CDKN2A inhibits formation of homotypic cell-in-cell structures
Open accessAbstract
Cell-in-cell (CIC) structures, characterized by enclosure of one or more cells within another cell, were extensively documented in human cancers. Although elevated CIC formation was found in cancers with CDKN2A inactivation, a causal link between them remains to be established. We reported here that inhibiting CDKN2A expression effectively promoted homotypic CIC formation, whereas ectopic overexpression of p16INK4a or p14ARF, two proteins encoded by CDKN2A gene, significantly suppressed CIC formation in MCF7 cells. The regulation of CIC formation by CDKN2A was tightly correlated with subcellular redistribution of E-cadherin, F-actin rearrangement and reduced phosphorylation of myosin light chain 2 (p-MLC2), consistent with which, CDKN2A expression imparted cells winner/outer identity in competition assay. Moreover, CIC formation negatively correlates with p16INK4a expression in human breast cancers. Thus, our work identifies CDKN2A as the first tumor suppressor whose inactivation promotes homotypic CIC formation in human cancer cells.
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CDKN2A promotes apoptosis and senescence, inhibits cell-in-cell structure formation and anchorage-independent growth, and modulates anti-tumor immunity by influencing immune-cell infiltration.
“Additionally, CDKN2A promotes apoptosis and senescence and inhibits cancer-associated processes like cell-in-cell structure formation and anchorage-independent growth, while it modulates anti-tumor immunity by influencing immune-cell infiltration [38,58,109,111].”
From Significance of TP53, CDKN2A, SMAD4 and KRAS in Pancreatic Cancer (2024) · cites this paper as [38]
The Results (no page number available) show that CDKN2A expression inhibits cell-in-cell formation and note that persistent expression is known to induce senescence. The Discussion links inhibition of cell-in-cell formation to increased anchorage-independent growth, but does not directly show that CDKN2A inhibits that growth. The paper does not support the attributed claims about CDKN2A promoting apoptosis or modulating anti-tumor immunity through immune-cell infiltration. (LLM, conf=0.88)
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- Authors
- Liang, J., Fan, J., Wang, M., Niu, Z., Zhang, Z., Yuan, L., Tai, Y., Chen, Z., Song, S., Wang, X., Liu, X., Huang, H., & Sun, Q.
- Affiliations
- Capital Medical University (CN)
- 307th Hospital of Chinese People’s Liberation Army (CN)
- South China University of Technology (CN)
- Corresponding author
- Liu, Xiaoqing
- Huang, Hongyan
- Sun, Qiang
- ORCID
- Venue
- Oncogenesis
- Published
- 2018-06-05
- Volume
- 7
- Issue
- 6
- Pages
- 50-50
- ISSN
- 2157-9024 (ISSN-L)
- PMC
- PMC6002405
- OpenAlex
- W2808191735
- Cited by
- 49
- References
- 27
- Citations by year
- 2026: 2 · 2025: 7 · 2024: 7 · 2023: 9 · 2022: 10 · 2021: 4 · 2020: 4 · 2019: 4 · 2018: 2
- FWCI
- 1.32
- Type
- journal article
- Language
- en
- Open access
- gold
- doi.org
- Locations
- Oncogenesis (publishedVersion, cc-by)
- Europe PMC (PubMed Central) (publishedVersion, cc-by)
- PubMed Central (publishedVersion, cc-by)
- PubMed (publishedVersion)
- DOAJ (DOAJ: Directory of Open Access Journals) (submittedVersion)
- Funders
- Memorial Sloan-Kettering Cancer Center
- National Natural Science Foundation of China (81372834, 31671432, 31770975, 81471578, 81472588, 81572799)
- National Key Research and Development Program of China (2015CB553704)
- Topics
- Health Sciences › Medicine › Oncology › Cancer Cells and Metastasis
- Health Sciences › Medicine › Oncology › Cancer-related Molecular Pathways
- Life Sciences › Biochemistry, Genetics and Molecular Biology › Cell Biology › Cellular Mechanics and Interactions
- Keywords
- CDKN2A, cell-in-cell structures, p16INK4a, p14ARF, tumor suppressor inactivation, F-actin rearrangement, myosin light chain 2 phosphorylation, MCF-7 cells, breast cancer, cell competition
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