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Stem-like Human Breast Cancer Cells Initiate Vasculogenic Mimicry on Matrigel.
Acta Histochemica et Cytochemica ( IF 1.6 ) Pub Date : 2019-01-17 , DOI: 10.1267/ahc.18041
Yuki Izawa 1 , Karin Kashii-Magaribuchi 1 , Kana Yoshida 2 , Mayu Nosaka 2 , Nanami Tsuji 2 , Ai Yamamoto 2 , Kana Kuroyanagi 2 , Kanoko Tono 2 , Misato Tanihata 2 , Moe Imanishi 2 , Momoka Onishi 2 , Mayu Sakiyama 2 , Sana Inoue 2 , Rei Takahashi 1, 2
Affiliation  

Vasculogenic mimicry (VM), referring to vasculogenic structures lined by tumor cells, can be distinguished from angiogenesis, and is responsible for the aggressiveness and metastatic potential of tumors. HCC1937/p53 cells were derived from triple-negative breast cancer (TNBC), and used to investigate the roles of breast cancer stem cells (CSCs) in the formation of VM. HCC1937/p53 cells formed mesh-like structures on matrigel culture in which expression of VM-related genes, vascular endothelial (VE)-cadherin, matrix metalloproteinase (MMP)-2 and MMP-9 was confirmed by droplet digital polymerase chain reaction (PCR). In immunofluorescence microscopy, aldehyde dehydrogenase (ALDH)1A3+ cells with properties of CSCs or progenitors and GATA binding protein 3 (GATA3)+ cells with more differentiated characteristics were localized in the bridging region and aggregated region of VM structures, respectively. In fluorescence-activated cell sorting analysis, ALDH+ cells, considered to be a subpopulation of CSCs sorted by the aldefluor assay, exhibited marked VM formation on matrigel in 24 hr, whereas ALDH- cells did not form VM, indicating possible roles of CSCs in VM formation. The stem-like cancer cells resistant to p53-induced apoptosis, which expressed a high rate of ALDH1A3 and Sex-determining region Y (SRY)-box binding protein-2 (Sox-2), completed VM formation much faster than the control. These findings may provide clues to elucidate the significance of VM formed by treatment-resistant CSCs in the metastatic potential and poor prognosis associated with TNBC.

中文翻译:

人体干细胞样干细胞在基质胶上引发血管生成模仿。

血管生成模拟物(VM)是指由肿瘤细胞排列的血管生成结构,可与血管生成区分开,并负责肿瘤的侵袭性和转移潜力。HCC1937 / p53细胞源自三阴性乳腺癌(TNBC),用于研究乳腺癌干细胞(CSC)在VM形成中的作用。HCC1937 / p53细胞在基质胶培养中形成网状结构,其中通过液滴数字聚合酶链反应(PCR)确认了VM相关基因,血管内皮(VE)-钙黏着蛋白,基质金属蛋白酶(MMP)-2和MMP-9的表达)。在免疫荧光显微镜下,具有CSCs或祖细胞特性的乙醛脱氢酶(ALDH)1A3 +细胞和具有更高分化特性的GATA结合蛋白3(GATA3)+细胞分别位于VM结构的桥接区和聚集区。在荧光激活的细胞分选分析中,ALDH +细胞(被认为是通过醛荧光法分选的CSC的一个亚群)在24小时内在基质胶上显示出明显的VM形成,而ALDH-细胞未形成VM,表明CSC在VM中的可能作用编队。对p53诱导的细胞凋亡具有抗性的干细胞状癌细胞,其表达率较高,其ALDH1A3和性别决定区Y(SRY)-box结合蛋白2(Sox-2)的表达比对照快得多。
更新日期:2019-11-01
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