Department of Hepatobiliary and Pancreatic Surgery, The First Hospital of Jilin University, Changchun, 130021 Jilin Province, China.
Comput Math Methods Med. 2021 Oct 28;2021:3267536. doi: 10.1155/2021/3267536. eCollection 2021.
The estimation of hepatocellular carcinoma (HCC) is tremendously inferior because of the formation of chemoresistance, integrated with essentially increased stemness belongings. At present, the relevance between miR-122 and cancer development was mostly undisclosed with single study reflecting its importance in glioblastoma. . The research here was focused to investigate the task of miR-122 to modulate tumorigenesis in hepatocellular carcinoma by aiming AKT3 in the management of hepatocellular carcinoma stemness and chemosensitivity. The method of QRT-PCR was performed to investigate the aspect of miR-122 and AKT3 in tissue sample and cell lines. The evaluation was done using gain- or loss-of-function in order to retrieve the function of miR-122 in the hepatocellular carcinoma cells, including cell multiplication and stemness effects. The properties of hepatocellular carcinoma were discovered by the development of sphere development, cell feasibility, and the emergence of colony. RNA immunoprecipitation (RIP), luciferase reporter, and the RNA pull down evaluation were conducted to investigate the communication between the miR-122 and AKT3. Therefore, a naked mouse xenograft specimen was set up for the in vivo analysis.
Here, we determined the new role of AKT3 and unmediated target of miR-122. The reimposition of miR-122 appearance in the hepatocellular carcinoma cell lines reduces the levels of AKT3 and also hinders the relocation and expansion of cells by prompting apoptosis. These phenotypes are antitumor in nature and can be retrieved by the reorganization of the AKT3 expression which signals the crucial role of AKT3 in the miR-122 arbitrated HCC modification. The in vivo analysis demonstrated the reimposition of miR-122 entirely obstructing the xenograft expansion to manage tumorigenesis in hepatocellular carcinoma and a prospective remedial entrant for the liver cancer.
In this study, it was observed that miR-122 encourages the stemness role of hepatocellular carcinoma and diminishes the chemosensitivity by cleaning the miR-122 in order to initiate the AKT3. The in vivo study reflected the restoration of miR-122 which completely hinders the xenograft growth to regulate the tumorigenesis in the HCC.
由于形成化学抗性，与本质上增加的干细胞特性相结合，肝细胞癌（HCC）的估计非常差。目前，miR-122 与癌症发展之间的相关性主要是通过单个研究来揭示的，该研究反映了其在神经胶质瘤中的重要性。本研究旨在通过 AKT3 调节肝细胞癌干细胞特性和化学敏感性来研究 miR-122 调节肝细胞癌发生的作用。通过 QRT-PCR 方法研究组织样本和细胞系中 miR-122 和 AKT3 的情况。通过增益或功能丧失来评估，以检索 miR-122 在肝细胞癌细胞中的功能，包括细胞增殖和干细胞作用。通过球体发育、细胞可行性和集落形成来发现肝细胞癌的特性。进行 RNA 免疫沉淀（RIP）、荧光素酶报告基因和 RNA 下拉实验来研究 miR-122 和 AKT3 之间的通讯。因此，建立了裸鼠异种移植标本进行体内分析。
在这里，我们确定了 AKT3 的新作用和 miR-122 的直接靶标。在肝细胞癌细胞系中重新引入 miR-122 会降低 AKT3 的水平，并通过促进细胞凋亡来阻碍细胞的迁移和扩增。这些表型具有抗肿瘤作用，并且通过 AKT3 表达的重组可以恢复，这表明 AKT3 在 miR-122 介导的 HCC 修饰中起关键作用。体内分析表明，重新引入 miR-122 完全阻止了异种移植的扩张，从而控制了肝细胞癌的肿瘤发生，并为肝癌提供了一种潜在的治疗方法。
在这项研究中，观察到 miR-122 通过清除 miR-122 来促进肝细胞癌的干细胞作用并降低化学敏感性，从而启动 AKT3。体内研究反映了 miR-122 的恢复，它完全阻止了异种移植的生长，从而调节 HCC 的肿瘤发生。
