ArticleEnvironmental science and pollution research international2022
CTBP1-AS2 promoted non-small cell lung cancer progression via sponging the miR-623/MMP3 axis.
Article in Environmental science and pollution research international, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 3 papers.
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3 citing papers in PubMed, 4 citations in OpenAlex.
- NAD(H)-dependent corepressor CTBP1 integrates metabolic signals to drive oncogenic programs.Frontiers in immunology · 2026Review
- Development of a Mitochondrial Permeability Transition-Driven Necrosis-Related Prognostic Signature in Cervical Cancer: Integrating Bulk Transcriptomic and Single-Cell Data.Cancer medicine · 2025Article
- The Intricate Interplay between the ZNF217 Oncogene and Epigenetic Processes Shapes Tumor Progression.Cancers · 2022Review
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Authors and funding
2 authors at 1 institution in 1 country.
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Abstract
Mounting evidence indicates that lncRNAs (long noncoding RNAs) are involved in the initiation and development of tumors, including non-small cell lung cancer (NSCLC). However, the involvement of C-terminal binding protein-antisense RNA 2 (CTBP1-AS2) in NSCLC remains to be studied. RT-qPCR was carried out to detect CTBP1-AS2 and miR-623 expression in NSCLC cells and tissues. CCK-8 and flow cytometry were performed to measure cell proliferation and cell cycle progression. Luciferase reporter analysis was performed to study the potential target of CTBP1-AS2. We found that CTBP1-AS2 expression was upregulated in NSCLC cells (SPC-A1, A549, H23, and H1299) compared to 16HBE cells. We demonstrated that the CTBP1-AS2 level was higher in NSCLC specimens than in paired non-tumor specimens. Elevated expression of CTBP1-AS2 increased cell growth and induced cell cycle progression and epithelial-mesenchymal transition (EMT). We also found that ectopic expression of CTBP1-AS2 inhibited miR-623 expression. MMP3 was a direct target of miR-623, and luciferase reporter assays suggested that miR-623 overexpression suppressed the luciferase expression driven by the MMP3 wild-type reporter but not the mutant reporter. Overexpression of miR-623 suppressed MMP3 expression in A549 cells, and overexpression of CTBP1-AS2 increased MMP3 expression in A549 cells. Moreover, the miR-623 level was lower in NSCLC specimens than in paired non-tumor specimens, and CTBP1-AS2 expression was negatively correlated with miR-623 expression in NSCLC samples. Furthermore, overexpression of CTBP1-AS2 enhanced cell growth, cell cycle progression, and EMT progression by modulating MMP3 expression.
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