Establishment and characterization of NCC-ASPS1-C1: a novel patient-derived cell line of alveolar soft-part sarcoma
Establishment and characterization of NCC-ASPS1-C1: a novel patient-derived cell line of alveolar soft-part sarcoma
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NCC-ASPS1-C1 的建立和表征：一种新型患者来源的肺泡软组织肉瘤细胞系
DOI：
10.1007/s13577-020-00382-2
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发表时间：
2020
期刊：
影响因子：
4.3
通讯作者：
Kondo Tadashi
中科院分区：
文献类型：
--
作者：
Yoshimatsu Yuki;Noguchi Rei;Tsuchiya Ryuto;Sei Akane;Sugaya Jun;Fukushima Suguru;Yoshida Akihiko;Kawai Akira;Kondo Tadashi
腺泡状软组织肉瘤是一种间叶性恶性肿瘤，其特征是ASPSCR 1和TFE 3的重排和组织学上独特的假腺泡样结构。虽然腺泡状软组织肉瘤的病程较缓慢，但由于其晚期远处转移，其长期预后较差。目前，尚未发现腺泡状软组织肉瘤的根治性治疗方法，因此，长期以来一直需要一种新的治疗策略。患者来源的细胞系是基础和临床前研究的重要工具。然而，腺泡状软组织肉瘤的细胞系很少在文献中报道，因为它是一种非常罕见的恶性肿瘤，占所有软组织肉瘤的不到1%。本研究旨在建立一种新的腺泡状软组织肉瘤细胞系。利用腺泡状软组织肉瘤组织块，成功建立了一株腺泡状软组织肉瘤细胞系，命名为NCC-ASPS 1-C1。NCC-ASPS 1-C1细胞具有ASPSCR 1-TFE 3融合基因，并表现出缓慢生长和球体形成。另一方面，NCC-ASPS 1-C1没有表现出入侵能力。我们筛选了195种抗癌药物的抗增殖作用，包括食品和药物管理局批准的抗癌药物。我们发现MET抑制剂tivantinib和多激酶抑制剂orantinib抑制NCC-ASPS 1-C1细胞的增殖。NCC-ASPS 1-C1细胞为腺泡状软组织肉瘤的体外研究提供了一种有效的工具。
Alveolar soft-part sarcoma is a mesenchymal malignancy characterized by the rearrangement ofASPSCR1andTFE3and a histologically distinctive pseudoalveolar pattern. Although alveolar soft-part sarcoma takes an indolent course, its long-term prognosis is poor because of late distant metastases. Currently, curative treatments have not been found for alveolar soft-part sarcoma, and hence, a novel therapeutic strategy has long been required. Patient-derived cell lines comprise an important tool for basic and preclinical research. However, few cell lines from alveolar soft-part sarcoma have been reported in the literature because it is an extremely rare malignancy, accounting for less than 1% of all soft-tissue sarcomas. This study aimed to establish a novel alveolar soft-part sarcoma cell line. Using surgically-resected tumor tissue of alveolar soft-part sarcoma, we successfully established a cell line and named it NCC-ASPS1-C1. The NCC-ASPS1-C1 cells harbored anASPSCR1-TFE3fusion gene and exhibited slow growth, and spheroid formation. On the other hand, NCC-ASPS1-C1 did not show the capability of invasion. We screened the antiproliferative effects of 195 anticancer agents, including Food and Drug Administration-approved anticancer drugs. We found that the MET inhibitor tivantinib and multi-kinase inhibitor orantinib inhibited the proliferation of NCC-ASPS1-C1 cells. The clinical utility and molecular mechanisms of antitumor effects of these drugs are worth investigating in the further studies, and NCC-ASPS1-C1 cells will be a useful tool for the in vitro study of alveolar soft-part sarcoma.