Haemmerle Monika, Taylor Morgan L, Gutschner Tony, Pradeep Sunila, Cho Min Soon, Sheng Jianting, Lyons Yasmin M, Nagaraja Archana S, Dood Robert L, Wen Yunfei, Mangala Lingegowda S, Hansen Jean M, Rupaimoole Rajesha, Gharpure Kshipra M, Rodriguez-Aguayo Cristian, Yim Sun Young, Lee Ju-Seog, Ivan Cristina, Hu Wei, Lopez-Berestein Gabriel, Wong Stephen T, Karlan Beth Y, Levine Douglas A, Liu Jinsong, Afshar-Kharghan Vahid, Sood Anil K
Department of Gynecologic Oncology and Reproductive Medicine, The University of Texas MD Anderson Cancer Center, Houston, TX, 77030, USA.
Institute of Pathology, Martin-Luther-University Halle-Wittenberg, Halle (Saale), Saxony-Anhalt, 06112, Germany.
Nat Commun. 2017 Aug 21;8(1):310. doi: 10.1038/s41467-017-00411-z.
Thrombocytosis is present in more than 30% of patients with solid malignancies and correlates with worsened patient survival. Tumor cell interaction with various cellular components of the tumor microenvironment including platelets is crucial for tumor growth and metastasis. Although it is known that platelets can infiltrate into tumor tissue, secrete pro-angiogenic and pro-tumorigenic factors and thereby increase tumor growth, the precise molecular interactions between platelets and metastatic cancer cells are not well understood. Here we demonstrate that platelets induce resistance to anoikis in vitro and are critical for metastasis in vivo. We further show that platelets activate RhoA-MYPT1-PP1-mediated YAP1 dephosphorylation and promote its nuclear translocation which induces a pro-survival gene expression signature and inhibits apoptosis. Reduction of YAP1 in cancer cells in vivo protects against thrombocytosis-induced increase in metastasis. Collectively, our results indicate that cancer cells depend on platelets to avoid anoikis and succeed in the metastatic process.Platelets have been associated with increased tumor growth and metastasis but the mechanistic details of this interaction are still unclear. Here the authors show that platelets improve anoikis resistance of cancer cells and increase metastasis by activating Yap through a RhoA/MYPT-PP1 pathway.
血小板增多症存在于超过30%的实体恶性肿瘤患者中,且与患者生存率降低相关。肿瘤细胞与肿瘤微环境的各种细胞成分(包括血小板)之间的相互作用对于肿瘤生长和转移至关重要。虽然已知血小板可浸润肿瘤组织、分泌促血管生成和促肿瘤生成因子,从而促进肿瘤生长,但血小板与转移性癌细胞之间精确的分子相互作用尚不清楚。在此,我们证明血小板在体外诱导对失巢凋亡的抗性,并且在体内对转移至关重要。我们进一步表明,血小板激活RhoA-MYPT1-PP1介导的YAP1去磷酸化并促进其核转位,从而诱导促生存基因表达特征并抑制细胞凋亡。在体内降低癌细胞中的YAP1可防止血小板增多症诱导的转移增加。总体而言,我们的结果表明癌细胞依赖血小板来避免失巢凋亡并在转移过程中成功转移。血小板已被证明与肿瘤生长和转移增加有关,但这种相互作用的机制细节仍不清楚。在此,作者表明血小板通过RhoA/MYPT-PP1途径激活Yap,从而提高癌细胞对失巢凋亡的抗性并增加转移。