ArticleMolecular biology of the cell2012
MicroRNA-212 displays tumor-promoting properties in non-small cell lung cancer cells and targets the hedgehog pathway receptor PTCH1.
Article in Molecular biology of the cell, 2012. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 38 papers.
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Who cites it
38 citing papers in PubMed, 77 citations in OpenAlex.
- MicroRNA-regulated signaling and tumor microenvironment modulation in lung cancer: mechanistic insights and translational opportunities.Cancer cell international · 2026Review
- Hedgehog pathway and cancer: A new area (Review).Oncology reports · 2024Review
- Initial development and testing of an exhaled microRNA detection strategy for lung cancer case-control discrimination.Scientific reports · 2023Article
- Epigenetic regulation of stem cells in lung cancer oncogenesis and therapy resistance.Frontiers in genetics · 2023Review
- Prognostic significance of PD-L1 expression and CD8Journal of thoracic disease · 2022Article
- Noncoding RNAs related to the hedgehog pathway in cancer: clinical implications and future perspectives.Molecular cancer · 2022Review
- Resveratrol promotes skin wound healing by regulating the miR-212/CASP8 axis.Laboratory investigation; a journal of technical methods and pathology · 2021Article
- HEDGEHOG/GLI Modulates the PRR11-SKA2 Bidirectional Transcription Unit in Lung Squamous Cell Carcinomas.Genes · 2021Article
- RPB5-mediating protein promotes the progression of non-small cell lung cancer by regulating the proliferation and invasion.Journal of thoracic disease · 2021Article
- Functions and Targets of miR-335 in Cancer.OncoTargets and therapy · 2021Review
- miR-143 is implicated in growth plate injury by targeting IHH in precartilaginous stem cells.International journal of medical sciences · 2021Article
- Diagnostic and Therapeutic Implications of microRNAs in Non-Small Cell Lung Cancer.International journal of molecular sciences · 2020Review
- Identification and Validation of a Potent Multi-miRNA Signature for Prediction of Prognosis of Osteosarcoma Patients.Medical science monitor : international medical journal of experimental and clinical research · 2020Article
- The functions and targets of miR-212 as a potential biomarker of cancer diagnosis and therapy.Journal of cellular and molecular medicine · 2020Review
- miR‑512‑5p suppresses proliferation, migration and invasion, and induces apoptosis in non‑small cell lung cancer cells by targeting ETS1.Molecular medicine reports · 2019Article
- hsa-miR-212 modulates the radiosensitivity of glioma cells by targeting BRCA1.Oncology reports · 2018Article
- Human umbilical cord mesenchymal stem cell-derived extracellular vesicles promote lung adenocarcinoma growth by transferring miR-410.Cell death & disease · 2018Article
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- MicroRNA-212 suppresses the proliferation and migration of osteosarcoma cells by targeting forkhead box protein A1.Experimental and therapeutic medicine · 2016Article
Corrections and comments
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Authors and funding
6 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Dysexpression of microRNAs has been found in many tumors, including lung cancer. The hedgehog (Hh) signaling pathway plays an important role during normal development, and the abnormal regulation of its members has also been related to many tumors. However, little is known about the relationship between microRNA and the Hh pathway. In this paper, we report microRNA-212 (miR-212) playing a role in non-small cell lung cancer (NSCLC) and targeting PTCH1, a receptor of the Hh pathway. We found that miR-212 was up-regulated when cells were treated with 4ß-12-O-tetradecanoylphorbol-13-acetate (TPA). We ectopically expressed miR-212 in NSCLC cell lines to examine the influence of miR-212 overexpression. The results showed that overexpression of miR-212 in NSCLC cells promoted cell cycle progression and cell proliferation, migration, and invasion. The promoting effects of miR-212 on cell proliferation, migration, and invasion were partially reversed by the miR-212 inhibitor anti-miR-212. These results suggested that miR-212 might have tumor-promoting properties. Potential targets of miR-212 were predicted, and we showed tumor suppressor PTCH1 was a functional target of miR-212. PTCH1 may be responsible for the effect of miR-212 on cell proliferation. Altogether, our results indicated that miR-212 was involved in tumorigenesis, and the oncogenic activity of miR-212 in NSCLC cells was due, in part, to suppression of PTCH1.
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