A preliminary study on abnormal expression of long noncoding RNA CTD-2012K14.6 in placentas and its role in inducing macrosomia
10.3760/cma.j.issn.1000-6699.2019.02.009
- VernacularTitle:胎盘长链非编码RNA CTD-2012K14.6异常表达致胎儿巨大的初步功能研究
- Author:
Linping YAN
1
;
Lan WU
;
Tianying ZHONG
;
Lan LIU
Author Information
1. 南京
- Keywords:
Gestational diabetes mellitus;
Macrosomia;
Long noncoding RNA CTD-2012K14. 6;
CCCTC-binding factor;
Insulin-like growth factor 2
- From:
Chinese Journal of Endocrinology and Metabolism
2019;35(2):138-142
- CountryChina
- Language:Chinese
-
Abstract:
Objective To explore the role of long noncoding RNA ( lncRNA) CTD-2012K14. 6 in the development of gestational diabetes mellitus (GDM) related macrosomia. Methods The quantitative real-time PCR ( qRT-PCR) was performed to measure the expression of CTD-2012K14.6 in placentas of women with or without GDM, and the quantity of CTD-2012K14. 6 expression and its association with fetal weights were analyzed; Bioinformatic analysis was performed to predict the downstream molecules. CTD-2012K14. 6 over-expressing lentiviral and siRNA was constructed in human trophoblastic cell line HTR-8/SVneo cells, qRT-PCR and Western blot (WB) were used to invest its effect in modulating the expression of downstream molecules. Results The expression of CTD-2012K14.6 in GDM placentas was significantly higher than that in normal controls (1.70 ± 0.63 vs 1.00 ± 0.56,t=3.68,P＜0.01), and positively correlated with fetal weight (r=0.8501, P＜0.01); on-line analysis showed that CTD-2012K14.6 was located at chr16:67,549,214-67,563,958, which was located in the intron of CCCTC-binding factor( CTCF); Up-regulating CTD-2012K14.6 could significantly reduce the expression of CTCF mRNA and protein, and increase the expression of insulin-like growth factor-Ⅱ( IGF-Ⅱ) mRNA and protein, while down-regulating CTD-2012K14.6 could significantly increase the expression of CTCF mRNA and protein, and reduce the expression of IGF-ⅡmRNA and protein. Conclusion The CTD-2012K14. 6 may play an important role in the pathogenesis of GDM related macrosomia by upregulating the expression of CTCF and IGF-Ⅱ.
