Long noncoding RNA LINC00511 regulates the proliferation, apoptosis, invasion and autophagy of trophoblast cells to mediate pre‐eclampsia progression through modulating the miR‐31‐5p/homeobox protein A7 axis.

Aim: Pre‐eclampsia (PE) is the usual complication during pregnancy. Long noncoding RNAs are essential regulatory factors in many diseases. Nevertheless, the role of LINC00511 in the development of PE has not been fully elucidated. Methods: The expression of LINC00511, homeobox protein A7 (HOXA7) and miR‐31‐5p was determined by quantitative real‐time polymerase chain reaction. The levels of HOXA7 protein and autophagy‐related proteins were measured by western blot analysis. Besides, cell proliferation was evaluated using cell counting kit 8 and colony formation assays. The apoptosis and invasion of cells were detected via flow cytometry and transwell assay, respectively. Further, the interaction between miR‐31‐5p and LINC00511 or HOXA7 was confirmed by dual‐luciferase reporter assay. Results: The LINC00511 and HOXA7 expression levels were decreased in placental tissues of PE patients, and the expression levels of both were positively correlated. LINC00511 knockdown suppressed proliferation, invasion and autophagy, while enhanced apoptosis in trophoblast cells. Meanwhile, the elevated HOXA7 expression promoted proliferation, invasion, autophagy, and inhibited the apoptosis of trophoblast cells. Besides, overexpression of HOXA7 also could reverse the effect of LINC00511 knockdown on the biological function of trophoblast cells. Further experiments confirmed that miR‐31‐5p could be sponged by LINC00511 and could target HOXA7. Also, miR‐31‐5p mimic could invert the promoting effect of LINC00511 overexpression on the biological function of trophoblast cells. Conclusion: LINC00511 expression was crucial for maintaining the normal function of trophoblast cells, and the decreased its expression might promote the progress of PE, which might provide some theoretical strategies for reducing the development of PE. [ABSTRACT FROM AUTHOR]