ATL1 inhibits the proliferation and invasion of trophoblast cells via inhibition of the mTOR signaling pathway

Pre‐eclampsia (PE) is a major cause of hypertension in maternal and fetal. Atlastin‐1 (ATL1), one regulator of endoplasmic reticulum (ER) morphology, participates in tubular ER formation and protein synthesis. The objective of this study is to investigate the role and molecular mechanism of ATL1 in...

Full description

Saved in:
Bibliographic Details
Published in:Journal of biochemical and molecular toxicology 2023-01, Vol.37 (1), p.e23237-n/a
Main Authors: Zhang, Guanli, Feng, Yan, Wang, Min, Liu, Xin
Format: Article
Language:English
Subjects:
Cell migration
Cell Movement
Cell proliferation
Cell Proliferation - physiology
Cell viability
Eclampsia
Endoplasmic reticulum
Female
Fetuses
Humans
Hypertension
invasion
migration
mTOR pathway
Placenta - metabolism
Preeclampsia
Pregnancy
pre‐eclampsia
proliferation
Protein biosynthesis
Protein synthesis
Rapamycin
Signal Transduction
Signaling
TOR protein
TOR Serine-Threonine Kinases - metabolism
Trophoblasts - metabolism
Citations: Items that this one cites
Items that cite this one
Online Access:Get full text
Tags: Add Tag
No Tags, Be the first to tag this record!
Description
Summary:Pre‐eclampsia (PE) is a major cause of hypertension in maternal and fetal. Atlastin‐1 (ATL1), one regulator of endoplasmic reticulum (ER) morphology, participates in tubular ER formation and protein synthesis. The objective of this study is to investigate the role and molecular mechanism of ATL1 in PE. GEO databases showed that ATL1 was upregulated in PE patients. Our data also found that ATL1 was highly expressed in PE placental tissues. The cell viability, proliferation, migration, and invasion of HTR‐8/SVneo cells increased/decreased after the downregulation/upregulation of ATL1. The mTOR pathway is the downstream pathway of ATL1. The levels of p‐p70S6K and p‐mTOR were increased/decreased after the downregulation/upregulation of ATL1. Moreover, rapamycin, an inhibitor of mTOR pathway, reversed the promotive effect of siATL1 on proliferation, migration, and invasion in HTR‐8/SVneo cells. In conclusion, ATL1 inhibits the proliferation and invasion of trophoblast cells via the inhibition of the mTOR signaling pathway in HTR‐8/SVneo cells.
ISSN:1095-6670
1099-0461
DOI:10.1002/jbt.23237