Abstract
Pancreatic cancer is a highly malignant digestive system tumor which is the leading cause of cancer-related deaths. The basic and clinical research of pancreatic cancer has made great progress in recent years, and kinds of signaling pathways have been found in the tumorigenesis and progression in pancreatic cancer. The Slit glycoprotein (Slit) and Roundabout receptor (Robo) signaling pathway acts as a neural targeting factor with the axonal remnant, axon guidance, and inhibition of neuronal migration in the nervous system. In recent years, it has been found that the Slit/Robo signaling pathway has different degrees of expression changes in various tumor cells. In different tumor cells, the signaling pathway gene expression is different and regulates tumor angiogenesis, cell invasion, metastasis, and nerve infiltration. Herein, we summarize the mechanisms of the Slit/Robo pathway in the development and progression of pancreatic cancer, in order to have more understanding of the role of Slit/Robo in pancreatic cancer.
Highlights
Pancreatic ductal adenocarcinoma (PDAC), generally known as pancreatic cancer, is a highly lethal malignancy disease
Pancreatic cancer is characterized as aggressive local invasion, early lymphatic and hematogenous dissemination, distant metastasis, and chemotherapeutic resistance. e difficulty of early diagnosis is a major obstacle to long-term survival
Despite extensive research in adjuvant therapy in recent decades, there has been no breakthrough in overall treatment outcomes due to the dense interstitial and chemotherapy resistance of pancreatic cancer. e high invasiveness of pancreatic cancer enables the rapid tumor to grow rapidly and metastasis to the liver, peritoneum, and lungs
Summary
Pancreatic ductal adenocarcinoma (PDAC), generally known as pancreatic cancer, is a highly lethal malignancy disease. In the United States, pancreatic cancer is expected to kill 23,800 men and 21,950 women each year [1,2,3]. E newest statistics showed that the overall 5-year survival rate of pancreatic cancer was about 9% [1]. Pancreatic cancer is characterized as aggressive local invasion, early lymphatic and hematogenous dissemination, distant metastasis, and chemotherapeutic resistance. E high invasiveness of pancreatic cancer enables the rapid tumor to grow rapidly and metastasis to the liver, peritoneum, and lungs. Pancreatic cancer results from the complex interaction of multiple genetic mutations and environmental factors. Enhanced expression and signaling via these pathways lead to increased proliferation, invasion, metastasis, and immune evasion by pancreatic cancer cells
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