Institute for Cell Engineering, School of Medicine, Johns Hopkins University, Baltimore, MD, United States; Division of Pediatric Oncology, Sidney Kimmel Comprehensive Cancer Center at Johns Hopkins, Baltimore, MD, United States.
Biochimie. 2013 Dec;95(12):2235-45. doi: 10.1016/j.biochi.2013.05.010. Epub 2013 Jun 5.
Cancer treatment generally relies on tumor ablative techniques that can lead to major functional or disfiguring defects. These post-therapy impairments require the development of safe regenerative therapy strategies during cancer remission. Many current tissue repair approaches exploit paracrine (immunomodulatory, pro-angiogenic, anti-apoptotic and pro-survival effects) or restoring (functional or structural tissue repair) properties of mesenchymal stem/stromal cells (MSC). Yet, a major concern in the application of regenerative therapies during cancer remission remains the possible triggering of cancer recurrence. Tumor relapse implies the persistence of rare subsets of tumor-initiating cancer cells which can escape anti-cancer therapies and lie dormant in specific niches awaiting reactivation via unknown stimuli. Many of the components required for successful regenerative therapy (revascularization, immunosuppression, cellular homing, tissue growth promotion) are also critical for tumor progression and metastasis. While bi-directional crosstalk between tumorigenic cells (especially aggressive cancer cell lines) and MSC (including tumor stroma-resident populations) has been demonstrated in a variety of cancers, the effects of local or systemic MSC delivery for regenerative purposes on persisting cancer cells during remission remain controversial. Both pro- and anti-tumorigenic effects of MSC have been reported in the literature. Our own data using breast cancer clinical isolates have suggested that dormant-like tumor-initiating cells do not respond to MSC signals, unlike actively dividing cancer cells which benefited from the presence of supportive MSC. The secretome of MSC isolated from various tissues may partially diverge, but it includes a core of cytokines (i.e. CCL2, CCL5, IL-6, TGFβ, VEGF), which have been implicated in tumor growth and/or metastasis. This article reviews published models for studying interactions between MSC and cancer cells with a focus on the impact of MSC secretome on cancer cell activity, and discusses the implications for regenerative therapy after cancer.
癌症治疗通常依赖于肿瘤消融技术,这些技术可能导致主要的功能或毁容缺陷。这些治疗后损伤需要在癌症缓解期间开发安全的再生治疗策略。许多当前的组织修复方法利用间充质干细胞/基质细胞(MSC)的旁分泌(免疫调节、促血管生成、抗凋亡和生存促进作用)或恢复(功能或结构组织修复)特性。然而,在癌症缓解期间应用再生疗法的一个主要关注点仍然是癌症复发的可能触发。肿瘤复发意味着肿瘤起始癌细胞的罕见亚群仍然存在,这些细胞可以逃避抗癌治疗,并在特定的龛位中休眠,等待通过未知刺激重新激活。成功再生治疗所需的许多成分(再血管化、免疫抑制、细胞归巢、组织生长促进)对于肿瘤进展和转移也是至关重要的。虽然在各种癌症中已经证明了肿瘤发生细胞(特别是侵袭性癌细胞系)与 MSC(包括肿瘤基质驻留群体)之间的双向串扰,但在缓解期间局部或系统递送 MSC 以进行再生对持续存在的癌细胞的影响仍然存在争议。MSC 的促肿瘤和抗肿瘤作用都在文献中有所报道。我们自己使用乳腺癌临床分离物的数据表明,休眠样肿瘤起始细胞不会对 MSC 信号做出反应,而活跃分裂的癌细胞则受益于支持性 MSC 的存在。从各种组织中分离的 MSC 的分泌组可能部分分化,但它包括一组细胞因子(即 CCL2、CCL5、IL-6、TGFβ、VEGF),这些细胞因子与肿瘤生长和/或转移有关。本文综述了已发表的研究 MSC 与癌细胞相互作用的模型,重点讨论了 MSC 分泌组对癌细胞活性的影响,并讨论了癌症后再生治疗的意义。