Evidence map›Paper›PMID 42484731›Full record

ArticleMolecular genetics and genomics : MGG2026

Long non-coding RNA LOXL1 antisense RNA 1 promotes the malignancy of non-small cell lung cancer cells via modulating the microRNA-122-5p/E2F transcription factor 3 axis.

Zhijian Wang, Zhenkui Zhang, Liqiang Zhao, Aiwen Sun, Min Wang

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Article in Molecular genetics and genomics : MGG, 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Not yet cited in PubMed.

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3 · Its place in the literature

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4 · The record

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5 · Who and what money

Authors and funding

5 authors.

Zhijian WangDepartment of Thoracic Surgery, Beijing Chao-Yang Hospital, Capital Medical University, Beijing, 100043, China.
Zhenkui ZhangDepartment of Thoracic Surgery, Beijing Chao-Yang Hospital, Capital Medical University, Beijing, 100043, China.
Liqiang ZhaoDepartment of Thoracic Surgery, Beijing Chao-Yang Hospital, Capital Medical University, Beijing, 100043, China.
Aiwen SunDepartment of Laboratory Medicine, Beijing Chao-Yang Hospital, Capital Medical University, Beijing, 100043, China.
Min WangDepartment of Respiratory Medicine, Guang'anmen Hospital, China Academy of Chinese Medical Sciences, No. 5, Beixiange, Xicheng District, Beijing, 100053, China. wm_med@163.com.

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Long non-coding RNA (lncRNA) antisense RNA 1 (LOXL1-AS1), reportedly, exerts carcinogenic effects in cancers including non-small cell lung cancer (NSCLC) via competitive endogenous RNA (ceRNA) mechanism. Additionally, previous studies have implied that microRNA-122-5p (miR-122-5p) and E2F transcription factor 3 (E2F3) have cancer-promoting properties and tumor-suppressive properties, respectively. Here we aim to further explore the function and mechanism of LOXL1-AS1 in NSCLC. In this experimental study, we found that LOXL1-AS1 was high expression in NSCLC tissues and cell lines. High LOXL1-AS1 expression was significantly relevant to the advanced tumor node metastasis (TNM) stage and positive lymph node metastasis of NSCLC patients. LOXL1-AS1 overexpression promoted proliferation, migration and invasion of NSCLC cells, while LOXL1-AS1 knockdown had the opposite effect. LOXL1-AS1 could sponge miR-122-5p. E2F3 was a downstream target of miR-122-5p. LOXL1-AS1 increased E2F3 expression through repressing miR-122-5p. In addition, miR-122-5p up-regulation or E2F3 knockdown could offset the promoting effect of LOXL1-AS1 overexpression on proliferation, migration and invasion of NSCLC cells. Overall, this study demonstrates that LOXL1-AS1 promotes NSCLC cell proliferation and migration in vitro, and correlates with poor clinical outcomes, partially via modulating miR-122-5p/E2F3 axis.

Indexed as

Carcinoma, Non-Small-Cell LungE2F3 Transcription FactorLung NeoplasmsMicroRNAsRNA, Long NoncodingAmino Acid OxidoreductasesCell Line, TumorCell MovementCell ProliferationFemaleGene Expression Regulation, NeoplasticHumansMaleMiddle AgedRNA, AntisenseRNA, Competitive EndogenousAmino Acid OxidoreductasesE2F3 protein, humanE2F3 Transcription FactorLOXL1 protein, humanMicroRNAsMIRN122 microRNA, humanRNA, AntisenseRNA, Competitive EndogenousRNA, Long NoncodingE2F3LOXL1-AS1miR-122-5pNSCLC

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Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.