCAPG contributes to the development of endometrial cancer by activating the PI3K-AKT signaling pathway, making it a potential tumor marker.
- The study utilized advanced techniques like ATAC-Seq, CHIP, and CoIP to demonstrate how NCAPG influences cell proliferation and invasion by modulating LEF1's interaction with chromatin, which subsequently affects the transcription of SEMA7A.
- The NCAPG/LEF1/SEMA7A pathway is linked to cancer progression and severity in patients, suggesting that targeting this molecular pathway could lead to new treatments for endometrial cancer.
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