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Abstract：
BACKGROUND: The tetraspanin family plays a pivotal role in the genesis of migrasomes, and Tetraspanin CD151 is also implicated in neovascularization within tumorous contexts. Nevertheless, research pertaining to the involvement of CD151 in hepatocellular carcinoma (HCC) neovascularization and its association with migrasomes remains inadequate.
METHODS: To investigate the correlation between CD151 and migrasome marker TSPAN4 in liver cancer, we conducted database analysis using clinical data from HCC patients. Expression levels of CD151 were assessed in HCC tissues and correlated with patient survival outcomes. In vitro experiments were performed using HCC cell lines to evaluate the impact of CD151 expression on migrasome formation and cellular invasiveness. Cell lines with altered CD151 expression levels were utilized to study migrasome generation and in vitro invasion capabilities. Additionally, migrasome function was explored through cellular aggregation assays and phagocytosis studies. Subsequent VEGF level analysis and tissue chip experiments further confirmed the role of CD151 in mediating migrasome involvement in angiogenesis and cellular signal transduction.
RESULTS: Our study revealed a significant correlation between CD151 expression and migrasome marker TSPAN4 in liver cancer, based on database analysis of clinical samples. High expression levels of CD151 were closely associated with poor survival outcomes in HCC patients. Experimentally, decreased CD151 expression led to reduced migrasome generation and diminished in vitro invasion capabilities, resulting in attenuated in vivo metastatic potential. Migrasomes were demonstrated to facilitate cellular aggregation and phagocytosis, thereby promoting cellular invasiveness. Furthermore, VEGF-enriched migrasomes were implicated in signaling and angiogenesis, accelerating HCC progression.
CONCLUSIONS: In summary, our findings support the notion that elevated CD151 expression promotes migrasome formation, and migrasomes play a pivotal role in the invasiveness and angiogenesis of liver cancer cells, thereby facilitating HCC progression. This finding implies that migrasomes generated by elevated CD151 expression may constitute a promising high-priority target for anti-angiogenic therapy in HCC, offering crucial insights for the in-depth exploration of migrasome function and a renewed comprehension of the mechanism underlying liver cancer metastasis.
METHODS: To investigate the correlation between CD151 and migrasome marker TSPAN4 in liver cancer, we conducted database analysis using clinical data from HCC patients. Expression levels of CD151 were assessed in HCC tissues and correlated with patient survival outcomes. In vitro experiments were performed using HCC cell lines to evaluate the impact of CD151 expression on migrasome formation and cellular invasiveness. Cell lines with altered CD151 expression levels were utilized to study migrasome generation and in vitro invasion capabilities. Additionally, migrasome function was explored through cellular aggregation assays and phagocytosis studies. Subsequent VEGF level analysis and tissue chip experiments further confirmed the role of CD151 in mediating migrasome involvement in angiogenesis and cellular signal transduction.
RESULTS: Our study revealed a significant correlation between CD151 expression and migrasome marker TSPAN4 in liver cancer, based on database analysis of clinical samples. High expression levels of CD151 were closely associated with poor survival outcomes in HCC patients. Experimentally, decreased CD151 expression led to reduced migrasome generation and diminished in vitro invasion capabilities, resulting in attenuated in vivo metastatic potential. Migrasomes were demonstrated to facilitate cellular aggregation and phagocytosis, thereby promoting cellular invasiveness. Furthermore, VEGF-enriched migrasomes were implicated in signaling and angiogenesis, accelerating HCC progression.
CONCLUSIONS: In summary, our findings support the notion that elevated CD151 expression promotes migrasome formation, and migrasomes play a pivotal role in the invasiveness and angiogenesis of liver cancer cells, thereby facilitating HCC progression. This finding implies that migrasomes generated by elevated CD151 expression may constitute a promising high-priority target for anti-angiogenic therapy in HCC, offering crucial insights for the in-depth exploration of migrasome function and a renewed comprehension of the mechanism underlying liver cancer metastasis.
摘要：
背景：四跨膜蛋白家族在迁移体的发生中起关键作用，TetraspaninCD151也与肿瘤环境中的新生血管形成有关。然而，关于CD151参与肝细胞癌(HCC)新生血管形成及其与迁移体相关的研究仍然不足.
方法：为了探讨CD151与迁移体标志物TSPAN4在肝癌中的相关性，我们使用HCC患者的临床数据进行了数据库分析.在HCC组织中评估CD151的表达水平，并与患者的生存结果相关。使用HCC细胞系进行体外实验以评估CD151表达对迁移体形成和细胞侵袭性的影响。使用具有改变的CD151表达水平的细胞系来研究迁移体的产生和体外侵袭能力。此外,通过细胞聚集试验和吞噬作用研究探讨了迁移体的功能.随后的VEGF水平分析和组织芯片实验进一步证实了CD151在介导迁移体参与血管生成和细胞信号转导中的作用。
结果：我们的研究揭示了CD151表达和迁移体标志物TSPAN4在肝癌中的显著相关性，基于临床样本的数据库分析。CD151的高表达水平与HCC患者的不良生存预后密切相关。实验上,CD151表达减少导致偏头痛小体生成减少，体外侵袭能力减弱，导致体内转移潜能减弱。迁移体被证明有助于细胞聚集和吞噬作用，从而促进细胞侵袭。此外，富含VEGF的迁移体与信号传导和血管生成有关，加速HCC进展。
结论：总之，我们的研究结果支持CD151表达升高促进迁移体形成的观点，迁移体在肝癌细胞的侵袭和血管生成中起着关键作用，从而促进HCC进展。这一发现表明，由CD151表达升高产生的迁移体可能构成HCC抗血管生成治疗的有希望的高优先级靶标。为深入探索迁移体功能和重新理解肝癌转移的潜在机制提供了重要见解。
方法：为了探讨CD151与迁移体标志物TSPAN4在肝癌中的相关性，我们使用HCC患者的临床数据进行了数据库分析.在HCC组织中评估CD151的表达水平，并与患者的生存结果相关。使用HCC细胞系进行体外实验以评估CD151表达对迁移体形成和细胞侵袭性的影响。使用具有改变的CD151表达水平的细胞系来研究迁移体的产生和体外侵袭能力。此外,通过细胞聚集试验和吞噬作用研究探讨了迁移体的功能.随后的VEGF水平分析和组织芯片实验进一步证实了CD151在介导迁移体参与血管生成和细胞信号转导中的作用。
结果：我们的研究揭示了CD151表达和迁移体标志物TSPAN4在肝癌中的显著相关性，基于临床样本的数据库分析。CD151的高表达水平与HCC患者的不良生存预后密切相关。实验上,CD151表达减少导致偏头痛小体生成减少，体外侵袭能力减弱，导致体内转移潜能减弱。迁移体被证明有助于细胞聚集和吞噬作用，从而促进细胞侵袭。此外，富含VEGF的迁移体与信号传导和血管生成有关，加速HCC进展。
结论：总之，我们的研究结果支持CD151表达升高促进迁移体形成的观点，迁移体在肝癌细胞的侵袭和血管生成中起着关键作用，从而促进HCC进展。这一发现表明，由CD151表达升高产生的迁移体可能构成HCC抗血管生成治疗的有希望的高优先级靶标。为深入探索迁移体功能和重新理解肝癌转移的潜在机制提供了重要见解。
