European journal of medical research · 2025
CAF derived IL-33 mediated EMT to promote the metastasis of LSCC cells.
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Yang Liyun, Zhou Jieyu, Chen Shiyan, Wang Yanmei, Huang Shuixian
Аннотация
BACKGROUND: The metastasis of laryngeal squamous cell carcinoma (LSCC) is not only caused by the tumor itself but is also closely related to cancer-associated fibroblasts (CAFs). The epithelial-mesenchymal transition (EMT) serves as a key event during its metastasis. However, the specific mechanisms underlying LSCC metastasis remain uncertain.
METHODS: A wound healing assay was utilized to evaluate the migratory capacity of LSCC cells (TU686 and TU212 cells). Immunofluorescence staining and Western blot analysis were conducted to demonstrate the expression levels of associated proteins. Migration and invasion assays were employed to assess the migration and invasion abilities of LSCC cells in vitro. A nude mouse metastasis model was used to detect LSCC metastasis in vivo.
RESULTS: Our results revealed that interleukin-33 (IL-33) enhanced the migratory, invasive, and EMT capabilities of LSCC cells. In the co-culture model of LSCC cells and CAFs, silencing the expression of IL-33 inhibited the migratory, invasive, and metastasis potential of LSCC cells both in vitro and in vivo.
CONCLUSION: IL-33 derived from CAFs mediates EMT to promote the metastasis of LSCC cells. The findings of our study not only provide a new mechanism for the activation of CAFs and the metastasis of LSCC but also offer theoretical significance and application value for more effective prevention and treatment strategies in clinical practice.
METHODS: A wound healing assay was utilized to evaluate the migratory capacity of LSCC cells (TU686 and TU212 cells). Immunofluorescence staining and Western blot analysis were conducted to demonstrate the expression levels of associated proteins. Migration and invasion assays were employed to assess the migration and invasion abilities of LSCC cells in vitro. A nude mouse metastasis model was used to detect LSCC metastasis in vivo.
RESULTS: Our results revealed that interleukin-33 (IL-33) enhanced the migratory, invasive, and EMT capabilities of LSCC cells. In the co-culture model of LSCC cells and CAFs, silencing the expression of IL-33 inhibited the migratory, invasive, and metastasis potential of LSCC cells both in vitro and in vivo.
CONCLUSION: IL-33 derived from CAFs mediates EMT to promote the metastasis of LSCC cells. The findings of our study not only provide a new mechanism for the activation of CAFs and the metastasis of LSCC but also offer theoretical significance and application value for more effective prevention and treatment strategies in clinical practice.