ArticleScientific reports2012
Reversal of aberrant cancer methylome and transcriptome upon direct reprogramming of lung cancer cells.
Article in Scientific reports, 2012. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 25 papers.
What it found
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Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
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Who cites it
25 citing papers in PubMed, 49 citations in OpenAlex.
- Engineered immune cell therapies for solid tumors: pharmacological advances, clinical outcomes, and future directions.Frontiers in pharmacology · 2025Review
- Possible Strategies to Reduce the Tumorigenic Risk of Reprogrammed Normal and Cancer Cells.International journal of molecular sciences · 2024Review
- Application of Induced Pluripotent Stem Cells in Malignant Solid Tumors.Stem cell reviews and reports · 2023Review
- Connecting the dots: Melanoma cell of origin, tumor cell plasticity, trans-differentiation, and drug resistance.Pigment cell & melanoma research · 2023Review
- Cancer cells as a new source of induced pluripotent stem cells.Stem cell research & therapy · 2022Review
- Revisiting Epithelial Carcinogenesis.International journal of molecular sciences · 2022Article
- Pluripotency Stemness and Cancer: More Questions than Answers.Advances in experimental medicine and biology · 2022Article
- "Reprogram Enablement" as an Assay for Identifying Early Oncogenic Pathways by Their Ability to Allow Neoplastic Cells to Reacquire an Epiblast State.Stem cell reports · 2020Article
- Modeling cancer using patient-derived induced pluripotent stem cells to understand development of childhood malignancies.Cell death discovery · 2018Review
- Modeling Hematological Diseases and Cancer With Patient-Specific Induced Pluripotent Stem Cells.Frontiers in immunology · 2018Review
- Development of hepatoma-derived, bidirectional oval-like cells as a model to study host interactions with hepatitis C virus during differentiation.Oncotarget · 2017Article
- Current status in cancer cell reprogramming and its clinical implications.Journal of cancer research and clinical oncology · 2017Review
- Article
- Attractor landscape analysis of colorectal tumorigenesis and its reversion.BMC systems biology · 2016Article
- In vitro models of cancer stem cells and clinical applications.BMC cancer · 2016Review
- The reverse control of irreversible biological processes.Wiley interdisciplinary reviews. Systems biology and medicine · 2016Review
- SFRP1 is a possible candidate for epigenetic therapy in non-small cell lung cancer.BMC medical genomics · 2016Article
- Autophagy in stem and progenitor cells.Cellular and molecular life sciences : CMLS · 2016Review
- Sendai virus-mediated expression of reprogramming factors promotes plasticity of human neuroblastoma cells.Cancer science · 2015Article
- Epigenetic biomarker to support classification into pluripotent and non-pluripotent cells.Scientific reports · 2015Article
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
6 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Recent reports on direct reprogramming of cancer cells (iPCs) which results in reduced tumorigenic potential has attributed the importance of epigenetics in tumorigenesis, but lacked genome-wide analysis. Here we describe successful generation of iPCs from non-small cell lung cancer (NSCLC) cell lines. Following reprogramming, they resembled embryonic stem and induced pluripotent stem cells in pluripotency markers expression, gene expression patterns and in vitro differentiation ability. Genome-wide methylation analysis revealed that aberrantly methylated promoters which were mostly developmental-associated genes and tumor suppressors; as well as commonly upregulated genes in NSCLC i.e. KRT19 and S100P were reversed in iPCs upon reprogramming. Also, the reversal of oncogenes and tumor suppressors status were partially explainable by DNA methylation. These findings suggest that DNA methylation patterns explain the downstream transcriptional effects, which potentially caused the reduced tumorigenicity in iPCs, thus providing evidence that reprogramming reverses the aberrantly dysregulated genes in NSCLC both epigenetically and transcriptionally.
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Registered trials
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.