Search Result

Basic Information

Classification Information

Regulatory Mechanism		Biological Function		Clinical Application
TF		Immune		Survival
Enhancer		Apoptosis	apoptosis	Drug
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, in vitro knockdown, etc.
Sample	Human breast cancer cell line MDA-MB-231 and breast cell line MCF7
Expression Pattern	down-regulated
Function Description	Ectopic overexpression of MEG3 using a lentiviral vector Lv MEG3 significantly inhibited breast cancer cell growth in vitro and a cancer xenograft growth in vivo. MEG3 overexpression led to marked increase of apoptosis in breast cancer cells as determined using flow cytometry and fragmented DNA labeling. Moreover, ectopic expression of MEG3 increased the expression of endoplasmic reticulum (ER) stress related proteins required for unfolded protein response, including glucose regulated protein 78 (GRP78), inositol requiring enzyme 1 (IRE1), protein kinase RNA (PKR) like ER kinase (PERK), and activated transcription factor 6 (ATF6), as well as proapoptotic proteins CCAAT/enhancer binding protein homologous protein (CHOP) and caspase 3. Finally, MEG3 overexpression markedly increased nuclear factor ?B (NF ?B) expression, NF ?B translocation to the nucleus, and p53 expression, whereas pharmacological inhibition of NF ?B completely abolished MEG3 induced activation of p53.
Pubmed ID	30556250
Year	2018
Title	Long Noncoding RNA MEG3 Inhibits Breast Cancer Growth via Upregulating Endoplasmic Reticulum Stress and Activating NF-?B and p53

External Links