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m6A-YTHDF1-mediated TRIM29 upregulation facilitates the stem cell-like phenotype of cisplatin-resistant ovarian cancer cells
Biochimica et Biophysica Acta (BBA) - Molecular Cell Research ( IF 5.1 ) Pub Date : 2020-10-01 , DOI: 10.1016/j.bbamcr.2020.118878
Liang Hao , Jia-Mei Wang , Bao-Qin Liu , Jing Yan , Chao Li , Jing-Yi Jiang , Fu-Ying Zhao , Huai-Yu Qiao , Hua-Qin Wang

Ovarian cancer is the deadliest gynaecologic malignancy, and the five-year survival rate of patients is less than 35% worldwide. Cancer stem cells (CSCs) are a population of cells with stem-like characteristics that are thought to cause chemoresistance and recurrence. TRIM29 is aberrantly expressed in various cancers and associated with cancer development and progression. Previous studies showed that the upregulation of TRIM29 expression in pancreatic cancer is related to stem-like characteristics. However, the role of TRIM29 in ovarian cancer is poorly understood. In this study, we found that TRIM29 expression was increased at the translational level in both the cisplatin-resistant ovarian cancer cells and clinical tissues. Increased TRIM29 expression was associated with a poor prognosis of patients with ovarian cancer. In addition, TRIM29 could enhance the CSC-like characteristics of the cisplatin-resistant ovarian cancer cells. Recruitment of YTHDF1 to m6A-modified TRIM29 was involved in promoting TRIM29 translation in the cisplatin-resistant ovarian cancer cells. Knockdown of YTHDF1 suppressed the CSC-like characteristics of the cisplatin-resistant ovarian cancer cells, which could be rescued by ectopic expression of TRIM29. This study suggests TRIM29 may act as an oncogene to promote the CSC-like features of cisplatin-resistant ovarian cancer in an m6A-YTHDF1-dependent manner. Due to the roles of TRIM29 and YTHDF1 in the promotion of CSC-like features, they may become potential therapeutic targets to combat the recurrence of ovarian cancer.



中文翻译:

m6A-YTHDF1介导的TRIM29上调促进顺铂耐药卵巢癌细胞的干细胞样表型

卵巢癌是最致命的妇科恶性肿瘤,全球患者的五年生存率不到35%。癌症干细胞(CSC)是具有干样特征的细胞群,被认为会引起化学抗性和复发。TRIM29在各种癌症中异常表达,并与癌症的发展和进程有关。先前的研究表明,胰腺癌中TRIM29表达的上调与茎样特征有关。然而,对TRIM29在卵巢癌中的作用了解甚少。在这项研究中,我们发现在顺铂耐药的卵巢癌细胞和临床组织中,TRIM29表达在翻译水平上均增加。TRIM29表达增加与卵巢癌患者预后不良有关。此外,TRIM29可以增强顺铂耐药卵巢癌细胞的CSC样特征。YTHDF1到m6A修饰的TRIM29的募集参与促进顺铂耐药性卵巢癌细胞中TRIM29的翻译。击倒YTHDF1抑制了顺铂耐药卵巢癌细胞的CSC样特征,可以通过异位表达TRIM29来挽救它。这项研究表明,TRIM29可能作为致癌基因,以m6A-YTHDF1依赖性方式促进顺铂耐药性卵巢癌的CSC样特征。由于TRIM29和YTHDF1在促进CSC样特征中的作用,它们可能成为对抗卵巢癌复发的潜在治疗靶标。YTHDF1到m6A修饰的TRIM29的募集参与促进顺铂耐药性卵巢癌细胞中TRIM29的翻译。击倒YTHDF1抑制了顺铂耐药卵巢癌细胞的CSC样特征,可以通过异位表达TRIM29来挽救它。这项研究表明,TRIM29可能作为致癌基因,以m6A-YTHDF1依赖性方式促进顺铂耐药性卵巢癌的CSC样特征。由于TRIM29和YTHDF1在促进CSC样特征中的作用,它们可能成为对抗卵巢癌复发的潜在治疗靶标。YTHDF1到m6A修饰的TRIM29的募集参与促进顺铂耐药性卵巢癌细胞中TRIM29的翻译。击倒YTHDF1抑制了顺铂耐药卵巢癌细胞的CSC样特征,可以通过异位表达TRIM29来挽救它。这项研究表明,TRIM29可能作为致癌基因,以m6A-YTHDF1依赖性方式促进顺铂耐药性卵巢癌的CSC样特征。由于TRIM29和YTHDF1在促进CSC样特征中的作用,它们可能成为对抗卵巢癌复发的潜在治疗靶标。可以通过异位表达TRIM29来挽救它。这项研究表明,TRIM29可能作为致癌基因,以m6A-YTHDF1依赖性方式促进顺铂耐药性卵巢癌的CSC样特征。由于TRIM29和YTHDF1在促进CSC样特征中的作用,它们可能成为对抗卵巢癌复发的潜在治疗靶标。可以通过异位表达TRIM29来挽救它。这项研究表明,TRIM29可能作为致癌基因,以m6A-YTHDF1依赖性方式促进顺铂耐药性卵巢癌的CSC样特征。由于TRIM29和YTHDF1在促进CSC样特征中的作用,它们可能成为对抗卵巢癌复发的潜在治疗靶标。

更新日期:2020-10-13
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