Interleukin-6 affects cell death escaping mechanisms acting on Bax-Ku70-Clusterin interactions in human colon cancer progression
Open accessAbstract
Activation of pro-survival pathways and apoptotic cell death escape are considered hallmarks of oncogenic cell transformation. Tissue microenvironment strongly influences tumorigenesis, redirecting some pathways versus a persisting pro-survival state. Here, we report evidence on the role of interleukin 6 (IL-6) in affecting pro-survival pathways in colon cancer progression, modulating the expression and the molecular interactions among the pro-apoptotic factor Bax, the DNA repair proteins Ku70/86 and Clusterin isoforms. In human colorectal carcinomas (n = 50) at different stages of disease, we found an increased IL-6 production, the loss of Ku86 and Clusterin 50-55 kDa pro-apoptotic isoform. Conversely, we observed the overexpression of Bax and the 40 kDa prosurvival sClusterin (sCLU) isoform. Bax co-localized with Ku70 that was found atypically expressed in the cytoplasm of advanced stage colon cancers (Dukes'C-D; n = 22). IL-6 treatment of a colon cancer cell line, Caco-2, modulated the expression of genes involved in tumor invasion and apoptosis, as observed by microarrays. In particular, IL-6 downmodulated Bax expression at mRNA level. Concomitantly, IL-6 exposure influenced Bax also at protein level acting on the Bax-Ku70-sCLU physical interactions in the cytoplasm, by affecting the Ku70 acetylation and phosphorylation state, thus leading to the inhibition of Bax pro-apoptotic activity. In addition, we found that IL-6 treatment induced a significant downregulation of Ku86 and a strong increase of sCLU, confirming tumor biopsies data. In contrast Somatostatin treatment of Caco-2 cells was able to restore apoptosis, demonstrating that Ku70-Bax-CLU interactions could be dynamically modulated. Hence, IL-6 could favor tumor expansion, promoting cell survival and apoptosis escape throughout the different stages of tumor evolution. Uncovering the molecular mechanisms of action of these factors may offer strategies for selectively manipulate the cancer cells sensitivity to therapy.
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IL6 seems to influence CLU expression.
“IL6 appears to play a role in modulating expression of CLU (Pucci, et al., 2009)”
From A potential endophenotype for Alzheimer's disease: cerebrospinal fluid clusterin (2016) · cites this paper as Pucci, et al., 2009
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- Authors
- Pucci, S., Mazzarelli, P., Sesti, F., Boothman, D. A., & Spagnoli, L. G.
- Affiliations
- University of Rome Tor Vergata (IT)
- Corresponding author
- Pucci, Sabina
- Venue
- Cell Cycle
- Publisher
- Informa UK Limited
- Published
- 2009-02
- Volume
- 8
- Issue
- 3
- Pages
- 473-481
- ISSN
- 1538-4101 (ISSN-L)
- 1551-4005
- PMC
- PMC2853871
- OpenAlex
- W2005025018
- Cited by
- 46
- References
- 33
- Citations by year
- 2024: 5 · 2023: 1 · 2022: 3 · 2021: 2 · 2020: 2 · 2019: 3 · 2018: 2 · 2017: 3 · 2016: 3 · 2015: 4 · 2014: 1 · 2013: 2 · 2012: 2
- FWCI
- 1.88
- Type
- journal article
- Language
- en
- Open access
- bronze
- doi.org
- Locations
- Cell Cycle (publishedVersion)
- PubMed (publishedVersion)
- PubMed Central (acceptedVersion)
- Cineca Institutional Research Information System (Tor Vergata University) (submittedVersion, cc-by-nc-nd)
- Funders
- Istituto Superiore di Sanità
- Alleanza Contro il Cancro
- National Cancer Institute (R01CA078530, R01CA102792, P30CA013148, P30CA142543)
- National Institute of Allergy and Infectious Diseases (U19AI067773)
- Topics
- Life Sciences › Biochemistry, Genetics and Molecular Biology › Molecular Biology › Cell death mechanisms and regulation
- Health Sciences › Medicine › Oncology › Clusterin in disease pathology
- Health Sciences › Medicine › Oncology › Cytokine Signaling Pathways and Interactions
- Keywords
- interleukin-6, colon cancer progression, Bax, Ku70, Ku80, survival signaling, somatostatin, Caco-2 cells, tumor microenvironment, DNA repair proteins
- MeSH terms
- Ku Autoantigen, Colonic Neoplasms, DNA Helicases, DNA-Binding Proteins, Humans, Interleukin-6, Gene Expression, Cell Death, Disease Progression, Protein Isoforms, Antigens, Nuclear, Cell Line, Tumor, bcl-2-Associated X Protein, Clusterin
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