The DOI matches its Crossref record; 53 of the 53 references it cites were found in a registry or an index.
Senescent tumor cells lead the collective invasion in thyroid cancer
Open accessAbstract
Cellular senescence has been perceived as a barrier against carcinogenesis. However, the senescence-associated secretory phenotype (SASP) of senescent cells can promote tumorigenesis. Here, we show senescent tumour cells are frequently present in the front region of collective invasion of papillary thyroid carcinoma (PTC), as well as lymphatic channels and metastatic foci of lymph nodes. In in vitro invasion analysis, senescent tumour cells exhibit high invasion ability as compared with non-senescent tumour cells through SASP expression. Collective invasion in PTC is led by senescent tumour cells characterized by generation of a C-X-C-motif ligand (CXCL)12 chemokine gradient in the front region. Furthermore, senescent cells increase the survival of cancer cells via CXCL12/CXCR4 signalling. An orthotopic xenograft in vivo model also shows higher lymphatic vessels involvement in the group co-transplanted with senescent cells and cancer cells. These findings suggest that senescent cells are actively involved in the collective invasion and metastasis of PTC.
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“Recent studies revealed that besides cancer cells (7), other cells in the tumor microenvironment (TME), such as fibroblasts (8–11) and endothelial cells (12–14), undergo cellular senescence or display senescence-like phenotypic alterations that promote cancer progression.”
From Chromatin conformational changes at human satellite II contribute to the senescence phenotype in the tumor microenvironment (2023) · cites this paper as [7]
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“we and other groups have reported that cancer cells exhibit senescence-like phenotypes (7, 42).”
From Chromatin conformational changes at human satellite II contribute to the senescence phenotype in the tumor microenvironment (2023) · cites this paper as [7]
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“However, OIS cells reportedly can also associate with nonsenescent cancer cells during metastasis to assist in cancer cell survival and invasion through SASP factors [42].”
From The role of cellular senescence and SASP in tumour microenvironment (2023) · cites this paper as [42]
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“In a murine model of papillary thyroid carcinoma, senescent cancer cells located in the front region of collective invasion site and lymph nodes generate a CXCL12 gradient propaedeutic for cancer invasion.197”
From Meta-hallmarks of aging and cancer (2023) · cites this paper as [197]
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Cites
Hallmarks of Cancer: The Next Generation
Hanahan, D., & Weinberg, R. A. (2011) · Cell · doi:10.1016/j.cell.2011.02.013 · Cited by 66,590
Oncogenic ras provokes premature cell senescence associated with accumulation of p53 and p16INK4a
Serrano, M., Lin, A. W., McCurrach, M. E., Beach, D., & Lowe, S. W. (1997) · Cell · doi:10.1016/s0092-8674(00)81902-9 · Cited by 5,218
The senescence-associated secretory phenotype: the dark side of tumor suppression
Coppé, J.-P., Desprez, P.-Y., Krtolica, A., & Campisi, J. (2010) · Annual Review of Pathology: Mechanisms of Disease · doi:10.1146/annurev-pathol-121808-102144 · Cited by 5,206
BRAFE600-associated senescence-like cell cycle arrest of human naevi
Michaloglou, C., Vredeveld, L. C. W., Soengas, M. S., Denoyelle, C., Kuilman, T., van der Horst, C. M. A. M., Majoor, D. M., Shay, J. W., Mooi, W. J., & Peeper, D. S. (2005) · Nature · doi:10.1038/nature03890 · Cited by 2,160
The lymphocyte chemoattractant SDF-1 is a ligand for LESTR/fusin and blocks HIV-1 entry
Bleul, C. C., Farzan, M., Choe, H., Parolin, C., Clark‐Lewis, I., Sodroski, J., & Springer, T. A. (1996) · Nature · doi:10.1038/382829a0 · Cited by 1,953
Metastasis: a question of life or death
Mehlen, P., & Puisieux, A. (2006) · Nature reviews. Cancer · doi:10.1038/nrc1886 · Cited by 1,919
Cellular senescence and the senescent secretory phenotype: therapeutic opportunities
Tchkonia, T., Zhu, Y., van Deursen, J., Campisi, J., & Kirkland, J. L. (2013) · Journal of Clinical Investigation · doi:10.1172/jci64098 · Cited by 1,774
Senescence surveillance of pre-malignant hepatocytes limits liver cancer development
Kang, T.-W., Yevsa, T., Woller, N., Hoenicke, L., Wuestefeld, T., Dauch, D., Hohmeyer, A., Gereke, M., Rudalska, R., Potapova, A., et al. (2011) · Nature · doi:10.1038/nature10599 · Cited by 1,621
Senescence in premalignant tumours
Collado, M., Gil, J., Efeyan, A., Guerra, C., Schuhmacher, A. J., Barradas, M., Benguría, A., Zaballos, A., Flores, J. M., Barbacid, M., et al. (2005) · Nature · doi:10.1038/436642a · Cited by 1,482
CXCL12 (SDF-1)/CXCR4 Pathway in Cancer
Teicher, B. A., & Fricker, S. P. (2010) · Clinical Cancer Research · doi:10.1158/1078-0432.ccr-09-2329 · Cited by 1,453
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Mechanisms of Cellular Senescence: Cell Cycle Arrest and Senescence Associated Secretory Phenotype
Kumari, R., & Jat, P. (2021) · Frontiers in Cell and Developmental Biology · doi:10.3389/fcell.2021.645593 · Cited by 1,622
The senescence-associated secretory phenotype and its physiological and pathological implications
Wang, B., Han, J., Elisseeff, J. H., & Demaria, M. (2024) · Nature Reviews Molecular Cell Biology · doi:10.1038/s41580-024-00727-x · Cited by 948
Unmasking senescence: context-dependent effects of SASP in cancer
Faget, D. V., Ren, Q., & Stewart, S. A. (2019) · Nature Reviews Cancer · doi:10.1038/s41568-019-0156-2 · Cited by 863
Senescence and cancer — role and therapeutic opportunities
Schmitt, C. A., Wang, B., & Demaria, M. (2022) · Nature Reviews Clinical Oncology · doi:10.1038/s41571-022-00668-4 · Cited by 794
Meta-hallmarks of aging and cancer
López-Otín, C., Pietrocola, F., Roiz-Valle, D., Galluzzi, L., & Kroemer, G. (2023) · Cell Metabolism · doi:10.1016/j.cmet.2022.11.001 · Cited by 529
Metadata
- Authors
- Kim, Y. H., Choi, Y. W., Lee, J., Soh, E. Y., Kim, J.-H., & Park, T. J.
- Affiliations
- Ajou University (KR)
- Corresponding author
- Kim, Jang-Hee
- Park, Tae Jun
- Venue
- Nature Communications
- Published
- 2017-05-10
- Volume
- 8
- Issue
- 1
- Pages
- 15208-15208
- ISSN
- 2041-1723 (ISSN-L)
- PMC
- PMC5436223
- OpenAlex
- W2612090342
- Cited by
- 253
- References
- 53
- Citations by year
- 2026: 22 · 2025: 27 · 2024: 39 · 2023: 42 · 2022: 27 · 2021: 37 · 2020: 33 · 2019: 12 · 2018: 13 · 2017: 1
- FWCI
- 12.14
- Type
- journal article
- Language
- en
- Open access
- gold
- doi.org
- Locations
- Nature Communications (publishedVersion, cc-by)
- Europe PMC (PubMed Central) (publishedVersion, cc-by)
- PubMed Central (publishedVersion, cc-by)
- PubMed (publishedVersion)
- RePEc: Research Papers in Economics (submittedVersion)
- DOAJ (DOAJ: Directory of Open Access Journals) (submittedVersion, cc-by-sa)
- AJOU Open Repository (Ajou University) (submittedVersion)
- Funders
- Clinical Trial Center, China Medical University Hospital
- National Research Foundation
- Ajou University
- National Research Foundation of Korea (NRF-2016R1D1A1B02010452, 2016R1D1A1B02010452)
- Topics
- Life Sciences › Biochemistry, Genetics and Molecular Biology › Cell Biology › Telomeres, Telomerase, and Senescence
- Health Sciences › Medicine › Endocrinology, Diabetes and Metabolism › Thyroid Cancer Diagnosis and Treatment
- Health Sciences › Medicine › Oncology › Cancer Cells and Metastasis
- Keywords
- cellular senescence, senescence-associated secretory phenotype, papillary thyroid carcinoma, collective invasion, lymph node metastasis, chemokine gradients, tumor cell survival, lymphatic vessel invasion, tumor microenvironment
- MeSH terms
- Thyroid Epithelial Cells, Animals, Carcinoma, Papillary, Cell Movement, Cells, Cultured, Female, Humans, Lymphatic Metastasis, Mice, Inbred BALB C, Mice, Nude, Neoplasm Invasiveness, Thyroid Neoplasms, Transplantation, Heterologous, Cellular Senescence, Receptors, CXCR4, Gene Expression Profiling, Cell Line, Tumor, Chemokine CXCL12
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