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超声靶向微泡破坏介导的 si-CyclinD1 通过抑制 PI3K/AKT 信号通路遏制肝细胞癌的发展
Authors Yan W, Cheng L, Zhang D
Received 28 May 2020
Accepted for publication 1 September 2020
Published 29 October 2020 Volume 2020:12 Pages 10829—10839
DOI https://doi.org/10.2147/CMAR.S263590
Checked for plagiarism Yes
Review by Single anonymous peer review
Peer reviewer comments 2
Editor who approved publication: Professor Bilikere Dwarakanath
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.
Keywords: hepatocellular carcinoma, ultrasound-targeted microbubble destruction, CCND1, PI3K/AKT signaling pathway