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骨膜蛋白:一种可能参与肿瘤对抗血管生成治疗的中介物?

Periostin: a putative mediator involved in tumour resistance to anti-angiogenic therapy?

机构信息

Center for the Study of Liver Cancer and Department of Hepatic Surgery, Anhui Provincial Hospital, Anhui Medical University, Hefei, Peoples Republic of China.

出版信息

Cell Biol Int. 2011 Nov;35(11):1085-8. doi: 10.1042/CBI20110171.

DOI:10.1042/CBI20110171
PMID:21999314
Abstract

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.

摘要

尽管在开发用于癌症治疗的抗血管生成药物方面取得了进展,但癌症患者的生存时间仍然相当有限。抗血管生成治疗的一个主要障碍是耐药性的出现。了解肿瘤逃避抗血管生成治疗的分子机制对于提高治疗效果很有价值。靶向血液供应通常会导致肿瘤缺氧反应,触发一系列适应性变化,导致耐药表型。骨膜蛋白是一种分泌型 ECM(细胞外基质)蛋白,主要在缺氧应激下由 CAFs(癌相关成纤维细胞)产生。由于 CAFs 与肿瘤对血管生成阻断的耐药性偶然相关,并且骨膜蛋白可以影响肿瘤生物学的许多方面,我们假设骨膜蛋白可能是癌症治疗中抗血管生成耐药性的关键介质。这一假设间接得到以下事实的支持:(a) 高水平的骨膜蛋白促进肿瘤血管生成;(b) 骨膜蛋白在缺氧条件下提高癌细胞的存活率;和 (c) 骨膜蛋白的遗传调节诱导 EMT(上皮-间充质转化),并增强癌细胞的侵袭和转移,这代表了逃避抗癌治疗的一种机制。对这一假设的验证将更深入地了解耐药机制,并为改善抗血管生成治疗的治疗效果提供依据。

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引用本文的文献

1
Cancer-associated fibroblast regulation of tumor neo-angiogenesis as a therapeutic target in cancer.癌症相关成纤维细胞对肿瘤新生血管生成的调控作为癌症治疗靶点
Oncol Lett. 2019 Mar;17(3):3055-3065. doi: 10.3892/ol.2019.9973. Epub 2019 Jan 25.
2
High-level expression of periostin is closely related to metastatic potential and poor prognosis of hepatocellular carcinoma.骨膜蛋白的高水平表达与肝癌的转移潜能和不良预后密切相关。
Med Oncol. 2013 Mar;30(1):385. doi: 10.1007/s12032-012-0385-7. Epub 2012 Dec 30.
3
Cancer stem cell-related gene periostin: a novel prognostic marker for breast cancer.
癌干细胞相关基因 periostin:乳腺癌的一种新型预后标志物。
PLoS One. 2012;7(10):e46670. doi: 10.1371/journal.pone.0046670. Epub 2012 Oct 9.
4
Controlling escape from angiogenesis inhibitors.控制抗血管生成抑制剂的逃逸。
Nat Rev Cancer. 2012 Oct;12(10):699-709. doi: 10.1038/nrc3366.