ArticleOncotarget2017
Feedback circuitry via let-7c between lncRNA CCAT1 and c-Myc is involved in cigarette smoke extract-induced malignant transformation of HBE cells.
Article in Oncotarget, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 20 papers.
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Who cites it
20 citing papers in PubMed, 45 citations in OpenAlex.
- Hsa_circ_0003611 hinders the transformation of mesenchymal stem cells into osteosarcoma cells through suppressing MYC by IGF2BP3 via mBiological research · 2025Article
- Downregulation ofeLife · 2024Article
- Deep sequencing of candidate genes identified 14 variants associated with smoking abstinence in an ethnically diverse sample.Scientific reports · 2024Article
- Downregulation ofbioRxiv : the preprint server for biology · 2024Article
- LncRNA in tumorigenesis of non-small-cell lung cancer: From bench to bedside.Cell death discovery · 2022Review
- Antioxidant Systems, lncRNAs, and Tunneling Nanotubes in Cell Death Rescue from Cigarette Smoke Exposure.Cells · 2022Review
- miRNA-34b/c regulates mucus secretion in RSV-infected airway epithelial cells by targeting FGFR1.Journal of cellular and molecular medicine · 2021Article
- Long Non-coding RNA CCAT1 Acts as an Oncogene and Promotes Sunitinib Resistance in Renal Cell Carcinoma.Frontiers in oncology · 2020Article
- LncRNA CCAT1 functions as apoptosis inhibitor in podocytes via autophagy inhibition.Journal of cellular biochemistry · 2020Article
- LncRNA & Wnt signaling in colorectal cancer.Cancer cell international · 2020Review
- MicroRNAs as Potential Regulators of Immune Response Networks in Asthma and Chronic Obstructive Pulmonary Disease.Frontiers in immunology · 2020Review
- Long non-coding RNAs in non-small cell lung cancer: functions and distinctions from other malignancies.Translational cancer research · 2019Review
- Transcriptomic and barrier responses of human airway epithelial cells exposed to cannabis smoke.Physiological reports · 2019Article
- The effects of cigarette smoking extracts on cell cycle and tumor spread: novel evidence.Future science OA · 2019Review
- Pivotal prognostic and diagnostic role of the long non‑coding RNA colon cancer‑associated transcript 1 expression in human cancer (Review).Molecular medicine reports · 2019Review
- Crosstalk mechanisms between the WNT signaling pathway and long non-coding RNAs.Non-coding RNA research · 2018Review
- [Progress of Long Non-coding RNA in Non-small Cell Lung Cancer].Zhongguo fei ai za zhi = Chinese journal of lung cancer · 2018Review
- To Wnt or Lose: The Missing Non-Coding Linc in Colorectal Cancer.International journal of molecular sciences · 2017Review
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Authors and funding
15 authors at 3 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Cigarette smoking is a primary risk factor for the development of lung cancer, which is regarded as the leading cause of cancer-related deaths. The process of malignant transformation of cells, however, is complex and elusive. The present study investigated the roles of an lncRNA, CCAT1, and a transcriptional factor, c-Myc, in human bronchial epithelial (HBE) cell transformation induced by cigarette smoke extract. With acute and chronic treatment of HBE cells, cigarette smoke extract induced increases of CCAT1 and c-Myc levels and decreases of levels of let-7c, a microRNA. Down-regulation of c-Myc reduced the degree of malignancy and the invasion/migration capacity of HBE cells transformed by cigarette smoke extract. ChIP assays established that c-Myc, increased by cigarette smoke extract, binds to the promoter of CCAT1, activating its transcription. Further, let-7c suppressed the expression of c-Myc through binding to its 3'-UTR. In turn, CCAT1 promoted the accumulation of c-Myc through binding to let-7c and decreasing free let-7c, which influenced the neoplastic capacity of HBE cells transformed by cigarette smoke extract. These results indicate that a positive feedback loop ensures expression of cigarette smoke extract-induced CCAT1 and c-Myc via let-7c, which is involved in cigarette smoke extract-induced malignant transformation of HBE cells. Thus, the present research establishes a new mechanism for the reciprocal regulation between CCAT1 and c-Myc and provides an understanding of cigarette smoke extract-induced lung carcinogenesis.
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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.