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Basic Information

Classification Information

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

Cancer&Entry Information

Cancer Name	ovarian cancer
ICD-0-3	C56.9
Methods	qPCR, Western blot, RNAi, RIP, other
Sample	ovarian cancer tissues and cell lines (SKOV3, HO-8910, HO-8910PM, A2780) and cisplatin-resistant cell line (A2780/DDP)
Expression Pattern	up-regulated
Function Description	Our data showed that among the drugs commonly used in ovarian cancer therapy, cisplatin induces higher levels of PANDAR compared with doxorubicin and paclitaxel. We also proved that PANDAR exhibited higher expression in cisplatin-resistant ovarian cancer tissues and cells, compared with cisplatin-sensitive ones, and this expression pattern depends on wild-type p53 (wt-p53), not mutant-p53 (mt-p53). In vitro and in vivo, PANDAR overexpression improved cell survival rate and tumor growth in response to cisplatin, while depletion of PANDAR leads to a reduced tumor growth. Further investigation revealed that PANDAR-reduced cisplatin sensitivity was likely or partly due to the PANDAR-binding protein SFRS2 (arginine/serine-rich 2), a splicing factor with the ability to negative regulate p53 and its phosphorylation at Serine 15 (Ser15). This feedback regulation of PANDAR-SFRS2-p53 leads to a reduced transactivation of p53-related pro-apoptotic genes, such as PUMA (p53-upregulated modulator of apoptosis).
Pubmed ID	30375398
Year	2018
Title	The Cisplatin-Induced lncRNA PANDAR Dictates the Chemoresistance of Ovarian Cancer via Regulating SFRS2-mediated p53 Phosphorylation

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