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FAM225A facilitates colorectal cancer progression by sponging miR‐613 to regulate NOTCH3

机译:FAM225A通过使miR‐613海绵化以调节NOTCH3促进结直肠癌的进展

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摘要

Colorectal cancer (CRC) is a fatal disease ranking the third among the commonplace cancer types around the world. It is extremely significant to exploit effective treatments against CRC. FAM225A was proved to influence cell progression and forecast unfavorable prognosis in nasopharyngeal carcinoma. The role and function mechanism of FAM225A are still unclear in CRC. In this research, FAM225A was discovered presenting much higher expression in CRC tissues and cell lines. In addition, depleting FAM225A was capable of inhibiting cell proliferation, migration, and epithelial‐to‐mesenchymal transition (EMT) progress, and enhancing cell apoptosis ability. Furthermore, miR‐613 exerted important effects as a mediator between FAM225A and NOTCH3. NOTCH3 was negatively correlated with miR‐613, whereas was positively associated with FAM225A. Via competitively binding with miR‐613, FAM225A positively regulated NOTCH3 expression. FAM225A facilitated CRC occurrence and development through positively regulating NOTCH3 expression by binding with miR‐613. In a word, FAM225A/miR‐613/NOTCH3 axis may play a tumor‐facilitator in CRC cell progression. These data manifested the pivotal effect of FAM225A/miR‐613/NOTCH3 pathway in CRC cell proliferation, apoptosis, and migration process. The findings may provide some theoretical basis and different perspective for CRC treatment.
机译:结直肠癌(CRC)是一种致命疾病,在世界各地常见的癌症类型中排名第三。开发有效的抗CRC治疗方法极其重要。 FAM225A被证明可影响鼻咽癌的细胞进程并预测不良预后。 FAM225A的作用和功能机制在CRC中尚不清楚。在这项研究中,发现FAM225A在CRC组织和细胞系中表现出更高的表达。此外,消耗FAM225A能够抑制细胞增殖,迁移和上皮-间质转化(EMT)进展,并增强细胞凋亡能力。此外,miR‐613作为FAM225A和NOTCH3之间的介体发挥了重要作用。 NOTCH3与miR-613负相关,而与FAM225A正相关。通过与miR-613竞争结合,FAM225A可以正向调节NOTCH3的表达。 FAM225A通过与miR-613结合正调控NOTCH3表达,促进了CRC的发生和发展。简而言之,FAM225A / miR‐613 / NOTCH3轴可能在CRC细胞进程中起肿瘤促进作用。这些数据表明FAM225A / miR-613 / NOTCH3途径在CRC细胞增殖,凋亡和迁移过程中起关键作用。这些发现可能为CRC治疗提供一些理论依据和不同观点。

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