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PML/RARα Fusion Gene and Response to Retinoic Acid and Arsenic Trioxide Treatment
Published in Sherry X. Yang, Janet E. Dancey, Handbook of Therapeutic Biomarkers in Cancer, 2021
Alicja M. Gruszkaa, Myriam Alcalay
The interaction between PML/RARa and transcription factors is not limited to inter-protein binding, but is detected also at the level of DNA binding. A very recent genome-wide study of PML/RARa binding sites revealed that the fusion protein binds to additional regulators of haematopoiesis, including RUNX1, RUNX3 and GFI1. Significantly, these are not classical targets of RA signalling [53].
Intraepithelial T cells: Specialized T cells at epithelial surfaces
Published in Phillip D. Smith, Richard S. Blumberg, Thomas T. MacDonald, Principles of Mucosal Immunology, 2020
The binding of α4β7 to the mucosal addressin cell adhesion molecule-1 (MAdCAM-1), expressed by vascular endothelium in lamina propria, MLN, and PP blood vessels, promotes translocation into the respective tissues. After local or systemic infection, α4β7 is transiently induced, which provides a finite window of time to migrate to the intestinal epithelium. Following entry into the mucosa, α4β7 is lost; concomitant with this αEβ7 is induced and appears to be important for retention in the epithelium via interaction with its ligand, E-cadherin, expressed by epithelial cells. Induction of αEβ7 is mediated by transforming growth factor-beta (TGF-β), and the transcription factor Runx3 and is enhanced by signaling through CCR9. Similarly, reinduction of CD69 occurs when activated T cells enter the mucosa; however, its function on these mucosal T cells remains unknown.
Breast cancer epigenetic targets for precision medicine
Published in Debmalya Barh, Precision Medicine in Cancers and Non-Communicable Diseases, 2018
In addition, in the ER+ breast cancers, the RUNX3 hypermethylation was frequently observed and a higher RUNX3 mRNA expression was associated with better relapse-free survival (Lu et al., 2017). Thus, RUNX3 methylation could be a therapeutic target for the development of personalized therapy.
Molecular Genetics of Cleidocranial Dysplasia
Published in Fetal and Pediatric Pathology, 2021
Jamshid Motaei, Arash Salmaninejad, Ebrahim Jamali, Imaneh Khorsand, Mohammad Ahmadvand, Sasan Shabani, Farshid Karimi, Mohammad Sadegh Nazari, Golsa Ketabchi, Fatemeh Naqipour
Thirty percent of patients with acute myeloid leukemia (AML) and ten percent of patients with myelodysplasia (MDS) have mutations in the RUNX1 gene [12]. RUNX1 plays an important role in hematopoietic cells. Hereditary mutation in RUNX1 causes familial platelet disorder with predisposition to myeloid malignancy (FPD/AML) with autosomal dominate inheritance pattern [13]. RUNX2 plays an important role in the development of the skeletal system and the morphogenesis of other organs, such as thyroid and breast. The role of RUNX2 is increasingly recognized in various cancers, including thyroid, prostate, lung and breast cancer. Many studies have shown that the deregulation of RUNX2 is associated with the progression and metastasis of various tumors [14–17]. RUNX3 is a tumor suppressor gene that plays a role in various biological processes, including development of the cranial and dorsal root ganglia, gastrointestinal tract and T-cell differentiation. Mutations in RUNX3 have been reported in various diseases including colon and gastric cancers, glioma, melanoma, prostate cancer, renal cell carcinoma and neural disorders [18].
LncRNA PART1/miR-185-5p/RUNX3 feedback loop modulates osteogenic differentiation of bone marrow mesenchymal stem cells
Published in Autoimmunity, 2021
Junjie Zhang, Nanwei Xu, Changlin Yu, Kaisong Miao, Qiugen Wang
Previous research suggested that abnormal osteogenic differentiation of BMSCs is the main cause of OP [21,22]. Thus, regulation of BMSCs osteogenic differentiation is a vital focus in OP pathogenesis research. Emerging evidence unravelled that lncRNAs served essential roles in various diseases, including OP [23,24]. Moreover, previous researches exhibited that PART1 was involved in the development of bone disease. For example, PART1 acted as an oncogene in osteosarcoma by regulating miR-20b-5p to enhance BAMBI [25]. Upregulated PART1 promoted the viability and decreased cell apoptosis of chondrocytes through miR-590-3p/TGFBR2 in osteoarthritis [26]. Nevertheless, the molecular mechanism of PART1 in OP is unclear. In this work, we found that PART1 was overexpressed during osteogenic differentiation of hBMSCs, and knockdown of PART1 impaired hBMSC osteogenic differentiation. In addition, the upstream regulatory mechanism of PART1 was further explored. Runt-related transcription factor 3 (RUNX3) is a member of the RUNX family, which has been reported to be an inducer of osteoblast differentiation [27,28]. In addition, RUNX3 was identified as a transcription activator of various genes, including lncRNAs [29,30]. Herein, we demonstrated that RUNX3 served as a transcriptional activator of PART1.
Caudal type homeoboxes as a driving force in Helicobacter pylori infection-induced gastric intestinal metaplasia
Published in Gut Microbes, 2020
Hong-Yan Chen, Yi Hu, Nong-Hua Lu, Yin Zhu
The Smad complex must be guided by the Runt-related transcription factor gene (RUNX) protein (including the RUNX3 protein) before it can be transferred from the cytoplasm to a specific target site. The Smad complex must co-transcribe and activate target genes with the RUNX protein, thereby affecting cell differentiation, cell cycle regulation, apoptosis and tumorigenesis. RUNX3 is an important transcription factor downstream of the TGF-β signaling pathway as a tumor suppressor gene for GC.96 In the progression of GC, RUNX3 can also undergo epigenetic changes. Low expression of RUNX3 caused by RUNX3 hypermethylation97 and abnormal cytoplasmic localization of RUNX3 were observed in most IM patients with H. pylori infection, which is related to Src-mediated tyrosine phosphorylation, cytoplasmic RUNX3 cannot enter the nucleus and exert biological activity.98 Ito et al.99found that the gastric epithelium of Runx3−/- mice was transformed by SPEM, demonstrating MUC6 and TFF2 expression, and the expression of Cdx2 was detected in the metaplastic area. This evidence indicates that the inactivation of RUNX3 may promote the expression of CDX2 and accelerate the formation of IM (Figure 2).