Background <p>Cervical cancer (CC) is a common malignancy. And long non-coding RNAs (lncRNAs) have been identified as pivotal molecular modulators in tumorigenesis, with particular relevance to cervical carcinoma pathogenesis.</p> Aim <p>This study sought to examine the expression, biological functions, and mechanisms of IGFL2-AS1 in CC, and to evaluate its association with clinical prognosis.</p> Methods <p>The present investigation examined IGFL2-AS1 expression levels in paired tumor and paracancerous normal specimens obtained from a cohort of 131 CC cases. Next, the biological functions of IGFL2-AS1 were evaluated in CC cells through proliferation, migration, and invasion assays. Mechanistic studies were conducted using bioinformatics prediction, dual-luciferase reporter assays, and functional experiments (CCK-8 proliferation assays, Transwell migration and invasion assays, and RT-qPCR) to elucidate the IGFL2-AS1/miR-126-5p/MACC1 axis.</p> Results <p>Elevated expression of IGFL2-AS1 was observed in CC tissues, showing significant correlations with disease progression (large tumor size, advanced International Federation of Gynecology and Obstetrics (FIGO) stage, and lymph node metastasis) and unfavorable clinical prognosis. Functional analyses revealed that it promoted CC cell proliferation, migration, invasion, and stemness maintenance. Mechanistically, IGFL2-AS1 acted as a ceRNA to sponge miR-126-5p, consequently relieving its suppression of MACC1. The IGFL2-AS1/miR-126-5p/MACC1 axis was shown to drive the malignant phenotype of CC cells.</p> Conclusions <p>IGFL2-AS1 is upregulated in CC and correlates with poor prognosis. Mechanistically, it promotes malignant phenotypes in CC cells via the miR-126-5p/MACC1 axis.</p>

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IGFL2-AS1 is associated with poor prognosis in cervical cancer and promotes disease progression via the miR-126-5p/MACC1 axis

  • Zhibing Wu,
  • Donglian Lan,
  • Chao He,
  • Na Li

摘要

Background

Cervical cancer (CC) is a common malignancy. And long non-coding RNAs (lncRNAs) have been identified as pivotal molecular modulators in tumorigenesis, with particular relevance to cervical carcinoma pathogenesis.

Aim

This study sought to examine the expression, biological functions, and mechanisms of IGFL2-AS1 in CC, and to evaluate its association with clinical prognosis.

Methods

The present investigation examined IGFL2-AS1 expression levels in paired tumor and paracancerous normal specimens obtained from a cohort of 131 CC cases. Next, the biological functions of IGFL2-AS1 were evaluated in CC cells through proliferation, migration, and invasion assays. Mechanistic studies were conducted using bioinformatics prediction, dual-luciferase reporter assays, and functional experiments (CCK-8 proliferation assays, Transwell migration and invasion assays, and RT-qPCR) to elucidate the IGFL2-AS1/miR-126-5p/MACC1 axis.

Results

Elevated expression of IGFL2-AS1 was observed in CC tissues, showing significant correlations with disease progression (large tumor size, advanced International Federation of Gynecology and Obstetrics (FIGO) stage, and lymph node metastasis) and unfavorable clinical prognosis. Functional analyses revealed that it promoted CC cell proliferation, migration, invasion, and stemness maintenance. Mechanistically, IGFL2-AS1 acted as a ceRNA to sponge miR-126-5p, consequently relieving its suppression of MACC1. The IGFL2-AS1/miR-126-5p/MACC1 axis was shown to drive the malignant phenotype of CC cells.

Conclusions

IGFL2-AS1 is upregulated in CC and correlates with poor prognosis. Mechanistically, it promotes malignant phenotypes in CC cells via the miR-126-5p/MACC1 axis.