Mechanistic study of Bushen Antai formula regulating biological effects of trophoblast cells via the LncRNA-MALAT1/miR-200C-3p/SOCS3 signaling axis
Abstract
Objectives This study aimed to investigate the mechanisms by which the Bushen Antai Formula regulates the biological effects of trophoblast cells through the LncRNA-MALAT1/miR-200c-3p/SOCS3 Signaling Axis. Methods This study utilized RNA-FISH to localize LncRNA-MALAT1 in HTR-8/SVneo trophoblasts. CRISPR-based overexpression/knockdown vectors were used to assess MALAT1's role in regulating proliferation, migration, invasion, and the cell cycle. Western blotting analyzed MALAT1's impact on miR-200c-3p, SOCS3, and Caspase-3 expression. Dual-luciferase reporter assays confirmed direct interactions between MALAT1 and miR-200c-3p, as well as between miR-200c-3p and SOCS3, revealing how the Bushen Antai Formula modulates trophoblast biology via this axis. Results LncRNA-MALAT1, localized in the cytoplasm of HTR-8/Svneo cells, regulates vital cellular processes. Silencing it decreases cell viability, hampers migration, and triggers G0/G1 cell cycle arrest. RT-qPCR confirms reduced miR-200c-3p and elevated SOCS3 and Caspase-3 upon MALAT1 knockdown. Luciferase assays validate the MALAT1-miR-200c-3p-SOCS3 axis. CCK-8 and Transwell tests demonstrate MALAT1's role in suppressing cell proliferation and invasion by targeting miR-200c-3p. Flow cytometry revealed that the combination of LncRNA-MALAT1 knockdown and miR-200c-3p silencing inhibited the cell cycle in both the G0/G1 and S phases. Furthermore, Western blot analyses reveal that MALAT1, by targeting miR-200c-3p, promotes the expression of SOCS3, Caspase-3, and β-catenin. Bushen Antai formula potently inhibits HTR-8/Svneo proliferation and invasion, with additional these processes via the MALAT1-miR-200c-3p axis. It also significantly increases S-phase cell cycle arrest and upregulates SOCS3, Caspase-3, and β-catenin, primarily through modulating the MALAT1-miR-200c-3p interaction. Conclusions The upregulation of LncRNA-MALAT1 in HTR-8/SVneo trophoblast cells is associated with increased cellular proliferation and invasive capacity. Functionally, Bushen Antai Formula modulates these proliferative and invasive phenotypes by targeting the LncRNA-MALAT1/miR-200c-3p/SOCS3 regulatory network. These findings position this regulatory pathway as a promising therapeutic target for managing pregnancy-related complications.
Fields of Study & Subjects
Cancer-related molecular mechanisms research
Reproductive System and Pregnancy
Pregnancy and preeclampsia studies
Publication details
- Journal / source
- Journal of Radiation Research and Applied Sciences
- Volume
- 19
- Issue
- 1
- Pages
- 102221–102221
- Publication date
- 1 March 2026
- Language
- EN