The host microenvironment influences prostate cancer invasion, systemic spread, bone colonization, and osteoblastic metastasis.
The host microenvironment influences prostate cancer invasion, systemic spread, bone colonization, and osteoblastic metastasis.
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DOI：
10.3389/fonc.2014.00364
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发表时间：
2014
影响因子：
4.7
通讯作者：
Miranti CK
中科院分区：
文献类型：
--
作者：
Ganguly SS;Li X;Miranti CK
前列腺癌（PCa）是全球男性癌症死亡的第二大原因。大多数PCa死亡是由于成骨细胞骨转移。什么触发PCa转移到骨和什么导致成骨细胞病变仍然没有答案。PCa转移的主要贡献者是宿主微环境。在这里，我们讨论了原发性肿瘤微环境如何通过整合素，细胞外蛋白酶和瞬时上皮间质转化（EMT）影响PCa转移，以促进PCa进展，侵袭和转移。我们讨论了骨微环境如何影响转移;趋化细胞因子有利于骨归巢，粘附分子促进定植，骨源性信号诱导成骨细胞病变。需要完全概括人类PCa从原发性肿瘤到骨转移的进展的动物模型来理解导致骨转移的PCa病理生理学。更好地描绘涉及PCa骨转移的特定过程是预防或治疗转移性PCa所必需的。关注肿瘤微环境的治疗方案可以添加到PCa药典中。
Prostate cancer (PCa) is the second leading cause of cancer death in men worldwide. Most PCa deaths are due to osteoblastic bone metastases. What triggers PCa metastasis to the bone and what causes osteoblastic lesions remain unanswered. A major contributor to PCa metastasis is the host microenvironment. Here, we address how the primary tumor microenvironment influences PCa metastasis via integrins, extracellular proteases, and transient epithelia-mesenchymal transition (EMT) to promote PCa progression, invasion, and metastasis. We discuss how the bone-microenvironment influences metastasis; where chemotactic cytokines favor bone homing, adhesion molecules promote colonization, and bone-derived signals induce osteoblastic lesions. Animal models that fully recapitulate human PCa progression from primary tumor to bone metastasis are needed to understand the PCa pathophysiology that leads to bone metastasis. Better delineation of the specific processes involved in PCa bone metastasize is needed to prevent or treat metastatic PCa. Therapeutic regimens that focus on the tumor microenvironment could add to the PCa pharmacopeia.