Abstract |
In our previous studies, we found that isocorydine (ICD) could be a potential antitumor agent in hepatocellular carcinoma (HCC). Derivate isocorydine (d-ICD), a more effective antitumor agent, has been demonstrated to inhibit proliferation and drug resistance in HCC. In order to investigate the potential role of d-ICD on HCC cell migration and its possible mechanism, wound healing assay, trans-well invasion assay, western blot analysis, and qRT-PCR were performed to study the migration and invasion ability of HCC cells as well as relevant molecular alteration following d-ICD treatment. Results indicated that the migration and invasion ability of HCC cells were suppressed when cultured with d-ICD. Meanwhile, the expression level of ITGA1 was markedly reduced. Furthermore, we found that ITGA1 promotes HCC cell migration and invasion in vitro, and that ITGA1 can partly reverse the effect of d-ICD-induced migration and invasion suppression in HCC cells. In addition, dual luciferase reporter assay and chromatin immunoprecipitation assay were used to study the expression regulation of ITGA1, and found that E2F1 directly upregulates ITGA1 expression and d-ICD inhibits E2F1 expression. Taken together, these results reveal that d-ICD inhibits HCC cell migration and invasion may partly by downregulating E2F1/ITGA1 expression.
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Authors | Xiaoqin Liu, Hua Tian, Hong Li, Chao Ge, Fangyu Zhao, Ming Yao, Jinjun Li |
Journal | International journal of molecular sciences
(Int J Mol Sci)
Vol. 18
Issue 3
(Feb 27 2017)
ISSN: 1422-0067 [Electronic] Switzerland |
PMID | 28264467
(Publication Type: Journal Article)
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Chemical References |
- Antineoplastic Agents, Phytogenic
- Aporphines
- E2F1 Transcription Factor
- Integrin alpha1
- MicroRNAs
- isocorydine
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Topics |
- Antineoplastic Agents, Phytogenic
(pharmacology)
- Aporphines
(pharmacology)
- Carcinoma, Hepatocellular
(metabolism)
- Cell Line, Tumor
- Cell Movement
(drug effects)
- E2F1 Transcription Factor
(metabolism)
- Gene Expression
- Gene Silencing
- Humans
- Integrin alpha1
(genetics)
- Liver Neoplasms
(metabolism)
- MicroRNAs
(genetics)
- Promoter Regions, Genetic
- Transcriptional Activation
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