Long non-coding RNA MSC-AS1 confers imatinib resistance of gastrointestinal stromal tumor cells by activating FNDC1 and ANLN-mediated PI3K/AKT pathway.

IF 3.4 3区 生物学 Q3 CELL BIOLOGY Human Cell Pub Date : 2025-01-03 DOI:10.1007/s13577-024-01167-7
Lin Chen, Yongjian Gao, Huaixi Yang, Yanzhuo Su, Yunxin Zhang, Lin Lou, Xuefeng Wang, Dayong Ding
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Abstract

Imatinib resistance is a major obstacle to the successful treatment of gastrointestinal stromal tumors (GIST). Long non-coding RNAs (LncRNAs) have been identified as important regulatory factors in chemotherapy resistance. This study aimed to identify key lncRNAs involved in imatinib resistance of GISTs. First, MSC-AS1 was found to be upregulated in imatinib-resistant GIST tissues and imatinib-resistant GIST cells. Cellular experiments demonstrated that MSC-AS1 overexpression decreased imatinib sensitivity of GIST cells, evidenced by increased cell survival, colony formation, migration, and invasion. Moreover, suppression of MSC-AS1 improved the imatinib resistance of imatinib-resistant GIST cells. Furthermore, MSC-AS1 upregulated the expression of FNDC1 and Anillin via sponging miR-200b-3p, activated the phosphatidylinositol-3-kinase-AKT signaling pathway, and thereby driving imatinib resistance in vitro and in vivo. Overall, this study elucidates the crucial role and mechanism of MSC-AS1 in the imatinib resistance of GIST, providing the potential therapeutic strategy for overcoming the imatinib resistance of GIST.

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长链非编码RNA MSC-AS1通过激活FNDC1和anln介导的PI3K/AKT通路,赋予胃肠道间质肿瘤细胞伊马替尼耐药。
伊马替尼耐药是胃肠道间质瘤(GIST)成功治疗的主要障碍。长链非编码rna (LncRNAs)已被确定为化疗耐药的重要调控因子。本研究旨在确定参与gist伊马替尼耐药的关键lncrna。首先,发现MSC-AS1在耐伊马替尼GIST组织和耐伊马替尼GIST细胞中表达上调。细胞实验表明,MSC-AS1过表达降低了GIST细胞对伊马替尼的敏感性,证明了细胞存活率、集落形成、迁移和侵袭的增加。此外,抑制MSC-AS1可改善耐伊马替尼GIST细胞的伊马替尼耐药性。此外,MSC-AS1通过海绵化miR-200b-3p上调FNDC1和Anillin的表达,激活磷脂酰肌醇-3-激酶- akt信号通路,从而在体外和体内驱动伊马替尼耐药。总的来说,本研究阐明了MSC-AS1在GIST伊马替尼耐药中的关键作用和机制,为克服GIST伊马替尼耐药提供了潜在的治疗策略。
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来源期刊
Human Cell
Human Cell CELL BIOLOGY-
CiteScore
5.90
自引率
2.30%
发文量
176
审稿时长
4.5 months
期刊介绍: Human Cell is the official English-language journal of the Japan Human Cell Society. The journal serves as a forum for international research on all aspects of the human cell, encompassing not only cell biology but also pathology, cytology, and oncology, including clinical oncology. Embryonic stem cells derived from animals, regenerative medicine using animal cells, and experimental animal models with implications for human diseases are covered as well. Submissions in any of the following categories will be considered: Research Articles, Cell Lines, Rapid Communications, Reviews, and Letters to the Editor. A brief clinical case report focusing on cellular responses to pathological insults in human studies may also be submitted as a Letter to the Editor in a concise and short format. Not only basic scientists but also gynecologists, oncologists, and other clinical scientists are welcome to submit work expressing new ideas or research using human cells.
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