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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	pancreatic ductal adenocarcinoma
ICD-0-3	C25.3
Methods	qPCR, Western blot, Luciferase reporter assay, RIP
Sample	pancreatic cancer cell lines MIA PaCa-2 and BxPC-3, pancreatic tumor, normal pancreatic tissue, pancreatic tumor, normal pancreatic tissue
Expression Pattern	up-regulated
Function Description	We first show that LINC00346 is highly expressed in pancreatic tumor specimens as compared to normal pancreatic tissue based on interrogation of The Cancer Genome Atlas (TCGA) pancreatic adenocarcinoma dataset. Of significance, this upregulation of LINC00346 is associated with overall survival (OS) and disease-free survival (DFS), respectively. We further show that knockout (KO) of LINC00346 impairs pancreatic cancer cell proliferation, tumorigenesis, migration, and invasion ability. Importantly, these phenotypes can be restored by LINC00346 re-expression in KO cells (i.e., rescue experiment). RNA precipitation assays combined with mass spectrometry analysis indicate that LINC00346 interacts with CCCTC-binding factor (CTCF), a known transcriptional repressor of c-Myc. This interaction between LINC00346 and CTCF prevents the binding of CTCF to c-Myc promoter, relieving the CTCF-mediated repression of c-Myc.
Pubmed ID	31391552
Year	2019
Title	LINC00346 promotes pancreatic cancer progression through the CTCF-mediated Myc transcription

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