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Long noncoding RNA MALAT1 knockdown inhibits progression of anaplastic thyroid carcinoma by regulating miR-200a-3p/FOXA1.
Cancer Biology & Therapy ( IF 3.6 ) Pub Date : 2019-09-10 , DOI: 10.1080/15384047.2019.1617567 Lisha Gou 1 , Huawei Zou 2 , Beibei Li 1
Cancer Biology & Therapy ( IF 3.6 ) Pub Date : 2019-09-10 , DOI: 10.1080/15384047.2019.1617567 Lisha Gou 1 , Huawei Zou 2 , Beibei Li 1
Affiliation
Long noncoding RNAs (lncRNAs) have been reported to play essential roles in progression of thyroid carcinoma. However, the roles of lncRNA metastasis-associated lung adenocarcinoma transcript 1 (MALAT1) in anaplastic thyroid carcinoma (ATC) process and its mechanism remain not been fully established. In this study, we focused on the effect of MALAT1 on cell proliferation, apoptosis, migration, invasion, and autophagy formation in ATC and explored the interaction between miR-200a-3p and MALAT1 or FOXA1. Moreover, murine xenograft model was established to investigate the roles and mechanism of MALAT1 in ATC progression in vivo. Results showed that MALAT1 expression was enhanced and miR-200a-3p was reduced in ATC tissues and cells. Knockdown of MALAT1 or overexpression of miR-200a-3p inhibited cell proliferation, migration and invasion but increased apoptosis and autophagy formation in ATC cells. Moreover, miR-200a-3p was directly bound to MALAT1 and its inhibition reversed the inhibitory effect of MALAT1 knockdown on progression of ATC. In addition, FOXA1 was indicated as a target of miR-200a-3p and its restoration attenuated the anti-cancer role of miR-200a-3p in ATC cells. Furthermore, MALAT1 functioned as a competing endogenous RNA (ceRNA) via sponging miR-200a-3p to derepress FOXA1 expression. Besides, interference of MALAT1 decreased tumor growth by upregulating miR-200a-3p and downregulating FOXA1. Collectively, MALAT1 knockdown suppressed ATC progression by regulating miR-200a-3p/FOXA1, providing a novel avenue for treatment of ATC.
中文翻译:
长时非编码RNA MALAT1敲低可以通过调节miR-200a-3p / FOXA1抑制变性甲状腺癌的进展。
据报道,长非编码RNA(lncRNA)在甲状腺癌的进展中起重要作用。然而,lncRNA转移相关的肺腺癌转录本1(MALAT1)在变性甲状腺癌(ATC)过程中的作用及其机制尚未完全确立。在这项研究中,我们集中于MALAT1对ATC中细胞增殖,凋亡,迁移,侵袭和自噬形成的影响,并探讨了miR-200a-3p与MALAT1或FOXA1之间的相互作用。此外,建立了小鼠异种移植模型以研究MALAT1在体内ATC进展中的作用和机制。结果表明,ATC组织和细胞中MALAT1表达增强,miR-200a-3p降低。敲低MALAT1或过度表达miR-200a-3p会抑制细胞增殖,迁移和侵袭,但增加了ATC细胞的凋亡和自噬形成。而且,miR-200a-3p直接与MALAT1结合,其抑制作用逆转了MALAT1敲低对ATC进程的抑制作用。此外,FOXA1被指示为miR-200a-3p的靶标,其还原减弱了miR-200a-3p在ATC细胞中的抗癌作用。此外,MALAT1通过海绵化miR-200a-3p作为竞争性内源RNA(ceRNA)来抑制FOXA1表达。此外,MALAT1的干扰通过上调miR-200a-3p和下调FOXA1来降低肿瘤的生长。总的来说,MALAT1敲低通过调节miR-200a-3p / FOXA1抑制了ATC进程,为治疗ATC提供了一条新途径。miR-200a-3p直接与MALAT1结合,其抑制作用逆转了MALAT1敲低对ATC进程的抑制作用。此外,FOXA1被指示为miR-200a-3p的靶标,其还原减弱了miR-200a-3p在ATC细胞中的抗癌作用。此外,MALAT1通过海绵化miR-200a-3p作为竞争性内源RNA(ceRNA)来抑制FOXA1表达。此外,MALAT1的干扰通过上调miR-200a-3p和下调FOXA1来降低肿瘤的生长。总的来说,MALAT1敲低通过调节miR-200a-3p / FOXA1抑制了ATC进程,为治疗ATC提供了一条新途径。miR-200a-3p直接与MALAT1结合,其抑制作用逆转了MALAT1敲低对ATC进程的抑制作用。此外,FOXA1被指示为miR-200a-3p的靶标,其还原减弱了miR-200a-3p在ATC细胞中的抗癌作用。此外,MALAT1通过海绵化miR-200a-3p充当竞争性内源RNA(ceRNA),从而抑制FOXA1表达。此外,MALAT1的干扰通过上调miR-200a-3p和下调FOXA1来降低肿瘤的生长。总的来说,MALAT1敲低通过调节miR-200a-3p / FOXA1抑制了ATC进程,为治疗ATC提供了一条新途径。此外,MALAT1通过海绵化miR-200a-3p作为竞争性内源RNA(ceRNA)来抑制FOXA1表达。此外,MALAT1的干扰通过上调miR-200a-3p和下调FOXA1来降低肿瘤的生长。总的来说,MALAT1敲低通过调节miR-200a-3p / FOXA1抑制了ATC进程,为治疗ATC提供了一条新途径。此外,MALAT1通过海绵化miR-200a-3p作为竞争性内源RNA(ceRNA)来抑制FOXA1表达。此外,MALAT1的干扰通过上调miR-200a-3p和下调FOXA1来降低肿瘤的生长。总体而言,MALAT1敲低通过调节miR-200a-3p / FOXA1抑制了ATC进程,为治疗ATC提供了一条新途径。
更新日期:2019-11-01
中文翻译:
长时非编码RNA MALAT1敲低可以通过调节miR-200a-3p / FOXA1抑制变性甲状腺癌的进展。
据报道,长非编码RNA(lncRNA)在甲状腺癌的进展中起重要作用。然而,lncRNA转移相关的肺腺癌转录本1(MALAT1)在变性甲状腺癌(ATC)过程中的作用及其机制尚未完全确立。在这项研究中,我们集中于MALAT1对ATC中细胞增殖,凋亡,迁移,侵袭和自噬形成的影响,并探讨了miR-200a-3p与MALAT1或FOXA1之间的相互作用。此外,建立了小鼠异种移植模型以研究MALAT1在体内ATC进展中的作用和机制。结果表明,ATC组织和细胞中MALAT1表达增强,miR-200a-3p降低。敲低MALAT1或过度表达miR-200a-3p会抑制细胞增殖,迁移和侵袭,但增加了ATC细胞的凋亡和自噬形成。而且,miR-200a-3p直接与MALAT1结合,其抑制作用逆转了MALAT1敲低对ATC进程的抑制作用。此外,FOXA1被指示为miR-200a-3p的靶标,其还原减弱了miR-200a-3p在ATC细胞中的抗癌作用。此外,MALAT1通过海绵化miR-200a-3p作为竞争性内源RNA(ceRNA)来抑制FOXA1表达。此外,MALAT1的干扰通过上调miR-200a-3p和下调FOXA1来降低肿瘤的生长。总的来说,MALAT1敲低通过调节miR-200a-3p / FOXA1抑制了ATC进程,为治疗ATC提供了一条新途径。miR-200a-3p直接与MALAT1结合,其抑制作用逆转了MALAT1敲低对ATC进程的抑制作用。此外,FOXA1被指示为miR-200a-3p的靶标,其还原减弱了miR-200a-3p在ATC细胞中的抗癌作用。此外,MALAT1通过海绵化miR-200a-3p作为竞争性内源RNA(ceRNA)来抑制FOXA1表达。此外,MALAT1的干扰通过上调miR-200a-3p和下调FOXA1来降低肿瘤的生长。总的来说,MALAT1敲低通过调节miR-200a-3p / FOXA1抑制了ATC进程,为治疗ATC提供了一条新途径。miR-200a-3p直接与MALAT1结合,其抑制作用逆转了MALAT1敲低对ATC进程的抑制作用。此外,FOXA1被指示为miR-200a-3p的靶标,其还原减弱了miR-200a-3p在ATC细胞中的抗癌作用。此外,MALAT1通过海绵化miR-200a-3p充当竞争性内源RNA(ceRNA),从而抑制FOXA1表达。此外,MALAT1的干扰通过上调miR-200a-3p和下调FOXA1来降低肿瘤的生长。总的来说,MALAT1敲低通过调节miR-200a-3p / FOXA1抑制了ATC进程,为治疗ATC提供了一条新途径。此外,MALAT1通过海绵化miR-200a-3p作为竞争性内源RNA(ceRNA)来抑制FOXA1表达。此外,MALAT1的干扰通过上调miR-200a-3p和下调FOXA1来降低肿瘤的生长。总的来说,MALAT1敲低通过调节miR-200a-3p / FOXA1抑制了ATC进程,为治疗ATC提供了一条新途径。此外,MALAT1通过海绵化miR-200a-3p作为竞争性内源RNA(ceRNA)来抑制FOXA1表达。此外,MALAT1的干扰通过上调miR-200a-3p和下调FOXA1来降低肿瘤的生长。总体而言,MALAT1敲低通过调节miR-200a-3p / FOXA1抑制了ATC进程,为治疗ATC提供了一条新途径。