Entry Detail



General Information

Database ID:TRD00037
Confidence:Very High
Contents:>> tsRNA Information
>> tsRNA Association Statistics
>> Disease Information
>> Disease Association Statistics
>> Evidence Support
>> Reference



tsRNA Information

tsRNA Name:m7G-3' tiRNA LysTTT
tsRNA Type:3'-tiRNA
Amino acid and Anticodon:LysTTT
Sequence:N/A
Related Target:ANXA2
Predicted Target:N/A
External Links:
MINTbase ID:N/A
tRFdb ID:N/A



tsRNA Association Statistics

Total Associated Disease Number:1
More Information
Network:
(Display the first 15 nodes)



Disease Information

 MeSHDisease Ontology
Disease ID:D001749DOID:11054
Disease Name:Bladder Cancerurinary bladder cancer
Category:MeSHDisease Ontology
Type:Neoplasms//Urogenital Diseasesdisease of anatomical entity//disease of cellular proliferation
Define:Tumors or cancer of the URINARY BLADDER.An urinary system cancer that results_in malignant growth located_in the urinary bladder.
Alias:Bladder Cancer//Bladder Neoplasms//Bladder Tumors//Cancer of Bladder//Cancer of the Bladder//Malignant Tumor of Urinary Bladder//Neoplasms, Bladder//Urinary Bladder Cancerbladder cancer//tumor of the bladder



Disease Association Statistics

Total Associated tsRNA Number:1
More Information
Network:
(Display the first 15 nodes)



Evidence Support

Strong Evidence:RT-PCR//Northern blot//Western blot//RNA Pulldown
Weak Evidence:High-throughput sequencing



Reference

[1] PubMed ID:38894581
Disease Name:Bladder Cancer
Tissue:Bladder
Dysfunction Pattern:N/A
Validated Method:RT-PCR//Northern blot//Western blot//RNA Pulldown//High-throughput sequencing
Description:Currently, the functional role of m7G‐modified tsRNAs in tumors is unknown. In the present study, we identified mtiRL as a novel m7G‐modified tsRNA in transformed urothelial and BC cells for the first time and found that mtiRL was highly expressed in BC and involved in BC malignancy.
Comparision:Disease VS Control
Mechanism:Our in vitro and in vivo assays further indicated that mtiRL promotes BC growth. To probe the underlying mechanism, we performed a series of experiments and found that mtiRL specifically interacts with ANXA2 and increases the expression of p‐ANXA2‐Y24, but not total ANXA2. We further showed that mtiRL can enhance the binding between ANXA2 and Yes1, which phosphorylates ANXA2 at Tyr24. Collectively, these results describe the functional roles and regulatory mechanism of mtRL, which has an oncogenic role in BC.