Background <p>Cervical cancer (CC) represents a significant public health challenge globally.</p> Objectives <p>This research sought to explore the effect of the microRNA (miR)-1307-3p in CC.</p> Materials and methods <p>180 CC patients were recruited. The association between miR-1307-3p expression and patient survival was evaluated using the Kaplan-Meier method, while risk factors associated with patient mortality were identified by Cox regression analysis. Additionally, the expression of relevant genes was measured using reverse transcription‑quantitative polymerase chain reaction (RT‑qPCR). Cell viability was assessed using the cell counting kit-8 (CCK-8), and cell migration and invasion were analyzed using Transwell. Furthermore, the dual-luciferase reporter assay was performed to confirm the targeted regulatory relationship between miR-1307-3p and <i>forkhead box O3 (FOXO3)</i>.</p> Results <p>MiR-1307-3p was significantly upregulated in CC tissues, and its high expression was closely associated with the malignant progression of CC. MiR-1307-3p promoted the malignant progression of CC by directly targeting and inhibiting the <i>FOXO3</i> gene. Inhibition of miR-1307-3p significantly suppressed cell proliferation, migration, and invasion. However, knocking down <i>FOXO3</i> partially reversed the aforementioned biological effects induced by the miR-1307-3p inhibitor.</p> Conclusion <p>MiR-1307-3p was involved in promoting carcinogenesis during the occurrence and progression of CC.</p>

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miR-1307-3p promotes the progression of cervical cancer by targeting FOXO3

  • Yulan Lu,
  • Yuan Yuan,
  • Sheng Liang

摘要

Background

Cervical cancer (CC) represents a significant public health challenge globally.

Objectives

This research sought to explore the effect of the microRNA (miR)-1307-3p in CC.

Materials and methods

180 CC patients were recruited. The association between miR-1307-3p expression and patient survival was evaluated using the Kaplan-Meier method, while risk factors associated with patient mortality were identified by Cox regression analysis. Additionally, the expression of relevant genes was measured using reverse transcription‑quantitative polymerase chain reaction (RT‑qPCR). Cell viability was assessed using the cell counting kit-8 (CCK-8), and cell migration and invasion were analyzed using Transwell. Furthermore, the dual-luciferase reporter assay was performed to confirm the targeted regulatory relationship between miR-1307-3p and forkhead box O3 (FOXO3).

Results

MiR-1307-3p was significantly upregulated in CC tissues, and its high expression was closely associated with the malignant progression of CC. MiR-1307-3p promoted the malignant progression of CC by directly targeting and inhibiting the FOXO3 gene. Inhibition of miR-1307-3p significantly suppressed cell proliferation, migration, and invasion. However, knocking down FOXO3 partially reversed the aforementioned biological effects induced by the miR-1307-3p inhibitor.

Conclusion

MiR-1307-3p was involved in promoting carcinogenesis during the occurrence and progression of CC.