ArticleJournal of Zhejiang University. Science. B2022
Optimized thyroid transcription factor-1 core promoter-driven microRNA-7 expression effectively inhibits the growth of human non-small-cell lung cancer cells.
Article in Journal of Zhejiang University. Science. B, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 6 papers.
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Who cites it
6 citing papers in PubMed, 8 citations in OpenAlex.
- Dual-specific phosphatases-8: a new target for clinical disease intervention.Journal of translational medicine · 2025Review
- Bulk RNA-seq conjoined with ScRNA-seq analysis reveals the molecular characteristics of nucleus pulposus cell ferroptosis in rat aging intervertebral discs.Arthritis research & therapy · 2025Article
- Mitochondrial respiratory chain component NDUFA4: a promising therapeutic target for gastrointestinal cancer.Cancer cell international · 2024Review
- miR-124 as a Liquid Biopsy Prognostic Biomarker in Small Extracellular Vesicles from NSCLC Patients.International journal of molecular sciences · 2023Article
- MiRNA-Based Therapies for Lung Cancer: Opportunities and Challenges?Biomolecules · 2023Review
- Immunohistochemistry in the pathologic diagnosis and management of thyroid neoplasms.Frontiers in endocrinology · 2023Review
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Authors and funding
11 authors at 1 institution in 1 country.
Funding
Abstract
Targeted gene therapy has become a promising approach for lung cancer treatment. In our previous work, we reported that the targeted expression of microRNA-7 (miR-7) operated by thyroid transcription factor-1 (TTF-1) promoter inhibited the growth of human lung cancer cells in vitro and in vivo; however, the intervention efficiency needed to be further improved. In this study, we identified the core promoter of TTF-1 (from -1299 bp to -871 bp) by 5' deletion assay and screened out the putative transcription factors nuclear factor-1 (NF-1) and activator protein-1 (AP-1). Further analysis revealed that the expression level of NF-1, but not AP-1, was positively connected with the activation of TTF-1 core promoter in human non-small-cell lung cancer (NSCLC) cells. Moreover, the silencing of NF-1 could reduce the expression level of miR-7 operated by TTF-1 core promoter. Of note, we optimized four distinct sequences to form additional NF-1-binding sites (TGGCA) in the sequence of TTF-1 core promoter (termed as
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