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Reciprocal interaction between carcinoma-associated fibroblasts and squamous carcinoma cells through interleukin-1α induces cancer progression.

 Jung Yoon Bae  ;  Eun Kyoung Kim  ;  Dong Hyun Yang  ;  Xianglan Zhang  ;  Young Jin Park  ;  Doo Young Lee  ;  Chung Min Che  ;  Jin Kim 
 NEOPLASIA, Vol.16(11) : 928-938, 2014 
Journal Title
Issue Date
Actins/metabolism ; Animals ; Blotting, Western ; Carcinoma, Squamous Cell/genetics ; Carcinoma, Squamous Cell/metabolism ; Carcinoma, Squamous Cell/pathology* ; Cell Communication* ; Cell Line, Tumor ; Cell Proliferation/drug effects ; Cells, Cultured ; Cytokines/metabolism ; Fibroblasts/metabolism ; Fibroblasts/pathology* ; Gene Expression ; Humans ; Immunohistochemistry ; Interleukin-1alpha/genetics ; Interleukin-1alpha/metabolism* ; Interleukin-1alpha/pharmacology ; Kaplan-Meier Estimate ; Male ; Mice, Inbred BALB C ; Mouth Neoplasms/genetics ; Mouth Neoplasms/metabolism ; Mouth Neoplasms/pathology* ; Muscle, Smooth/chemistry ; Prognosis ; Reverse Transcriptase Polymerase Chain Reaction ; Transplantation, Heterologous ; Up-Regulation/drug effects
cancer progression ; carcinoma-associated fibroblasts ; interleukin-1 alpha ; oral squamous cell carcinoma ; reciprocal interaction
Crosstalk between cancer cells and carcinoma-associated fibroblasts (CAFs) has earned recognition as an interaction that plays a pivotal role in carcinogenesis. Thus, we attempted to clarify whether increase in the level of CAFs promotes cancer progression by proportionally enhancing the interaction between cancer cells and CAFs. We first analyzed clinical correlation between the levels of fibroblasts and cancer progression and found that the level of CAFs made a noticeable difference on the prognosis of patients with oral squamous cell carcinoma (OSCC). In vivo animal study also demonstrated that tumor volume depended on the dose of CAFs that was co-injected with OSCC cells. The same tendency was observed in an in vitro study. We also found that interleukin-1α (IL-1α) secreted from OSCC cells had dual effects on CAFs: IL-1α not only promoted the proliferation of CAFs but also upregulated the secretion of cytokines in CAFs such as CCL7, CXCL1, and IL-8. The induction activity of cytokine secretion by IL-1α surpassed that of proliferation in OSCC cells. In summary, we unraveled an important interactive mechanism of carcinogenesis: IL-1α released from carcinoma stimulates the proliferation of CAFs and the simultaneous increase in cytokine secretion from CAFs promotes cancer progression in human OSCC. On the basis of these findings, we propose that the level of CAFs is eligible for being selected as a prognostic factor that will be useful in routine diagnosis. We also propose that blockage of reciprocal interaction between cancer cells and CAFs will provide an insight for developing novel chemotherapeutic strategy.
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2. College of Dentistry (치과대학) > Research Institute (부설연구소) > 1. Journal Papers
1. College of Medicine (의과대학) > BioMedical Science Institute (의생명과학부) > 1. Journal Papers
2. College of Dentistry (치과대학) > Dept. of Oral Pathology (구강병리학교실) > 1. Journal Papers
Yonsei Authors
Kim, Eun Kyoung(김은경)
Kim, Jin(김진)
Park, Young Jin(박영진)
Bae, Jung Yoon(배정윤) ORCID logo https://orcid.org/0000-0001-8342-6987
Lee, Doo Young(이두영)
Zhang, Xiang Lan(장향란)
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