scholarly journals Identification ofTDRD1as a direct target gene ofERGin primary prostate cancer

2013 ◽  
Vol 133 (2) ◽  
pp. 335-345 ◽  
Author(s):  
Joost L. Boormans ◽  
Hanneke Korsten ◽  
Angelique J.C. Ziel-van der Made ◽  
Geert J.L.H. van Leenders ◽  
Carola V. de Vos ◽  
...  
Keyword(s):  
Prostate Cancer ◽  
Target Gene ◽  
Primary Prostate Cancer ◽  
Direct Target Gene ◽  
Direct Target

ZNF16 (HZF1) promotes erythropoiesis and megakaryocytopoiesis via regulation of the c-KIT gene

2014 ◽  
Vol 458 (1) ◽  
pp. 171-183 ◽  
Author(s):  
Jing Chen ◽  
Xiao-Bo Li ◽  
Rui Su ◽  
Li Song ◽  
Fang Wang ◽  
...  
Keyword(s):  
Progenitor Cells ◽  
Target Gene ◽  
Megakaryocytic Differentiation ◽  
Kit Gene ◽  
Direct Target Gene ◽  
Direct Target

The present study demonstrated that ZNF16 (HZF1) plays an important role in erythroid and megakaryocytic differentiation of human haematopoietic stem/progenitor cells, identified and validated c-KIT as a direct target gene of ZNF16, and demonstrated that ZNF16 functions via its regulation on the c-Kit/c-Raf/MEK/ERK/c-Jun/HEY1/GATA1 cascade.

scholarly journals The Receptor Tyrosine Kinase EphA2 Is a Direct Target Gene of Hypermethylated in Cancer 1 (HIC1)

2011 ◽  
Vol 287 (8) ◽  
pp. 5366-5378 ◽  
Author(s):  
Bénédicte Foveau ◽  
Gaylor Boulay ◽  
Sébastien Pinte ◽  
Capucine Van Rechem ◽  
Brian R. Rood ◽  
...  
Keyword(s):  
Tyrosine Kinase ◽  
Receptor Tyrosine Kinase ◽  
Target Gene ◽  
Direct Target Gene ◽  
Direct Target

scholarly journals Scavenger Chemokine (CXC Motif) Receptor 7 (CXCR7) Is a Direct Target Gene ofHIC1(Hypermethylated in Cancer 1)

2009 ◽  
Vol 284 (31) ◽  
pp. 20927-20935 ◽  
Author(s):  
Capucine Van Rechem ◽  
Brian R. Rood ◽  
Majid Touka ◽  
Sébastien Pinte ◽  
Mathias Jenal ◽  
...  
Keyword(s):  
Target Gene ◽  
Direct Target Gene ◽  
Direct Target

scholarly journals YTHDF2, a protein repressed by miR-145, regulates proliferation, apoptosis and migration in ovarian cancer cells

2020 ◽  
Author(s):  
Jie Li ◽  
Lei Wu ◽  
Meili Pei ◽  
Yun Zhang
Keyword(s):  
Ovarian Cancer ◽  
Feedback Loop ◽  
Target Gene ◽  
Epigenetic Modification ◽  
Ovarian Cancer Cells ◽  
Direct Target Gene ◽  
Direct Target ◽  
And Migration ◽  
Cancer Tissues ◽  
Proliferation And Migration

Abstract RNA methylation can reverse the methylation modification at RNA level, which is a kind of extremely important epigenetic modification. YTHDF2, as a reader of m6A modification, the function and mechanisms of in epithelial ovarian cancer(EOC) have not been elucidated so far. In this study, we demonstrated that YTHDF2 was significantly upregulated in EOC tissues compared with normal ovarian tissues, further function studies confirmed that YTHDF2 significantly promoted the proliferation and migration of EOC cell lines, and reduced the global mRNA m6A levels. Next, we found that the expression levels of miR-145 and YTHDF2 were inversely correlated in ovarian cancer tissues and cells, and YTHDF2 is the direct target gene of miR-145. Interestingly, there was a crucial crosstalk between miR-145 and YTHDF2 via a double-negative feedback loop. Overexpression of YTHDF2 rescues miR-145-induced reduction of proliferation and migration in EOC cells. To conclude, YTHDF2 and miR-145, as two crucial m6A regulators, are involved in the progression of EOC by indirectly modulating m6A levels. In view of these promising results, YTHDF2 and miR-145 may provide new insights into the carcinogenesis and new potential therapeutic targets for EOC.

scholarly journals Suppression of ANT2 by miR-137 Inhibits Prostate Tumorigenesis

2021 ◽  
Vol 12 ◽  
Author(s):  
Heyuan Zhang ◽  
Nanhui Chen ◽  
Zhihai Deng ◽  
Yang Mai ◽  
Limin Deng ◽  
...  
Keyword(s):  
Prostate Cancer ◽  
Target Gene ◽  
Inhibitory Effect ◽  
Luciferase Reporter ◽  
Migration And Invasion ◽  
Prostate Tumorigenesis ◽  
Direct Target Gene ◽  
Reporter Assays ◽  
Serious Disease ◽  
Cancer Tissues

Prostate cancer (PCa) is a serious disease that affects men’s health. To date, no effective and long-lasting treatment option for this condition is available in clinical practice. ANT2 is highly expressed in a variety of hormone-related cancers, but its relationship and regulatory mechanism with PCa are unclear. In this study, we found that ANT2 expression was significantly upregulated in PCa tissues relative to control samples. Genetic knockdown of ANT2 effectively inhibited, while overexpression promoted, proliferation, migration, and invasion of PCa cells. In addition, miR-137 expression was reduced in prostate cancer tissues relative to control tissues. We identified a regulatory site for miR-137 in the 3′-UTR of ANT2 mRNA; luciferase reporter assays indicated that ANT2 is a direct target gene for miR-137. Transfecting cells with miR-137 mimics and/or an ANT2-encoding plasmid revealed that ANT2 promotes proliferation, migration, and invasion of PCa, whereas co-expression of miR-137 mimics inhibited these behaviors. These observations suggest that miR-137 mimics inhibit development of PCa by antagonizing expression of ANT2. Furthermore, tumorigenic assays in nude mice showed that miR-137 inhibitors abolished the inhibitory effect of ANT2 knockdown on PCa tumor growth. Collectively, our findings suggest that ANT2, a target gene of miR-137, is intimately involved in development of PCa, providing new evidence for the mechanism underlying pathogenesis of PCa as well as new options for targeted therapy.

scholarly journals SEMA6D, Negatively Regulated by miR-7, Contributing to Chondrocyte Catabolic and Anabolic Activities via p38 Signaling Pathway

2020 ◽  
Author(s):  
Xindie Zhou ◽  
Yi Zhang ◽  
Junjie Zhang ◽  
Zhicheng Yang ◽  
Haoyu Yang ◽  
...  
Keyword(s):  
Target Gene ◽  
Regulatory Mechanism ◽  
Regulatory Factor ◽  
Regulatory Relation ◽  
Direct Target Gene ◽  
Direct Target ◽  
Novel Therapeutic ◽  
P38 Pathway

Abstract Background: MiR-7 has been recognized as a promoting factor of osteoarthritis (OA), but the specific down-stream pathway of miR-7 still remains unknown. Further investigation of the molecular regulatory mechanism of miR-7 might help develop a novel therapeutic method for OA.Results: Here we revealed that Semaphorin 6D (SEMA6D) was a direct target gene of miR-7, of which presented a negatively regulatory relation in vitro and in vivo. Lucubration of SEMA6D suggested that SEMA6D is validated to promote the anabolic metabolism and reduce the catabolism of chondrocytes via inhibiting the activation of p38 pathway.Conclusions: Present research illustrated that SEMA6D is a negatively regulatory factor of miR-7 and a pivotal mediator of the catabolism and anabolism of chondrocytes. SEMA6D exerts its function via inhibiting the activation of p38 pathway.

Clinical significance of serum miR-101-3p expression in patients with neonatal sepsis

2021 ◽  
Author(s):  
Juan Zhang ◽  
Xinwei Xu ◽  
Min Wang
Keyword(s):  
Neonatal Sepsis ◽  
Target Gene ◽  
Operating Characteristic ◽  
Characteristic Curve ◽  
Quantitative Real Time Pcr ◽  
Tnf Α ◽  
Direct Target Gene ◽  
Direct Target ◽  
Operating Characteristic Curve

Aim: This study aimed to evaluate the levels and functions of miR-101-3p in neonatal sepsis (NS). Materials & methods: Quantitative real-time PCR was conducted to investigate the expression of miR-101-3p and the receiver operating characteristic curve was applied to manifest its diagnostic effects. Results: MiR-101-3p was increased in the NS patients and the dysregulation of miR-101-3p was associated with levels of procalcitonin, CRP, IL-8 and TNF-α. The combination of miR-101-3p and procalcitonin could function as a promising indicator in distinguishing NS patients. The silenced miR-101-3p reversed the increased levels of TNF-α and IL-8 caused by lipopolysaccharide in vitro. DUSP1 was identified as a direct target gene of miR-101-3p in NS. Conclusion: The abundance of miR-101-3p facilitated the inflammation in NS by targeting DUSP1.

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