tsRNADisease

Entry Detail

General Information

Database ID:	TRD01882
Confidence:	Very High
Contents:	>> tsRNA Information >> tsRNA Association Statistics >> Disease Information >> Disease Association Statistics >> Evidence Support >> Reference

tsRNA Information

tsRNA Name:

3′tRF-AlaAGC

tsRNA Type:

tRF-3

Amino acid and Anticodon:

AlaAGC

Sequence:

N/A

Related Target:

Predicted Target:

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

	MeSH	Disease Ontology
Disease ID:	D001943	DOID:1612
Disease Name:	Breast Neoplasms	breast cancer
Category:	MeSH	Disease Ontology
Type:	Neoplasms//Skin and Connective Tissue Diseases	disease of anatomical entity//disease of cellular proliferation
Define:	Tumors or cancer of the human BREAST.	A thoracic cancer that originates in the mammary gland.
Alias:	Breast Cancer//Breast Carcinoma//Breast Tumors//Cancer of Breast//Cancer of the Breast//Human Mammary Carcinoma//Malignant Neoplasm of Breast//Malignant Tumor of Breast//Mammary Cancer//Mammary Carcinoma, Human//Mammary Neoplasm, Human//Mammary Neoplasms, Human//Neoplasms, Breast//Tumors, Breast	breast tumor//malignant neoplasm of breast//malignant tumor of the breast//mammary cancer//mammary neoplasm//mammary tumor//primary breast cancer

Disease Association Statistics

Total Associated tsRNA Number:	549 More Information
Network: (Display the first 15 nodes)

Evidence Support

Strong Evidence:	PCR//Western blot//FISH//Cell apoptosis assay//Luciferase reporter assay//Cell proliferation assay//Transwell assay//RIP
Weak Evidence:	Sequencing

Reference

[1] PubMed ID:	39080676
Disease Name:	Breast Neoplasms
Tissue:	Breast
Dysfunction Pattern:	Up-Regulation
Validated Method:	PCR//Western blot//FISH//Cell apoptosis assay//Luciferase reporter assay//Cell proliferation assay//Transwell assay//RIP//Sequencing
Description:	A 3′tRF fragment of 3′tRF-AlaAGC was screened, which is significantly overexpressed in BC specimens and Adriamycin-resistant cells. 3′tRF-AlaAGC could promote cell malignant activity and facilitate M2 polarization of macrophages in vitro and in vivo. Higher expression of M2 macrophages were more likely to have lymph node metastasis and deeper invasion in BC patients.
Comparision:	Cancer VS Normal
Mechanism:	Mechanistically, 3′tRF-AlaAGC binds Type 1-associated death domain protein (TRADD) in BC cells, and suppression of TRADD partially abolished the enhanced effect of 3′tRF-AlaAGC mimic on phenotype of M2. The NF-κb signaling pathway was activated in BC cells co-cultured with M2 macrophages transfected with 3′tRF-AlaAGC mimic.