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

Journal of biochemical and molecular toxicology (2022-10-05)
Guanli Zhang, Yan Feng, Min Wang, Xin Liu
RESUMEN

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.

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Sigma-Aldrich
Anti-phospho-p70 S6 Kinase (pThr389/412) antibody produced in rabbit, affinity isolated antibody
Sigma-Aldrich
Anti-ATL1 antibody produced in rabbit, Prestige Antibodies® Powered by Atlas Antibodies, affinity isolated antibody, buffered aqueous glycerol solution
Sigma-Aldrich
Anti-P70S6K/RPS6KB1 antibody produced in goat, affinity isolated antibody, buffered aqueous solution