ATF1 regulates MAL2 expression through inhibition of miR-630 to mediate the EMT process that promotes cervical cancer cell development and metastasis

  • 0Department of Oncology, The Third Xiangya Hospital of Central South University, Changsha, China.

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Summary

This summary is machine-generated.

Activating transcription factor 1 (ATF1) promotes cervical cancer progression by repressing miR-630, which targets MAL2. ATF1 may be a therapeutic target for cervical malignancies.

Area Of Science

  • Oncology
  • Molecular Biology
  • Biochemistry

Background

  • Activating transcription factor 1 (ATF1) is implicated in cervical cancer development, but its precise role and regulatory mechanisms remain unclear.
  • Understanding the molecular pathways governing cervical cancer progression is crucial for identifying novel therapeutic targets.

Purpose Of The Study

  • To elucidate the role of ATF1 in cervical cancer.
  • To investigate the regulatory relationship between ATF1, miR-630, and MAL2 in cervical carcinoma.
  • To explore the potential of ATF1 as a clinical marker and therapeutic target.

Main Methods

  • Quantitative reverse transcription polymerase chain reaction (qRT-PCR), immunohistochemistry, and Western blot assays were used to assess ATF1, miR-630, and MAL2 expression.
  • Cellular assays including colony formation, Transwell migration, and invasion assays were performed to evaluate the impact of ATF1 and miR-630 on cervical carcinoma cell behavior.
  • Chromatin immunoprecipitation (ChIP), RNA immunoprecipitation (RIP), and dual luciferase reporter assays were employed to confirm molecular interactions.

Main Results

  • Elevated ATF1 expression and decreased miR-630 expression were observed in cervical cancer tissues, with a negative correlation between them.
  • Inhibition of ATF1 suppressed cervical carcinoma cell proliferation, migration, invasion, and epithelial-mesenchymal transition (EMT).
  • Upregulation of miR-630 counteracted the aggressive phenotypes of cervical carcinoma cells, targeting MAL2 for repression.
  • ATF1 was confirmed to directly transcriptionally repress miR-630, establishing a regulatory axis.

Conclusions

  • ATF1 modulates the miR-630/MAL2 pathway, significantly influencing EMT and the aggressive behavior of cervical carcinoma cells.
  • The findings suggest that ATF1 plays a critical role in cervical cancer progression.
  • ATF1 represents a potential biomarker and therapeutic target for interventions in cervical malignancies.

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