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Long non-coding RNA LOXL1 antisense RNA 1 promotes the malignancy of non-small cell lung cancer cells via modulating

Zhijian Wang1, Zhenkui Zhang1, Liqiang Zhao1

  • 1Department of Thoracic Surgery, Beijing Chao-Yang Hospital, Capital Medical University, Beijing, 100043, China.

Molecular Genetics and Genomics : MGG
|July 22, 2026
PubMed

Insights

Long non-coding RNA (lncRNA) LOXL1-AS1 promotes non-small cell lung cancer (NSCLC) progression by sponging miR-122-5p, leading to increased E2F3 expression and poor patient outcomes.

Area of Science:

  • Oncology
  • Molecular Biology
  • Genetics

Background:

  • Long non-coding RNA (lncRNA) antisense RNA 1 (LOXL1-AS1) is implicated in cancer progression.
  • MicroRNA-122-5p (miR-122-5p) and E2F transcription factor 3 (E2F3) have known roles in cancer, with miR-122-5p potentially tumor-suppressive and E2F3 potentially tumor-promoting.
  • The specific role and mechanism of LOXL1-AS1 in non-small cell lung cancer (NSCLC) require further elucidation.

Purpose of the Study:

  • To investigate the function and molecular mechanism of LOXL1-AS1 in NSCLC.
  • To determine the relationship between LOXL1-AS1 expression and clinical outcomes in NSCLC patients.
  • To explore the interaction between LOXL1-AS1, miR-122-5p, and E2F3 in NSCLC cells.

Main Methods:

  • Quantitative real-time PCR to assess LOXL1-AS1 expression in NSCLC tissues and cell lines.
  • In vitro assays (proliferation, migration, invasion) to evaluate the functional impact of LOXL1-AS1.
  • RNA immunoprecipitation and luciferase reporter assays to confirm the interaction between LOXL1-AS1, miR-122-5p, and E2F3.

Main Results:

  • LOXL1-AS1 was significantly upregulated in NSCLC tissues and cell lines, correlating with advanced TNM stage and lymph node metastasis.
  • Overexpression of LOXL1-AS1 promoted NSCLC cell proliferation, migration, and invasion, while knockdown exerted opposite effects.
  • LOXL1-AS1 acted as a competing endogenous RNA (ceRNA) by sponging miR-122-5p, thereby increasing E2F3 expression. Upregulating miR-122-5p or downregulating E2F3 could counteract LOXL1-AS1's pro-tumorigenic effects.

Conclusions:

  • LOXL1-AS1 promotes NSCLC cell proliferation and migration in vitro.
  • LOXL1-AS1 expression correlates with poor clinical outcomes in NSCLC patients.
  • The LOXL1-AS1/miR-122-5p/E2F3 axis plays a crucial role in NSCLC progression, representing a potential therapeutic target.
Keywords:
E2F3LOXL1-AS1NSCLCmiR-122-5p

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