<p>Angiogenesis is a crucial process in cancer progression, particularly in malignant tumors, as it facilitates tumor growth and metastasis by generating new blood vessels that supply vital nutrients and oxygen. However, the regulatory mechanism governing the development of these tumor neo-vessels by endothelial cells is still not fully understood. This study investigates the role of long-form collapsin response mediator protein-1 (LCRMP-1) in angiogenesis within non-small cell lung cancer (NSCLC). Through in vitro tube formation, in vivo plaque angiogenesis assays, and immunohistochemical staining, we identify SERPINE1 as a crucial factor regulated by LCRMP-1. Mechanistically, LCRMP-1 functions as a co-transcriptional factor, enhancing the expression of SERPINE1 through its interactions with TP53. This enhancement promotes the secretion of SERPINE1, alters the tumor microenvironment, and assists endothelial cells in the formation of new blood vessels, thereby further advancing the progression of NSCLC.</p><p></p>

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LCRMP-1 induces tumor angiogenesis by transcriptionally upregulating SERPINE1 in lung adenocarcinoma

  • Yuan-Ling Hsu,
  • Pei-Fang Hung,
  • Chi-Chung Wang,
  • Yih-Leong Chang,
  • Chen-Tu Wu,
  • Pei-Shan Wu,
  • Xuan-Ren Chen,
  • Tse-Ming Hong,
  • Pan-Chyr Yang,
  • Szu-Hua Pan

摘要

Angiogenesis is a crucial process in cancer progression, particularly in malignant tumors, as it facilitates tumor growth and metastasis by generating new blood vessels that supply vital nutrients and oxygen. However, the regulatory mechanism governing the development of these tumor neo-vessels by endothelial cells is still not fully understood. This study investigates the role of long-form collapsin response mediator protein-1 (LCRMP-1) in angiogenesis within non-small cell lung cancer (NSCLC). Through in vitro tube formation, in vivo plaque angiogenesis assays, and immunohistochemical staining, we identify SERPINE1 as a crucial factor regulated by LCRMP-1. Mechanistically, LCRMP-1 functions as a co-transcriptional factor, enhancing the expression of SERPINE1 through its interactions with TP53. This enhancement promotes the secretion of SERPINE1, alters the tumor microenvironment, and assists endothelial cells in the formation of new blood vessels, thereby further advancing the progression of NSCLC.