An Epigenetic Switch Involving NF-κB, Lin28, Let-7 MicroRNA, and IL6 Links Inflammation to Cell Transformation
Open accessAbstract
Inflammation is linked clinically and epidemiologically to cancer, and NF-kappaB appears to play a causative role, but the mechanisms are poorly understood. We show that transient activation of Src oncoprotein can mediate an epigenetic switch from immortalized breast cells to a stably transformed line that forms self-renewing mammospheres that contain cancer stem cells. Src activation triggers an inflammatory response mediated by NF-kappaB that directly activates Lin28 transcription and rapidly reduces let-7 microRNA levels. Let-7 directly inhibits IL6 expression, resulting in higher levels of IL6 than achieved by NF-kappaB activation. IL6-mediated activation of the STAT3 transcription factor is necessary for transformation, and IL6 activates NF-kappaB, thereby completing a positive feedback loop. This regulatory circuit operates in other cancer cells lines, and its transcriptional signature is found in human cancer tissues. Thus, inflammation activates a positive feedback loop that maintains the epigenetic transformed state for many generations in the absence of the inducing signal.
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NF-κB increases IL-6 levels by inhibiting let-7 expression.
“NF-κB also increases IL-6 levels by inhibiting let-7 expression (89).”
From IL-6 in inflammation, autoimmunity and cancer (2021) · cites this paper as [89]
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- Authors
- Iliopoulos, D., Hirsch, H. A., & Struhl, K.
- Affiliations
- Harvard University (US)
- Corresponding author
- Struhl, Kevin
- Venue
- Cell
- Publisher
- Elsevier BV
- Published
- 2009-11
- Volume
- 139
- Issue
- 4
- Pages
- 693-706
- ISSN
- 0092-8674 (ISSN-L)
- PMC
- PMC2783826
- OpenAlex
- W2152310279
- Cited by
- 1,374
- References
- 1
- Citations by year
- 2026: 24 · 2025: 33 · 2024: 39 · 2023: 43 · 2022: 62 · 2021: 69 · 2020: 55 · 2019: 92 · 2018: 73 · 2017: 95 · 2016: 112 · 2015: 127 · 2014: 119 · 2013: 142 · 2012: 117
- FWCI
- 30.13
- Type
- journal article
- Language
- en
- Open access
- bronze
- doi.org
- Licence
- www.elsevier.com/tdm/userlicense/1.0/ (tdm)
- www.elsevier.com/legal/tdmrep-license (tdm)
- www.elsevier.com/open-access/userlicense/1.0/ (vor, 1354 d)
- doi.org/10.15223/policy-017 (stm-asf)
- doi.org/10.15223/policy-037 (stm-asf)
- doi.org/10.15223/policy-012 (stm-asf)
- doi.org/10.15223/policy-029 (stm-asf)
- doi.org/10.15223/policy-004 (stm-asf)
- Locations
- Cell (publishedVersion)
- PubMed (publishedVersion)
- Europe PMC (PubMed Central) (acceptedVersion)
- PubMed Central (acceptedVersion)
- Funders
- American Cancer Society
- National Institutes of Health
- National Cancer Institute (R01CA107486, CA107486)
- Topics
- Life Sciences › Biochemistry, Genetics and Molecular Biology › Cancer Research › NF-κB Signaling Pathways
- Life Sciences › Biochemistry, Genetics and Molecular Biology › Cancer Research › MicroRNA in disease regulation
- Health Sciences › Medicine › Oncology › Cytokine Signaling Pathways and Interactions
- Keywords
- inflammation, cancer, NF-κB, Lin28, let-7 microRNA, interleukin-6, STAT3, epigenetic switch, breast cancer, mammospheres, cancer stem cells, positive feedback loop, cell transformation, cell immortalization
- MeSH terms
- Animals, Cell Line, Cell Line, Transformed, Humans, Inflammation, Mice, Nude, Neoplasm Transplantation, Transplantation, Heterologous, Interleukin-6, Genes, src, RNA-Binding Proteins, Feedback, Physiological, MicroRNAs, Epigenesis, Genetic, Mice, NF-kappa B p50 Subunit
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