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甲状腺癌细胞中c-KIT表达缺失。

Loss of c-KIT expression in thyroid cancer cells.

作者信息

Franceschi Sara, Lessi Francesca, Panebianco Federica, Tantillo Elena, La Ferla Marco, Menicagli Michele, Aretini Paolo, Apollo Alessandro, Naccarato Antonio Giuseppe, Marchetti Ivo, Mazzanti Chiara Maria

机构信息

FPS-Pisa Science Foundation, Pisa, Italy.

Department of Translational Research and New Technologies in Medicine and Surgery, University Hospital of Pisa, Pisa, Italy.

出版信息

PLoS One. 2017 Mar 16;12(3):e0173913. doi: 10.1371/journal.pone.0173913. eCollection 2017.

Abstract

Papillary thyroid carcinoma is the most frequent histologic type of thyroid tumor. Few studies investigated the role of c-KIT expression in thyroid tumors, suggesting a role for this receptor and its ligand in differentiation and growth control of thyroid epithelium and a receptor loss following malignant transformation. We investigated and correlated c-KIT expression levels and two known markers of thyrocytes differentiation, PAX8 and TTF-1, in malignant and benign cytological thyroid samples. Moreover, we performed functional studies on human papillary thyroid carcinoma cell line to associated c-KIT expression to thyrocytes differentiation and tumor proliferation. c-KIT and PAX8 expression resulted higher in benign samples compared to the malignant ones, and the expression levels of these two genes were significantly correlated to each other. We also observed that c-KIT overexpression led to an increase of PAX8 expression level together with a decrease of proliferation. Furthermore, c-KIT overexpressing cells showed a regression of typical morphological features of malignancy. Taken together these results suggest that c-KIT could be involved in the differentiation of thyroid cells and in tumor progression.

摘要

乳头状甲状腺癌是最常见的甲状腺肿瘤组织学类型。很少有研究调查c-KIT表达在甲状腺肿瘤中的作用,提示该受体及其配体在甲状腺上皮细胞的分化和生长控制中发挥作用,且在恶性转化后受体缺失。我们研究了c-KIT表达水平与两种已知的甲状腺细胞分化标志物PAX8和TTF-1在甲状腺良恶性细胞学样本中的相关性。此外,我们对人乳头状甲状腺癌细胞系进行了功能研究,以将c-KIT表达与甲状腺细胞分化和肿瘤增殖相关联。与恶性样本相比,c-KIT和PAX8在良性样本中的表达更高,且这两个基因的表达水平彼此显著相关。我们还观察到c-KIT过表达导致PAX8表达水平增加,同时增殖减少。此外,c-KIT过表达的细胞显示出恶性典型形态特征的消退。综合这些结果表明,c-KIT可能参与甲状腺细胞的分化和肿瘤进展。

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