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Long non-coding RNA DIRC3 suppresses trophoblast invasion in preeclampsia via upregulating HOXD10

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Abstract

Background

Preeclampsia (PE) is a common and potentially serious pregnancy-related complication that contributes to morbidity and mortality of both mother and fetus. In this study, the association between long non-coding RNA (lncRNA) DIRC3 and the regulation of trophoblast invasion was analyzed.

Objective

This study aimed to identify gene modules associated with trophoblast invasion in the pathogenesis of PE.

Results

After the generation of weighted gene co-expression network analysis (WGCNA)-based modules, the green module was found to be most significantly correlated with PE. The Kyoto Encyclopedia of Genes and Genomes (KEGG) pathway enrichment analysis revealed that PE-associated hub genes were enriched in the T cell activation and antigen processing and presentation pathways. Compared with HTR-8 cells, lower expression levels of DIRC3 and HOXD10 were found in JEG-3 cells, and HOXD10 overexpression could reverse the accelerated proliferation and invasion of HTR-8 cells observed following DIRC3 downregulation.

Conclusion

The results suggested that DIRC3 could suppress PE progression by promoting HOXD10 expression.

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Authors and Affiliations

Authors

Contributions

JZ and ZZ designed the research plan. JZ, ZZ, and XW performed the experiments. JZ and ZZ drafted the manuscript.

Corresponding author

Correspondence to Zhendong Zhang.

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Conflict of interest

Jing Zhang declares that he/she has no conflict of interest. Zhendong Zhang declares that he/she has no conflict of interest. Xiaofeng Wu declares that he/she has no conflict of interest.

Ethical approval

This article does not contain any studies with human participants or animals performed by any of the authors.

Supplementary Information

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Supplementary file1 (XLSX 98 KB) Genes in each module

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Zhang, J., Zhang, Z. & Wu, X. Long non-coding RNA DIRC3 suppresses trophoblast invasion in preeclampsia via upregulating HOXD10. Mol. Cell. Toxicol. 19, 703–712 (2023). https://doi.org/10.1007/s13273-022-00297-z

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  • DOI: https://doi.org/10.1007/s13273-022-00297-z

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