Abstract
STOX1 is a transcription factor that is implicated in the high prevalence of human gestational diseases. It has been studied in various types of gestational diseases using different molecular and cellular biological technologies. However, the effect and detailed mechanism of storkhead box 1 (STOX1) in recurrent spontaneous abortion (RSA) remain unknown. This study aimed to explore the effect and detailed mechanism of STOX1 in human trophoblast cells. The result showed that downregulation of STOX1 by short hairpin RNA (shRNA) led to a decrease in proliferation and migration in HTR‐8/SVneo cells, while it induced the apoptosis of HTR‐8/SVneo cells. Moreover, the result showed that trophoblast cells expressed lower levels of pAKT and p85 subunits after treatment with STOX1 shRNA when compared with control. However, overexpression of STOX1 obviously increased the pAKT and p85 protein expressions. Transfection of pcDNA‐AKT plasmid increased cell proliferation and migration in HTR‐8/SVneo cells while suppressed the apoptosis of HTR‐8/SVneo cells. Furthermore, inhibition of the PI3K/Akt pathway by a specific inhibitor promoted cell apoptosis and aggravatedly suppressed cell proliferation and migration of HTR‐8/SVneo cells. On the other hand, upregulation of the PI3K/Akt pathway could increase the relative expression level of Bcl‐2 and decrease the relative expression levels of Bax and Bim, while inhibition of the PI3K/Akt pathway led to adverse results. Our results demonstrated that inhibition of STOX1 could suppress trophoblast cell proliferation and migration, while promote apoptosis through inhibiting the PI3K/Akt signaling pathway. These findings might provide a new fundamental mechanism for regulating RSA and could be used to prevent and treat RSA in clinic.
Highlights
Recurrent spontaneous abortion (RSA), an important factor affecting human reproduction, leads to various complications and even infertility, which seriously threatens women’s health around the world.[1]
storkhead box 1 (STOX1) is a transcription factor belonging to the forkhead family that is involved in diverse human gestational diseases.[19,20]
The result revealed that STOX1 knockdown could inhibit the proliferation of the cell in a time‐dependent manner, which was in accordance with the previous results
Summary
Recurrent spontaneous abortion (RSA), an important factor affecting human reproduction, leads to various complications and even infertility, which seriously threatens women’s health around the world.[1] The American Society of Reproductive Medicine defines two or more failed clinical pregnancies as RSA. A previous study revealed that overexpression of the transcription factor STOX1 could promote the proliferation of the inner ear epithelial cells via the AKT pathway.[16] HAM‐1, a homologous to STOX1 in nonmammals, has been reported to prevent neurons undergoing apoptosis and regulate the survival and fate of neural precursors cell.[17] In addition, Doridot et al[18] posit STOX1 as a genetic switch in the ROS/RNS balance of trophoblastic cell in pre‐eclampsia. Found a probable mechanism of recurrent spontaneous abortion and might provide a new method for preventing and treating RSA in clinic
Sign-in/Register to view highlights & summary Sign-in/Register to access full text options 
Talk to us
Join us for a 30 min session where you can share your feedback and ask us any queries you have
Schedule a callDisclaimer: All third-party content on this website/platform is and will remain the property of their respective owners and is provided on "as is" basis without any warranties, express or implied. Use of third-party content does not indicate any affiliation, sponsorship with or endorsement by them. Any references to third-party content is to identify the corresponding services and shall be considered fair use under The CopyrightLaw.
