Menin, encoded by the MEN1 gene, was initially identified as a tumor suppressor for endocrine neoplasia. Our previous report showed that Menin enhances PPARα transactivity preventing triglyceride accumulation in the liver. Here, we further explore the role of Menin in liver steatosis. Transient transfection assays demonstrate that Menin inhibits the transcriptional activity of nuclear receptor liver X receptor α (LXRα). Accordingly, Menin overexpression results in reduced expression of LXRα target genes, such as lipogenic enzymes including SREBP-1c, FASN and SCD-1. Co-immunoprecipitation assays revealed physical interaction between Menin and LXRα. Collectively, our data suggest that Menin acts as a novel corepressor of LXRα and functions as a negative regulator of hepatic lipogenesis.
Download full-text PDF |
Source |
---|---|
http://dx.doi.org/10.1016/j.febslet.2015.04.049 | DOI Listing |
Cir Cir
January 2025
Department of Genetics, Kocaeli University, Faculty of Medicine, Kocaeli, Turkey.
Objective: Understanding the relationship between genetic structure and the molecular changes involved in endometrial cancer (EC) provides an opportunity to personalize treatments and incorporate targeted therapies.
Method: We compared cytogenetic and molecular features observed in tumoral and adjacent healthy tissue endometrium samples in EC patients.
Results: Non-clonal chromosome aberrations (NCCAs) frequently in patients with EC, especially in 10,15,17,22, X chromosomes and were monitored in 73.
Oncol Lett
March 2025
Department of Hematology, Shengli Oilfield Central Hospital, Dongying, Shandong 257000, P.R. China.
The FAT atypical cadherin 1 (FAT1) gene is the ortholog of the fat gene and encodes the protocadherin FAT1. FAT1 belongs to the cadherin superfamily, a group of full-length membrane proteins that contain cadherin-like repeats. In various types of human cancer, FAT1 is one of the most commonly mutated genes, and is considered to be an emerging cancer biomarker and a potential target for novel therapies.
View Article and Find Full Text PDFCancer Discov
January 2025
Princess Margaret Cancer Centre, Toronto, ON, Canada.
Epigenetic therapies facilitate transcription of immunogenic repetitive elements that cull cancer cells through 'viral mimicry' responses. Paradoxically, cancer-initiating events also facilitate transcription of repetitive elements. Contributions of repetitive element transcription towards cancer initiation, and the mechanisms by which cancer cells evade lethal viral mimicry responses during tumor initiation remain poorly understood.
View Article and Find Full Text PDFJ Orthop Res
January 2025
Department of East Hospital Orthopaedic Trauma, Zibo Central Hospital, Zibo, China.
Ewing sarcoma (ES) is a malignant bone tumor prevalent among children and adolescents. Disulfidptosis represents a novel form of cell death; however, the mechanism of disulfidptosis in ES remains unclear. Our aim is to explore the disulfidptosis-related prognostic signature in ES.
View Article and Find Full Text PDFJ Clin Endocrinol Metab
January 2025
Metabolic Diseases Branch, Bldg. 10/Rm 8C-101, National Institute of Diabetes and Digestive and Kidney Diseases, Bethesda, MD 20892.
Establishing genotype-phenotype correlations in disorders of hereditary endocrine neoplasia is important for clinical screening, genetic counseling, prognostication, surveillance, and surgical strategy, and may also provide clues about disease pathogenesis. Important genotype-phenotype correlations are recognized, for example, in pheochromocytoma/paraganglioma and multiple endocrine neoplasia type 2A. The presence of such correlations has been less clear in other familial endocrine disorders associated with primary hyperparathyroidism including multiple endocrine neoplasia type 1 (MEN1), and the hyperparathyroidism-jaw tumor syndrome (HPT-JT).
View Article and Find Full Text PDFEnter search terms and have AI summaries delivered each week - change queries or unsubscribe any time!