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OBJECTIVE To detect the differentially expressed long non-coding RNA (lncRNA) EGFR-AS1 in the placenta tissues of preeclampsia (PE) patients and normal pregnancies. We also investigated the underlying mechanism of EGFR-AS1 in regulating PE development. PATIENTS AND METHODS 21 PE patients and 21 normal pregnancies admitted in our hospital were selected. The expression of EGFR Antisense RNA1 (EGFR-AS1) in the placenta tissues of PE patients and normal pregnancies was detected by quantitative reverse transcriptase-polymerase chain reaction (qRT-PCR). The regulatory effect of EGFR-AS1 on proliferation of HTR-8 cells was observed by Cell Counting Kit-8 (CCK-8) assay and colony formation assay. Cell cycle and apoptosis of HTR-8 cells after overexpression or knockdown of EGFR-AS1 were detected by flow cytometry. The expression changes of EGFR and proteins related to JAK/STAT signaling pathway after knockdown of EGFR-AS1 in HTR-8 cells were detected by Western blot. Rescue experiments were carried out after upregulating EGFR expression in HTR-8 cells. RESULTS QRT-PCR results showed that the mRNA expression of EGFR-AS1 in PE patients was lower than that in normal pregnancies. CCK-8 assay and colony formation assay showed that knockdown of EGFR-AS1 in HTR-8 cells inhibited cell proliferation. Flow cytometry results showed that knockdown of EGFR-AS1 blocked the cell cycle of HTR-8 cells. Overexpression of EGFR-AS1 obtained opposite results. Western blot results showed that the protein expressions of EGFR, p-JAK and p-STAT were decreased after knockdown of EGFR-AS1. Alterations in protein expressions of p-JAK and p-STAT, and proliferative ability of HTR-8 cells induced by EGFR-AS1 knockdown could be rescued after upregulation of EGFR. CONCLUSIONS The expression of lncRNA EGFR-AS1 is decreased in PE patients, which can promote the progression of preeclampsia by inhibiting EGFR-JAK/STAT signaling pathway.