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Basic Information

Classification Information

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

Cancer&Entry Information

Cancer Name	prostate cancer
ICD-0-3	C61.9
Methods	qRT-PCR, Western blot, Luciferase reporter assay, in vitro knockdown
Sample	prostate cancer cell lines (LNCaP and 22Rv1), Human umbilical vein endothelial cells (HuVECs)
Expression Pattern	up-regulated
Function Description	knockdown of PCAT3 and PCAT9 suppressed cellular proliferation, invasion, migration, angiogenesis and stemness in androgen-dependent LNCaP and 22Rv1 cells. both PCAT3 and PCAT9 transcripts had two conserved binding sties for miR-203. Meanwhile, dual luciferase report assays revealed that miR-203 could suppress the luciferase activities of reporter plasmids carrying the binding site of miR-203 on the mRNA of PCAT3 or PCAT9. Quantitative RT-PCR (qRT-PCR) and RNA fluorescence in situ hybridization (RNA-FISH) showed that miR-203 mimic reduced the expression of PCAT3 and PCAT9 both in LNCaP and 22Rv1 cells. We also noted that both PCAT3 and PCAT9 inhibited miR-203 expression and alleviated repression on the expression of SNAI2, a critical regulator of epithelial-mesenchymal transition directly targeted by miR-203.
Pubmed ID	29552304
Year	2018
Title	The PCAT3/PCAT9-miR-203-SNAI2 axis functions as a key mediator for prostate tumor growth and progression.

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