Duxiong Cai1, Chunji Chen2, Yexiong Su1, Yan Tan1, Xuyue Lin1, Rong Xing1. 1. Department of Gastroenterology, The First Affiliated Hospital of Hainan Medical University, Haikou, China. 2. Department of Pathology, Hainan Provincial People's Hospital, Haikou, China.
Abstract
Background: This study aimed to investigate the roles of leucine-rich alpha-2-glycoprotein 1 (LRG1) in regulating angiogenesis during pancreatic cancer (PC) pathogenesis. Methods: LRG1 expression in tissues was detected by qRT-PCR and immunohistochemistry. LRG1 in BxPC-3 and Capan-2 cells was knocked down or overexpressed. Cell viability and the migration and invasion abilities of cells were analyzed using the Cell Counting Kit-8 (CCK-8) assay and Transwell system, respectively. Interleukin-1 beta (IL-1β), IL-18, and vascular endothelial growth factor A (VEGFA) contents in cell culture were measured by ELISA, and the angiogenesis of HUVECs was assessed by the in vitro tube formation assay. In vitro LRG1 expression in BxPC-3 and Capan-2 cells was determined using immunofluorescence. Results: The results showed that LRG1 expression was significantly increased in pancreatic cancer tissues and cell lines. LRG1 knockdown inhibited the viability, migration, invasion, and IL-1β and IL-18 synthesis of BxPC-3 and Capan-2 cells. VEGFA synthesis in BxPC-3 and Capan-2 cells was also inhibited by LRG1 knockdown, which caused impaired tube formation of co-cultured HUVECs. LRG1 overexpression enhanced the viability, migration, and invasion of BxPC-3 and Capan-2 cells, also causing elevated tube formation of HUVECs and IL-1β and IL-18 synthesis in co-cultures of HUVECs and BxPC-3 or Capan-2 cells. Silencing of VEGF receptor (VEGFR) abrogated the enhanced tube formation and IL-1β and IL-18 synthesis in HUVECs co-cultured with BxPC-3 or Capan-2 cells overexpressing LRG1. Conclusions: In conclusion, LRG1, which is highly expressed in pancreatic cancer cells, promotes inflammatory factor synthesis and the angiogenesis of HUVECs though activating the VEGFR signaling pathway. 2022 Journal of Gastrointestinal Oncology. All rights reserved.
Background: This study aimed to investigate the roles of leucine-rich alpha-2-glycoprotein 1 (LRG1) in regulating angiogenesis during pancreatic cancer (PC) pathogenesis. Methods: LRG1 expression in tissues was detected by qRT-PCR and immunohistochemistry. LRG1 in BxPC-3 and Capan-2 cells was knocked down or overexpressed. Cell viability and the migration and invasion abilities of cells were analyzed using the Cell Counting Kit-8 (CCK-8) assay and Transwell system, respectively. Interleukin-1 beta (IL-1β), IL-18, and vascular endothelial growth factor A (VEGFA) contents in cell culture were measured by ELISA, and the angiogenesis of HUVECs was assessed by the in vitro tube formation assay. In vitro LRG1 expression in BxPC-3 and Capan-2 cells was determined using immunofluorescence. Results: The results showed that LRG1 expression was significantly increased in pancreatic cancer tissues and cell lines. LRG1 knockdown inhibited the viability, migration, invasion, and IL-1β and IL-18 synthesis of BxPC-3 and Capan-2 cells. VEGFA synthesis in BxPC-3 and Capan-2 cells was also inhibited by LRG1 knockdown, which caused impaired tube formation of co-cultured HUVECs. LRG1 overexpression enhanced the viability, migration, and invasion of BxPC-3 and Capan-2 cells, also causing elevated tube formation of HUVECs and IL-1β and IL-18 synthesis in co-cultures of HUVECs and BxPC-3 or Capan-2 cells. Silencing of VEGF receptor (VEGFR) abrogated the enhanced tube formation and IL-1β and IL-18 synthesis in HUVECs co-cultured with BxPC-3 or Capan-2 cells overexpressing LRG1. Conclusions: In conclusion, LRG1, which is highly expressed in pancreatic cancer cells, promotes inflammatory factor synthesis and the angiogenesis of HUVECs though activating the VEGFR signaling pathway. 2022 Journal of Gastrointestinal Oncology. All rights reserved.
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