Center of Cancer Systems Biology, Steward Research & Specialty Projects Corp., St. Elizabeth's Medical Center, Tufts University School of Medicine, Boston, Massachusetts, United States of America.
PLoS One. 2012;7(8):e44001. doi: 10.1371/journal.pone.0044001. Epub 2012 Aug 31.
Tumor dormancy refers to a critical stage in cancer development in which tumor cells remain occult for a prolonged period of time until they eventually progress and become clinically apparent. We previously showed that the switch of dormant tumors to fast-growth is angiogenesis dependent and requires a stable transcriptional reprogramming in tumor cells. Considering microRNAs (miRs) as master regulators of transcriptome, we sought to investigate their role in the control of tumor dormancy. We report here the identification of a consensus set of 19 miRs that govern the phenotypic switch of human dormant breast carcinoma, glioblastoma, osteosarcoma, and liposarcoma tumors to fast-growth. Loss of expression of dormancy-associated miRs (DmiRs, 16/19) was the prevailing regulation pattern correlating with the switch of dormant tumors to fast-growth. The expression pattern of two DmiRs (miR-580 and 190) was confirmed to correlate with disease stage in human glioma specimens. Reconstitution of a single DmiR (miR-580, 588 or 190) led to phenotypic reversal of fast-growing angiogenic tumors towards prolonged tumor dormancy. Of note, 60% of angiogenic glioblastoma and 100% of angiogenic osteosarcoma over-expressing miR190 remained dormant during the entire observation period of ∼ 120 days. Next, the ability of DmiRs to regulate angiogenesis and dormancy-associated genes was evaluated. Transcriptional reprogramming of tumors via DmiR-580, 588 or 190 over-expression resulted in downregulation of pro-angiogenic factors such as TIMP-3, bFGF and TGFalpha. In addition, a G-CSF independent downregulation of Bv8 was found as a common target of all three DmiRs and correlated with decreased tumor recruitment of bone marrow-derived CD11b+ Gr-1+ myeloid cells. In contrast, antiangiogenic and dormancy promoting pathways such as EphA5 and Angiomotin were upregulated in DmiR over-expressing tumors. This work suggests novel means to reverse the malignant tumor phenotype into an asymptomatic dormant state and may provide promising targets for early detection or prevention of cancer.
肿瘤休眠是癌症发展的一个关键阶段,在此阶段,肿瘤细胞会在很长一段时间内保持隐匿状态,直到最终进展并表现出临床症状。我们之前曾表明,休眠肿瘤向快速生长的转变依赖于血管生成,并需要肿瘤细胞中稳定的转录重编程。考虑到 microRNAs(miRs)作为转录组的主要调控因子,我们试图研究它们在控制肿瘤休眠中的作用。我们在此报告了一组识别共识的 19 个 miRs,它们控制着人类休眠乳腺癌、神经胶质瘤、骨肉瘤和脂肪肉瘤肿瘤向快速生长的表型转变。休眠相关 miRs(DmiRs,16/19)的表达缺失是与休眠肿瘤向快速生长转变相关的主要调控模式。两种 DmiRs(miR-580 和 190)的表达模式在人类神经胶质瘤标本中被证实与疾病阶段相关。单个 DmiR(miR-580、588 或 190)的重建导致快速生长的血管生成肿瘤向长期肿瘤休眠的表型逆转。值得注意的是,在大约 120 天的整个观察期内,过表达 miR190 的血管生成神经胶质瘤和 100%的血管生成骨肉瘤中有 60%保持休眠。接下来,评估了 DmiRs 调节血管生成和休眠相关基因的能力。通过 DmiR-580、588 或 190 的过表达对肿瘤进行转录重编程,导致促血管生成因子如 TIMP-3、bFGF 和 TGFalpha 的下调。此外,发现 Bv8 的 G-CSF 非依赖性下调是所有三种 DmiR 的共同靶标,与骨髓来源的 CD11b+Gr-1+髓样细胞对肿瘤的募集减少相关。相反,在 DmiR 过表达的肿瘤中,抗血管生成和促进休眠的途径,如 EphA5 和 Angiomotin,被上调。这项工作提出了将恶性肿瘤表型逆转到无症状休眠状态的新方法,可能为癌症的早期检测或预防提供有前途的靶点。