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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	non small cell lung cancer
ICD-0-3	C34
Methods	qPCR, RNAi, Western blot, Luciferase reporter assay etc.
Sample	non small cell lung cancer tissues, cell line (A549, H1975, H460 and H292)
Expression Pattern	up-regulated
Function Description	We demonstrated via real-time polymerase chain reaction that NEAT1 was significantly increased in NSCLC tissues and cell lines, suggesting a potential role of NEAT1 in NSCLC. CCK-8 assay and colony-formation assays showed that silencing of NEAT1 by siRNA pool inhibited NSCLC cell proliferation. An increased population of apoptotic cells was detected upon NEAT1 depletion by acridine orange/ethidium bromide staining compared to control cells. A549 cells depleted of NEAT1 exhibited reduced invasion and migration, characterized by wound healing assay and Transwell assay. To uncover the molecular mechanism of NEAT1 in lung cancer, we identified that NEAT1 could be a competing endogenous RNA against let-7a, and insulin-like growth factor (IGF)-2 could be a direct target of let-7a. These were characterized by reciprocal expression between NEAT1/IGF-2 and let-7a. Luciferase reporter assay validated direct binding of NEAT1/let-7a and let-7a/IGF-2. Exogenous IGF-2 expression reversed NEAT1-knockdown-induced growth inhibition assessed by CCK-8 assay and colony-formation assay.
Pubmed ID	29864936
Year	2018
Title	lncRNA NEAT1 competes against let-7a to contribute to non-small cell lung cancer proliferation and metastasis.

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