Tissue & cell · 2026
CAP2 promotes skin cutaneous melanoma progression by targeting epithelial-mesenchymal transition-like processes through the TLR4/NF-κB pathway.
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Li Lianchu, Zhao Zhengnan, Fang Yi, Zhao Zhuo, Zhang Yongxu, Chen Haoran, Ye Zhiqiang, Liang Haidong
Аннотация
BACKGROUND: CAP2 influences cellular behavior by regulating actin dynamics, and it is upregulated in malignant melanoma. The investigation intended to explore the mechanism of CAP2 in skin cutaneous melanoma (SKCM).
METHODS: Based on TCGA-SKCM and GTEx databases, the expression, clinical relevance, and potential molecular functions of CAP2 in SKCM were investigated using bioinformatics analysis. CAP2 expression in SKCM cell lines and normal cells was detected. CAP2 was knocked down in SKCM models, including A375 cells and subcutaneous nude mouse xenografts, to evaluate its involvement in tumor development and epithelial-mesenchymal transition (EMT)-like processes. TLR4 and p-NF-κB p65 levels were detected by Western blot. Dual-luciferase reporter assay and co-immunoprecipitation were used to explore the interaction between CAP2 and TLR4. TLR4 was overexpressed in SKCM models to further validate the underlying mechanism of CAP2 in SKCM.
RESULTS: Bioinformatics analysis indicated that the high expression of CAP2 in SKCM patients was associated with poor prognosis and had potential diagnostic value. Its function might be correlated with the Toll-like receptor (TLR) pathway. CAP2 was highly expressed in SKCM cell lines. CAP2 knockdown markedly suppressed tumor progression and EMT-like processes both in vivo and in vitro. Additionally, CAP2 knockdown significantly inhibited TLR4/NF-κB pathway. Notably, CAP2 regulated the activation of TLR4 at the transcriptional level. Overexpression of TLR4 partially altered the effects of CAP2 knockdown.
CONCLUSION: CAP2 accelerates SKCM development by promoting EMT-like processes through TLR4/NF-κB pathway. CAP2 may be a novel biomarker for SKCM management. Nevertheless, these findings require further validation in clinical studies.
METHODS: Based on TCGA-SKCM and GTEx databases, the expression, clinical relevance, and potential molecular functions of CAP2 in SKCM were investigated using bioinformatics analysis. CAP2 expression in SKCM cell lines and normal cells was detected. CAP2 was knocked down in SKCM models, including A375 cells and subcutaneous nude mouse xenografts, to evaluate its involvement in tumor development and epithelial-mesenchymal transition (EMT)-like processes. TLR4 and p-NF-κB p65 levels were detected by Western blot. Dual-luciferase reporter assay and co-immunoprecipitation were used to explore the interaction between CAP2 and TLR4. TLR4 was overexpressed in SKCM models to further validate the underlying mechanism of CAP2 in SKCM.
RESULTS: Bioinformatics analysis indicated that the high expression of CAP2 in SKCM patients was associated with poor prognosis and had potential diagnostic value. Its function might be correlated with the Toll-like receptor (TLR) pathway. CAP2 was highly expressed in SKCM cell lines. CAP2 knockdown markedly suppressed tumor progression and EMT-like processes both in vivo and in vitro. Additionally, CAP2 knockdown significantly inhibited TLR4/NF-κB pathway. Notably, CAP2 regulated the activation of TLR4 at the transcriptional level. Overexpression of TLR4 partially altered the effects of CAP2 knockdown.
CONCLUSION: CAP2 accelerates SKCM development by promoting EMT-like processes through TLR4/NF-κB pathway. CAP2 may be a novel biomarker for SKCM management. Nevertheless, these findings require further validation in clinical studies.