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DOI 10.1080/01443615.2023.2211681

Медицинская библиотека · Journal of obstetrics and gynaecology : the journal of the Institute of Obstetrics and Gynaecology · 2023

YKL-40 promotes proliferation and invasion of HTR-8/SVneo cells by activating akt/MMP9 signalling in placenta accreta spectrum disorders.

Liu Weifang, Wang Runfang, Liu Suxin, Yin Xiaoqian, Huo Yan, Zhang Ruiling, Li Jia

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Аннотация

YKL-40 is a secreted glycoprotein that can promote invasion, angiogenesis and inhibit apoptosis, and was highly expressed in a variety of tumours. In this paper, we investigated the impacts of YKL-40 on proliferation and invasion in HTR-8/SVneo cells during placenta accreta spectrum disorders (PAS) development. The levels of YKL-40 protein in late-pregnant placental tissue were detected using immunohistochemistry and Western blotting, and gene expression using reverse transcription-quantitative polymerase chain reaction (RT-qPCR). The proliferation, migration, invasion and apoptosis abilities of HTR-8/SVneo cells were detected by cell counting kit-8 (CCK-8), Transwell, scratch assay, and flow cytometry, respectively. Our current results showed that YKL-40 was significantly increased in the PAS group compared to the normal control group (P < 0.01). Biological function experiments showed that YKL-40 significantly promoted the proliferation, migration and invasion of HTR-8/SVneo cells, and inhibited cell apoptosis. Knockdown of YKL-40 inhibited the activation of Akt/MMP9 signalling in trophoblast cells. These data suggested that YKL-40 might be involved in the progression of PAS, which may be attributed to the regulation of Akt/MMP9 signalling pathway.

Для цитирования: Liu Weifang, Wang Runfang, Liu Suxin, Yin Xiaoqian, Huo Yan, Zhang Ruiling, Li Jia. YKL-40 promotes proliferation and invasion of HTR-8/SVneo cells by activating akt/MMP9 signalling in placenta accreta spectrum disorders.. Journal of obstetrics and gynaecology : the journal of the Institute of Obstetrics and Gynaecology. 2023. DOI: 10.1080/01443615.2023.2211681.

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