胰腺癌是非常致命和难以治疗的。低氧状况的存在已经被证明会增加癌症发生和扩散的可能性。胰管腺癌（PDAC/PC）由于早期转移的高发生率，传统上被视为一种高度致命的癌症形式。间质/导管周围纤维化通常很厚且胶原质，胰星型细胞是主要来源（PSCs）。癌细胞和其他间质细胞与PSC相互作用，促进疾病发展。肝细胞生长因子（HGF）/c-MET途径被提出作为介导此相互作用的生长因子机制。人类生长因子（HGF）由胰星型细胞（PSCs）分泌，其受体c-MET由胰腺癌细胞和内皮细胞产生。缺氧在恶性肿瘤中经常发生，特别是胰腺癌（PC）。缺氧由于无限的肿瘤发展并促进生存、进展和侵袭而发生。缺氧正成为胰腺癌的重要驱动因素和治疗靶点，因为其缺氧微环境已经被定义。最近癌症生物学的突破表明，缺氧促进肿瘤增殖、侵略性和治疗耐药性。缺氧诱导因子（HIFs）稳定缺氧信号。缺氧cMet是胰腺肿瘤微环境的关键组成部分，其还具有纤维化反应，缺氧促进和调节。c-Met是一种酪氨酸-蛋白激酶。简单来说，人类MET基因编码一种叫做肝细胞生长因子受体（HGFR）的蛋白质。大多数癌症肿瘤特别是胰腺癌，缺乏氧气（PC）。由于肿瘤发展不受限制，缺氧发生，积极促进肿瘤生存、进展和侵袭。随着缺氧信号促进侵袭和转移的过程变得清晰，c-MET已经成为胰腺癌恶性程度和潜在药理靶点的重要决定因素。本文提供了有关缺氧和HGF/c-MET在胰腺癌治疗中的最新发现。版权所有©2023年，由Elsevier BV出版。

Pancreatic cancer (PC) is very deadly and difficult to treat. The presence of hypoxia has been shown to increase the probability of cancer developing and spreading. Pancreatic ductal adenocarcinoma (PDAC/PC) has traditionally viewed a highly lethal form of cancer due to its high occurrence of early metastases. Desmoplasia/stroma is often thick and collagenous, with pancreatic stellate cells as the primary source (PSCs). Cancer cells and other stromal cells interact with PSCs, promoting disease development. The hepatocyte growth factor (HGF)/c-MET pathway have been proposed as a growth factor mechanism mediating this interaction. Human growth factor (HGF) is secreted by pancreatic stellate cells (PSCs), and its receptor, c-MET, is generated by pancreatic cancer cells and endothelial cells. Hypoxia is frequent in malignant tumors, particularly pancreatic (PC). Hypoxia results from limitless tumor development and promotes survival, progression, and invasion. Hypoxic is becoming a critical driver and therapeutic target of pancreatic cancer as its hypoxia microenvironment is defined. Recent breakthroughs in cancer biology show that hypoxia promotes tumor proliferation, aggressiveness, and therapeutic resistance. Hypoxia-inducible factors (HIFs) stabilize hypoxia signaling. Hypoxia cMet is a key component of pancreatic tumor microenvironments, which also have a fibrotic response, that hypoxia, promotes and modulates. c-Met is a tyrosine-protein kinase. As describe it simply, the MET gene in humans' codes for a protein called hepatocyte growth factor receptor (HGFR). Most cancerous tumors and pancreatic cancer in particular, suffer from a lack of oxygen (PC). Due to unrestrained tumor development, hypoxia develops, actively contributing to tumor survival, progression, and invasion. As the processes by which hypoxia signaling promotes invasion and metastasis become clear, c-MET has emerged as an important determinant of pancreatic cancer malignancy and a potential pharmacological target. This manuscript provides the most current findings on the role of hypoxia and HGF/c-MET expression in the treatment of pancreatic cancer.Copyright © 2023. Published by Elsevier B.V.