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SOX2-OT induced by PAI-1 promotes triple-negative breast cancer cells metastasis by sponging miR-942-5p and activating PI3K/Akt signaling

Triple-negative breast cancer (TNBC) has an aggressive biological behavior and poor outcome. Our published study showed that PAI-1 could induce the migration and metastasis of TNBC cells. However, the underlying mechanism by which PAI-1 regulates TNBC metastasis has not been addressed. Here, we demonstrated that PAI-1 is high expressed in TNBC and promotes TNBC cells tumorigenesis. Using microarray analysis of lncRNA expression profiles, we identified a lncRNA SOX2-OT, which is induced by PAI-1 and could function as an oncogenic lncRNA in TNBC. Mechanistic analysis demonstrated that SOX2-OT acts as a molecular sponge for miR-942-5p to regulate the expression of PIK3CA, ultimately leading to activating PI3K/Akt signaling pathway and promoting TNBC metastasis. Taken together, our findings suggest that SOX2-OT regulates PAI-1-induced TNBC cell metastasis through miR-942-5p/PIK3CA signaling and illustrate the great potential of developing new SOX2-OT-targeting therapy for TNBC patients.

 

Comments:

Your published study highlights the role of plasminogen activator inhibitor-1 (PAI-1) in triple-negative breast cancer (TNBC) metastasis and identifies a specific long non-coding RNA (lncRNA), SOX2-OT, as a mediator of this process. The study provides insights into the underlying mechanism by which PAI-1 regulates TNBC metastasis.

The research demonstrates that PAI-1 is highly expressed in TNBC and promotes tumorigenesis in TNBC cells. By conducting microarray analysis of lncRNA expression profiles, the study identifies SOX2-OT as an oncogenic lncRNA induced by PAI-1 in TNBC.

Further investigation reveals that SOX2-OT functions as a molecular sponge for a specific microRNA, miR-942-5p. This interaction between SOX2-OT and miR-942-5p regulates the expression of PIK3CA, a gene encoding the p110α catalytic subunit of PI3K (phosphoinositide 3-kinase). Consequently, the activation of the PI3K/Akt signaling pathway is promoted, ultimately leading to TNBC metastasis.

Overall, the findings of this study suggest that SOX2-OT plays a critical role in PAI-1-induced TNBC cell metastasis through the miR-942-5p/PIK3CA signaling axis. These insights into the molecular mechanisms involved in TNBC metastasis may have significant implications for the development of new therapeutic strategies targeting SOX2-OT in TNBC patients.

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