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超声靶向微泡破坏介导的si-CyclinD1通过抑制PI3K/AKT信号通路抑制肝细胞癌的发展。

Ultrasound-Targeted Microbubble Destruction Mediated si-CyclinD1 Inhibits the Development of Hepatocellular Carcinoma via Suppression of PI3K/AKT Signaling Pathway.

作者信息

Yan Wei, Cheng Li, Zhang Dongmei

机构信息

Department of Electrical Diagnosis, Changchun University of Traditional Chinese Medicine Affiliated Hospital, Changchun 130021, People's Republic of China.

出版信息

Cancer Manag Res. 2020 Oct 29;12:10829-10839. doi: 10.2147/CMAR.S263590. eCollection 2020.

Abstract

BACKGROUND AND AIM

In our study, we aimed to investigate the effect of ultrasound-targeted microbubble destruction (UTMD)mediated si-CyclinD1 (CCND1) on the growth of hepatocellular carcinoma (HCC) cells.

PATIENTS AND METHODS

Bioinformatics analysis was performed to detect the difference of CCND1 expression of HCC and normal liver tissues. After treatment with UTMDmediated si-CCND1, the growth and apoptosis of HepG2 cells were detected by flow cytometry, MTT, EdU staining, colony formation assay, Hoechst 33,258 staining and Western blot analysis. The growth of HepG2 cells in vivo was also studied via xenograft tumor in nude mice.

RESULTS

CCND1 was highly expressed in HCC tissues and HCC cell lines. UTMDmediated si-CCND1 could inhibit the growth of HepG2 cells and promote apoptosis via suppression of the PI3K/AKT signaling pathway. UTMDmediated si-CCND1 could also suppress the growth of HepG2 cells in vivo.

CONCLUSION

Our study provided evidence that UTMDmediated si-CCND1 could inhibit the growth of HepG2 cells and promote apoptosis via suppression of the PI3K/AKT signaling pathway.

摘要

背景与目的

在本研究中,我们旨在探讨超声靶向微泡破坏(UTMD)介导的si-CyclinD1(CCND1)对肝癌(HCC)细胞生长的影响。

患者与方法

进行生物信息学分析以检测HCC组织与正常肝组织中CCND1表达的差异。在用UTMD介导的si-CCND1处理后,通过流式细胞术、MTT、EdU染色、集落形成试验、Hoechst 33258染色和蛋白质印迹分析检测HepG2细胞的生长和凋亡情况。还通过裸鼠异种移植瘤研究了HepG2细胞在体内的生长情况。

结果

CCND1在HCC组织和HCC细胞系中高表达。UTMD介导的si-CCND1可通过抑制PI3K/AKT信号通路抑制HepG2细胞的生长并促进其凋亡。UTMD介导的si-CCND1也可在体内抑制HepG2细胞的生长。

结论

我们的研究提供了证据,表明UTMD介导的si-CCND1可通过抑制PI3K/AKT信号通路抑制HepG2细胞的生长并促进其凋亡。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/1628/7605614/4d4e6bfb4d7f/CMAR-12-10829-g0001.jpg

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