TENT5C

Last update 08 May 2025

Basic Info

Synonyms

FAM46C, FLJ20202, Non-canonical poly(A) polymerase FAM46C

+ [2]

Introduction

(Microbial infection) Seems to enhance replication of some viruses, including yellow fever virus, in response to type I interferon. Catalyzes the transfer of one adenosine molecule from an ATP to an mRNA poly(A) tail bearing a 3'-OH terminal group and enhances mRNA stability and gene expression (PubMed:28931820, PubMed:32009146, PubMed:34048638). Can also elongate RNA oligos ending with uridine molecule, provided that the sequence is adenosine-rich (PubMed:34048638). Mainly targets mRNAs encoding endoplasmic reticulum-targeted protein (PubMed:28931820).

100 Clinical Results associated with TENT5C

100 Translational Medicine associated with TENT5C

0 Patents (Medical) associated with TENT5C

Literatures (Medical) associated with TENT5C

01 Jan 2025·Cellular Signalling

Induction of FAM46C expression mediated by DNMT3A downregulation is involved in early-onset preeclampsia through gene body methylation

Article

Author: Dong, Jiaqi ; Ying, Hao ; Jia, Yuanhui ; Wu, Shengyu ; Xie, Han

BACKGROUNDAberrant methylation of genomic DNA has been found in preeclamptic placentas, which is characterized by elevated DNA methylation and hypermethylation of gene body regions, but the underlying mechanism is not yet fully understood.METHODSGlobal DNA methylation was assessed through ELISA and HPLC. The methylation sites were detected using the Illumina Human Methylation 450 K Microarray. The methylation level of FAM46C promoter and gene body was detected through the bisulfite sequencing. RNA-seq was utilized to investigate the mechanism by which DNMT3A and FAM46C mediate the migration and invasion of trophoblast cells.RESULTSWe discovered that DNMT3A knockdown led to elevated levels of gene body methylation and FAM46C transcription. FAM46C downregulation completely rescued the suppressive effects caused by DNMT3A knockdown on the migration and invasion of trophoblast cells. Mechanistically, DNMT3A reduction led to an increase in the enrichment of DNMT3B and DNMT1 in the gene body region of FAM46C. The results of transcriptome sequencing showed that DNMT3A and FAM46C regulate the adhesion of trophoblast cells. Elevated expression of FAM46C and increased methylation levels within its gene body region were observed in extravillous trophoblast cells of early-onset preeclamptic placentas.CONCLUSIONSDNMT3A-mediated aberrant FAM46C gene body methylation is relevant to the development of early-onset preeclampsia.

01 Aug 2024·Journal of Gastrointestinal Oncology

The emerging role of FAM46C as a biomarker and therapeutic target in gastric adenocarcinoma

Review

Author: Luu, Shelly ; Fu, Ning ; Conner, James ; Pacholczyk, Karina ; Swallow, Carol J. ; Savage, Paul ; Zaslavsky, Taylor ; Swallow, Carol J

On a global scale, gastric adenocarcinoma (GCa) accounts for a large burden of death from cancer. Despite advances in systemic therapy and surgical technique, the fatality rate for GCa remains unacceptably high in Europe and North America, where diagnosis is typically made at an advanced stage. Biomarkers that can accurately predict response to new therapies and provide novel therapeutic strategies are urgently sought. FAM46C, a putative noncanonical nucleotidyltransferase, has garnered interest for its tumor suppressor function in multiple myeloma. A frequent and profound depletion of FAM46C has been described in GCa patients from China, Japan and now Canada. Furthermore, the degree of FAM46C depletion meaningfully portends cancer recurrence following resection, and death from GCa. In this review, we provide an updated summary of the literature regarding FAM46C as a biomarker in GCa and explore the potential mechanism(s) through which FAM46C depletion promotes GCa progression, including dis-inhibition of oncogenic Plk4 kinase activity. We highlight the potential for restoration of FAM46C levels as a therapeutic strategy. Norcantharidin, a synthetic analogue of the traditional Chinese medicine cantharidin derived from the blister beetle, is the only bio-available compound presently known to upregulate FAM46C expression and is under investigation in phase one trials in cancer patients.

01 Jun 2024·Journal of Genetics and Genomics

The non-canonical poly(A) polymerase FAM46C promotes erythropoiesis

Article

Author: Han, Gaijing ; Lv, Xiang ; Xu, Weiyin ; Yin, Jiaying ; Fan, Hong ; Zhang, Qiaoli ; Li, Jing ; Yang, Ke ; Liu, Nan ; Zhu, Tianqi

The post-transcriptional regulation of mRNA is a crucial component of gene expression. The disruption of this process has detrimental effects on the normal development and gives rise to various diseases. Searching for novel post-transcriptional regulators and exploring their roles are essential for understanding development and disease. Through a multimodal analysis of red blood cell trait genome-wide association studies (GWAS) and transcriptomes of erythropoiesis, we identify FAM46C, a non-canonical RNA poly(A) polymerase, as a necessary factor for proper red blood cell development. FAM46C is highly expressed in the late stages of the erythroid lineage, and its developmental upregulation is controlled by an erythroid-specific enhancer. We demonstrate that FAM46C stabilizes mRNA and regulates erythroid differentiation in a polymerase activity-dependent manner. Furthermore, we identify transcripts of lysosome and mitochondria components as highly confident in vivo targets of FAM46C, which aligns with the need of maturing red blood cells for substantial clearance of organelles and maintenance of cellular redox homeostasis. In conclusion, our study unveils a unique role of FAM46C in positively regulating lysosome and mitochondria components, thereby promoting erythropoiesis.

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