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原花青素 B2 通过血管内皮生长因子 (VEGF)/VEGF 受体 2 (VEGFR2) 通路抑制口腔鳞状细胞癌细胞的血管生成和细胞生长。

Procyanidin B2 inhibits angiogenesis and cell growth in oral squamous cell carcinoma cells through the vascular endothelial growth factor (VEGF)/VEGF receptor 2 (VEGFR2) pathway.

机构信息

Department of Stomatology, The First Affiliated Hosital of Gannan Medical University, Ganzhou, Jiangxi, China.

Department of Oral Surgery, Daqing Longnan Hospital, Daqing, Heilongjiang, China.

出版信息

Bioengineered. 2022 Mar;13(3):6500-6508. doi: 10.1080/21655979.2022.2033013.

Abstract

This study aimed to explore the therapy role of procyanidin B2 (PB2) in inhibiting angiogenesis and cell growth in oral squamous cell carcinoma. After oral mucosa epithelial cell (OMEC) and human oral squamous cell carcinoma (OSCC) cell line (SCC-25) were treated with PB2 or SCC-25 were treated with PB2 and rhVEGF, cell counting kit-8 (CCK-8) assay was used to determine the cell viability. The apoptosis, migration, invasion and angiogenesis of SCC-25 after indicated treatment were detected by Tunel, wound healing, transwell and tube formation assays. The protein expression related to apoptosis, metastasis and epithelial-mesenchymal transition (EMT) and changed expression of vascular endothelial growth factor (VEGF)/VEGF receptor 2 (VEGFR2) signaling was analyzed by Western blot. As a result, PB2 inhibited viability, invasion, migration and EMT and promoted apoptosis of SCC-25 cells. In addition, PB2 inhibited VEGF/VEGFR2 signaling and tumor itangiogenesis in OSCC. As expected, activation of VEGF/VEGFR2 signaling suppressed the effect of PB2 on growth and metastasis of OSCC cells. In conclusion, PB2 inhibited the VEGF/VEGFR2 pathway to suppress the angiogenesis and cell growth of SCC-25 cells.

摘要

本研究旨在探讨原花青素 B2(PB2)在抑制口腔鳞状细胞癌血管生成和细胞生长中的治疗作用。用 PB2 处理口腔黏膜上皮细胞(OMEC)和人口腔鳞状细胞癌细胞系(SCC-25)后,或用 PB2 和 rhVEGF 处理 SCC-25 后,用细胞计数试剂盒-8(CCK-8)测定细胞活力。通过 Tunel、划痕愈合、Transwell 和管形成测定法检测经指示处理后 SCC-25 的细胞凋亡、迁移、侵袭和血管生成。通过 Western blot 分析与凋亡、转移和上皮-间充质转化(EMT)相关的蛋白表达以及血管内皮生长因子(VEGF)/VEGF 受体 2(VEGFR2)信号改变的表达。结果表明,PB2 抑制 SCC-25 细胞的活力、侵袭、迁移和 EMT,并促进细胞凋亡。此外,PB2 抑制 OSCC 中的 VEGF/VEGFR2 信号和肿瘤血管生成。正如预期的那样,VEGF/VEGFR2 信号的激活抑制了 PB2 对 OSCC 细胞生长和转移的作用。总之,PB2 通过抑制 VEGF/VEGFR2 通路抑制 SCC-25 细胞的血管生成和细胞生长。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/e071/8973926/e78ce65bd225/KBIE_A_2033013_UF0001_OC.jpg

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