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首页> 外文期刊>Cell biology international. >Periostin: a putative mediator involved in tumour resistance to anti-angiogenic therapy?
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Periostin: a putative mediator involved in tumour resistance to anti-angiogenic therapy?

机译：骨膜素：推测的介体参与了肿瘤对抗血管生成治疗的耐药性？

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摘要

Despite advances in the development of anti-angiogenic agents for cancer treatment, the increase in the survival duration of cancer patients is still rather modest. One major obstacle in anti-angiogenic therapy is the emergence of drug resistance. Understanding the molecular mechanisms that enable a tumour to evade anti-angiogenic treatment is valuable to improve therapeutic efficacy. Targeting blood supply usually causes hypoxic responses of tumours that trigger a series of adaptive changes leading to a resistant phenotype. Periostin, a secreted ECM (extracellular matrix) protein, is mainly produced by CAFs (cancer-associated fibroblasts) on hypoxic stress. As CAFs have been casually linked to tumour resistance to angiogenesis blockade and periostin can influence many aspects of tumour biology, we hypothesized that periostin might be a crucial mediator involved anti-angiogenic resistance in cancer treatment. This hypothesis is indirectly supported by the following facts: (a) high levels of periostin promote tumour angiogenesis; (b) periostin improves cancer cell survival under hypoxic conditions; and (c) genetic modulation of periostin induces EMT (epithelial-mesenchymal transition) and enhances cancer cell invasion and metastasis, which represents an escape mechanism from anticancer treatment. Testing and confirmation of this hypothesis will give more insight into the resistance mechanisms and provide the rationale for improvement of therapeutic outcome of anti-angiogenic therapy.
机译：尽管在用于癌症治疗的抗血管生成剂的开发方面取得了进展，但是癌症患者的存活时间的增加仍然相当适度。抗血管生成治疗的主要障碍之一是耐药性的出现。了解使肿瘤能够逃避抗血管生成治疗的分子机制对于提高治疗效果非常重要。靶向血液供应通常会引起肿瘤的低氧反应，从而引发一系列适应性变化，从而导致耐药表型。骨膜素是一种分泌的ECM（细胞外基质）蛋白，主要由CAF（与癌症相关的成纤维细胞）在低氧压力下产生。由于CAF已与肿瘤对血管生成阻滞的抗性偶然相关，并且骨膜素可影响肿瘤生物学的许多方面，因此我们假设骨膜素可能是癌症治疗中涉及抗血管生成抗性的关键介体。以下事实间接支持了这一假设：（a）高水平的骨膜素促进肿瘤血管生成; （b）骨膜素提高了低氧条件下癌细胞的存活率; （c）骨膜素的基因调节诱导EMT（上皮-间质转化）并增强癌细胞的侵袭和转移，这代表了抗癌治疗的逃逸机制。对这一假设的测试和证实将使人们对耐药机制有更多的了解，并为改善抗血管生成疗法的治疗结果提供依据。

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