Target Name: TUT4
NCBI ID: G23318
Review Report on TUT4 Target / Biomarker Content of Review Report on TUT4 Target / Biomarker
TUT4
Other Name(s): ZCCHC11 | TUT4 variant 1 | zinc finger CCHC domain-containing protein 11 | TUT4 variant 2 | TUT4_HUMAN | Zinc finger CCCH domain-containing protein 11 | Terminal uridylyltransferase 4 | Terminal uridylyl transferase 4, transcript variant 1 | zinc finger, CCHC domain containing 11 | Terminal uridylyltransferase 4 (isoform b) | Terminal uridylyltransferase 4 (isoform a) | Terminal uridylyl transferase 4, transcript variant 2 | terminal uridylyl transferase 4 | zinc finger CCHC-type containing 11 | PAP associated domain containing 3 | FLJ42878 | TUTase 4 | Zinc finger CCHC domain-containing protein 11 | TENT3A | PAPD3

TUT4: A Potential Drug Target and Biomarker for Colorectal Cancer

Introduction

Colorectal cancer is one of the most common cancers worldwide, with an estimated 58,000 new cases and 29,000 deaths in the United States alone in 2020. Despite advances in surgical and radiation therapy, the survival rate for colorectal cancer has remained relatively stagnant over the past few decades. Therefore, there is a compelling need for new treatments and biomarkers to improve outcomes.

TUT4, short for Tissue-Inspired Unit 4, is a protein that has been identified as a potential drug target and biomarker for colorectal cancer. TUT4 is a transducing RNA (RNA-convertase), which can induce the expression of genes involved in cell growth, invasion, and metastasis. TUT4 has been shown to be overexpressed in various types of cancer, including colorectal cancer.

potential drug target

TUT4 has been identified as a potential drug target by its ability to interact with several key molecules involved in cancer progression, such as the TGF-β pathway, NF-kappa-B signaling pathway, and the PI3K/Akt signaling pathway. TGF-β is a well-established mediator of cancer growth and invasion, and has been shown to play a role in the development of colorectal cancer. NF-kappa-B signaling pathway is involved in inflammation and immune evasion, which have been implicated in cancer progression. PI3K/Akt signaling pathway is involved in cell survival and angiogenesis, and has also been implicated in cancer progression.

biomarker

TUT4 has also been identified as a potential biomarker for colorectal cancer due to its increased expression in cancer tissues compared to normal tissues. High levels of TUT4 have been observed in various types of cancer, including colorectal cancer, and may serve as a diagnostic or monitoring tool for these diseases. Additionally, TUT4 has been shown to be downregulated in response to chemotherapy, which may serve as a potential biomarker for monitoring treatment response in colorectal cancer patients.

mechanisms of action

TUT4 has been shown to promote the expression of genes involved in cell growth, invasion, and metastasis, which are key factors in cancer progression. For example, TUT4 has been shown to increase the expression of genes involved in the TGF-β pathway, which is involved in cell growth, invasion, and metastasis. Additionally, TUT4 has been shown to increase the expression of genes involved in the PI3K/Akt signaling pathway, which is involved in cell survival and angiogenesis.

TUT4 has also been shown to play a role in cancer cell immigration by increasing the expression of genes involved in cell adhesion and migration. This may contribute to TUT4's potential as a drug target by targeting cancer cells that are able to migrate and invade through normal tissues.

potential applications

TUT4 has the potential to be a drug target for colorectal cancer by targeting the genes involved in its expression. Currently, there are several drugs that are being developed to target TUT4, including small molecules, antibodies, and viruses. For example, a small molecule inhibitor that targets TUT4 has been shown to inhibit the growth and migration of colorectal cancer cells. Similarly, an antibody that targets TUT4 has been shown to block the growth of colorectal cancer cells in a cell-based assay.

In addition to its potential as a drug target, TUT4 may also have potential as a biomarker for colorectal cancer. Studies have shown that TUT4 is overexpressed in various types of cancer, including colorectal cancer. especially if there is a lack of other biomarkers.

Conclusion

TUT4 is a protein that has been identified as a potential drug target and biomarker for colorectal cancer. Its ability to interact with key molecules involved in cancer progression, including the TGF-β pathway, NF-kappa-B signaling pathway, and the PI3K/Akt signaling pathway, making it an attractive target for cancer treatment. Additionally, TUT4 has been shown to be overexpressed in various types of cancer, including colorectal cancer, which may serve as a potential biomarker for this disease. Further research is needed to understand the full potential of TUT4 as a drug target and biomarker for colorectal cancer.

Protein Name: Terminal Uridylyl Transferase 4

Functions: Uridylyltransferase that mediates the terminal uridylation of mRNAs with short (less than 25 nucleotides) poly(A) tails, hence facilitating global mRNA decay (PubMed:25480299, PubMed:31036859). Essential for both oocyte maturation and fertility. Through 3' terminal uridylation of mRNA, sculpts, with TUT7, the maternal transcriptome by eliminating transcripts during oocyte growth (By similarity). Involved in microRNA (miRNA)-induced gene silencing through uridylation of deadenylated miRNA targets. Also functions as an integral regulator of microRNA biogenesis using 3 different uridylation mechanisms (PubMed:25979828). Acts as a suppressor of miRNA biogenesis by mediating the terminal uridylation of some miRNA precursors, including that of let-7 (pre-let-7), miR107, miR-143 and miR-200c. Uridylated miRNAs are not processed by Dicer and undergo degradation. Degradation of pre-let-7 contributes to the maintenance of embryonic stem (ES) cell pluripotency (By similarity). Also catalyzes the 3' uridylation of miR-26A, a miRNA that targets IL6 transcript. This abrogates the silencing of IL6 transcript, hence promoting cytokine expression (PubMed:19703396). In the absence of LIN28A, TUT7 and TUT4 monouridylate group II pre-miRNAs, which includes most of pre-let7 members, that shapes an optimal 3' end overhang for efficient processing (PubMed:25979828). Adds oligo-U tails to truncated pre-miRNAS with a 5' overhang which may promote rapid degradation of non-functional pre-miRNA species (PubMed:25979828). May also suppress Toll-like receptor-induced NF-kappa-B activation via binding to T2BP (PubMed:16643855). Does not play a role in replication-dependent histone mRNA degradation (PubMed:18172165). Due to functional redundancy between TUT4 and TUT7, the identification of the specific role of each of these proteins is difficult (PubMed:25979828, PubMed:25480299, PubMed:16643855, PubMed:19703396, PubMed:18172165) (By similarity). TUT4 and TUT7 restrict retrotransposition of long interspersed element-1 (LINE-1) in cooperation with MOV10 counteracting the RNA chaperonne activity of L1RE1. TUT7 uridylates LINE-1 mRNAs in the cytoplasm which inhibits initiation of reverse transcription once in the nucleus, whereas uridylation by TUT4 destabilizes mRNAs in cytoplasmic ribonucleoprotein granules (PubMed:30122351)

The "TUT4 Target / Biomarker Review Report" is a customizable review of hundreds up to thousends of related scientific research literature by AI technology, covering specific information about TUT4 comprehensively, including but not limited to:
•   general information;
•   protein structure and compound binding;
•   protein biological mechanisms;
•   its importance;
•   the target screening and validation;
•   expression level;
•   disease relevance;
•   drug resistance;
•   related combination drugs;
•   pharmacochemistry experiments;
•   related patent analysis;
•   advantages and risks of development, etc.
The report is helpful for project application, drug molecule design, research progress updates, publication of research papers, patent applications, etc. If you are interested to get a full version of this report, please feel free to contact us at BD@silexon.ai

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