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已发表论文
天然产物柳穿鱼黄素可抑制增殖，诱导细胞凋亡，并通过 PI3K/AKT/mTOR/ERK 信号通路引起 HCC 的 G2/M 期阻滞
Authors Wu T, Dong X, Yu D, Shen Z, Yu J, Yan S
Received 2 September 2018
Accepted for publication 6 November 2018
Published 3 December 2018 Volume 2018:11 Pages 8633—8642
DOI https://doi.org/10.2147/OTT.S186186
Checked for plagiarism Yes
Review by Single-blind
Peer reviewers approved by Dr Amy Norman
Peer reviewer comments 3
Editor who approved publication: Dr Carlos E Vigil
Background: Hepatocellular carcinoma (HCC) is characterized
by considerable phenotypic and molecular heterogeneity, but the overall
survival of HCC patients remains extremely poor. Thus, novel and efficient
alternatives to antitumor agents are urgently needed. Pectolinarigenin, a
flavonoid compound extract, has been previously reported for the treatment of
nasopharyngeal cancer. However, the potential antitumor roles of
pectolinarigenin in HCC have not been clearly elaborated. In the present study,
we investigated its role in HCC treatment and explored the potential molecular
mechanism(s).
Materials and methods: HCC cell lines SMMC7721 and PLC5 were cultured and treated with indicated concentrations of pectolinarigenin. For the HCC cell proliferation, after HCC cells were stimulated with indicated concentrations of pectolinarigenin, the cell viability was detected in CCK-8 and colony-forming assays. HCC cell invasion/migration assay was performed by Transwell and wound scratch methods. Additionally, cellular apoptosis and cell cycle arrest analysis was performed with flow cytometric analysis. Finally, the involved underlying signaling pathway, the PI3K/AKT/mTOR/ERK signaling-related molecular markers were detected through Western blot methods with indicated antibodies. Meanwhile, antitumor activity of pectolinarigenin was also assessed in tumor-bearing mice.
Results: The results indicated that the treatment with pectolinarigenin significantly inhibited cell proliferation and migratory and invasive abilities of SMMC7721 and PLC5 cells in concentration- and time-dependent manner. Meanwhile, pectolinarigenin markedly induced cell apoptosis and G2/M phase arrest in SMMC7721 and PLC5 cells, which was associated with apoptosis- and cell cycle-related protein levels, respectively. Furthermore, pectolinarigenin inhibited PI3K/AKT/mTOR/ERK signaling pathway. It also significantly suppressed HCC tumor growth in vivo.
Conclusion: Pectolinarigenin could suppress the viability and motility and cause apoptosis and G2/M phase arrest in HCC cell lines by inhibiting the PI3K/AKT/mTOR/ERK signaling pathway. This might be an appealing potential therapeutic agent for HCC treatment.
Keywords: hepatocellular carcinoma, pectolinarigenin, apoptosis, cell cycle arrest, antitumor
Materials and methods: HCC cell lines SMMC7721 and PLC5 were cultured and treated with indicated concentrations of pectolinarigenin. For the HCC cell proliferation, after HCC cells were stimulated with indicated concentrations of pectolinarigenin, the cell viability was detected in CCK-8 and colony-forming assays. HCC cell invasion/migration assay was performed by Transwell and wound scratch methods. Additionally, cellular apoptosis and cell cycle arrest analysis was performed with flow cytometric analysis. Finally, the involved underlying signaling pathway, the PI3K/AKT/mTOR/ERK signaling-related molecular markers were detected through Western blot methods with indicated antibodies. Meanwhile, antitumor activity of pectolinarigenin was also assessed in tumor-bearing mice.
Results: The results indicated that the treatment with pectolinarigenin significantly inhibited cell proliferation and migratory and invasive abilities of SMMC7721 and PLC5 cells in concentration- and time-dependent manner. Meanwhile, pectolinarigenin markedly induced cell apoptosis and G2/M phase arrest in SMMC7721 and PLC5 cells, which was associated with apoptosis- and cell cycle-related protein levels, respectively. Furthermore, pectolinarigenin inhibited PI3K/AKT/mTOR/ERK signaling pathway. It also significantly suppressed HCC tumor growth in vivo.
Conclusion: Pectolinarigenin could suppress the viability and motility and cause apoptosis and G2/M phase arrest in HCC cell lines by inhibiting the PI3K/AKT/mTOR/ERK signaling pathway. This might be an appealing potential therapeutic agent for HCC treatment.
Keywords: hepatocellular carcinoma, pectolinarigenin, apoptosis, cell cycle arrest, antitumor
