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Basic Information

Classification Information

Regulatory Mechanism		Biological Function		Clinical Application
TF		Immune		Survival
Enhancer		Apoptosis	apoptosis	Drug	Trastuzumab
Variant		Cell Growth		Circulating
MiRNA		EMT		Metastasis
Methylation		Coding Ability		Recurrence

Cancer&Entry Information

Cancer Name	breast Cancer
ICD-0-3	C50
Methods	qPCR, Western blot, Luciferase reporter assay, in vitro knockdown, RIP, etc.
Sample	primary cancer tissues, human HER-2+ breast cancer cell lines SKBR-3, BT474 and human normal breast epithelial cell line MCF-10A
Expression Pattern	up-regulated
Function Description	An increase in both, IC50 value of trastuzumab and EMT was observed in the established trastuzumab-resistant cell lines. The expression level of TINCR was significantly increased in trastuzumab-resistant cells when compared with sensitive cells. Knockdown of TINCR reversed the trastuzumab resistance and the acquired EMT in these cells. TINCR was detected in the cytoplasm of breast cancer cells and could spongemiR-125b, thereby releasing HER-2 and inducing trastuzumab resistance. In addition, Snail-1 was found to be the target gene of miR-125b and overexpression of Snail-1 could reverse the suppressed migration, invasion, and EMT caused by TINCR silencing. The upregulation of TINCR in breast cancer was attributed to the CREB-binding protein (CBP)-mediated H3K27 acetylation at the promoter region of TINCR. Clinically, HER-2 + breast cancer patients with high TINCR expression levels were associated with poor response to trastuzumab therapy and shorter survival time.
Pubmed ID	30621694
Year	2019
Title	Activation of LncRNA TINCR by H3K27 acetylation promotes Trastuzumab resistance and epithelial-mesenchymal transition by targeting MicroRNA-125b in breast Cancer.

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