Scientific reports, 2019-10, Vol.9 (1), p.14854-12, Article 14854
2019
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- Autor(en) / Beteiligte
- Titel
- Downregulation of B7-H4 suppresses tumor progression of hepatocellular carcinoma
- Ist Teil von
- Scientific reports, 2019-10, Vol.9 (1), p.14854-12, Article 14854
- Ort / Verlag
- London: Nature Publishing Group UK
- Erscheinungsjahr
- 2019
- Quelle
- MEDLINE
- Beschreibungen/Notizen
- B7-H4, as a member of the B7 superfamily, was overexpressed in various types of cancers. However, the effects of B7-H4 on the aggressiveness of HCC and the underlying mechanisms have not yet been fully explored. For this purpose, B7-H4 expression was detected by Flow cytometry and Western blotting, it was highly expressed in several HCC cell lines but not in normal LO2 cell line. Knockdown B7-H4 expression induced HCC cells apoptosis by flow cytometry and colony formation assays and increased several apoptosis-related proteins, including survivin, cleaved caspase-3, cleaved caspase-7, and Bax, while the pro-growth protein survivin was reduced. Then the proliferation and cell cycle were suppressed after treated by siB7-H4. Moreover, the level of B7-H4 was significantly correlated with cell migration. In vivo , intra-tumor injection of siRNA targeting B7-H4 can significantly inhibited the growth of HepG2 cells in nude mice. Finally, regions of interest were manually traced on T1WI, T2WI, DWI and ADC of MR images. ADC values were increased in HCC xenografts after B7-H4 siRNA treatment. These data indicated that downregulation of B7-H4 suppressed the proliferation and migration and promoted apoptosis in vitro and in vivo . Blocking the B7-H4 channel might be a potential therapeutic strategy for HCC.
- Sprache
- Englisch
- Identifikatoren
- ISSN: 2045-2322eISSN: 2045-2322DOI: 10.1038/s41598-019-51253-2Titel-ID: cdi_pubmedcentral_primary_oai_pubmedcentral_nih_gov_6795893
- Format
- –
- Schlagworte
- 13/51, 13/89, 14/63, 38/109, 38/77, 38/91, 59/57, 631/337, 631/67, 64/60, 82/51, 82/80, Animals, Antigens, CD - genetics, Antigens, CD - metabolism, Apoptosis, Apoptosis - genetics, B7 antigen, BAX protein, bcl-2-Associated X Protein - genetics, bcl-2-Associated X Protein - metabolism, Cadherins - genetics, Cadherins - metabolism, Carcinoma, Hepatocellular - genetics, Carcinoma, Hepatocellular - metabolism, Carcinoma, Hepatocellular - pathology, Carcinoma, Hepatocellular - therapy, Caspase 3 - genetics, Caspase 3 - metabolism, Caspase 7 - genetics, Caspase 7 - metabolism, Caspase-3, Caspase-7, Cell adhesion & migration, Cell cycle, Cell Line, Tumor, Cell migration, Cell Movement, Cell Proliferation, Disease Progression, Female, Flow cytometry, Gene Expression Regulation, Neoplastic, Hepatocellular carcinoma, Humanities and Social Sciences, Humans, Liver cancer, Liver Neoplasms - genetics, Liver Neoplasms - metabolism, Liver Neoplasms - pathology, Liver Neoplasms - therapy, Mice, Mice, Nude, multidisciplinary, RNA, Small Interfering - genetics, RNA, Small Interfering - metabolism, Science, Science (multidisciplinary), Signal Transduction, siRNA, Survivin, Survivin - genetics, Survivin - metabolism, Tumor Burden, V-Set Domain-Containing T-Cell Activation Inhibitor 1 - antagonists & inhibitors, V-Set Domain-Containing T-Cell Activation Inhibitor 1 - genetics, V-Set Domain-Containing T-Cell Activation Inhibitor 1 - metabolism, Vimentin - genetics, Vimentin - metabolism, Western blotting, Xenograft Model Antitumor Assays, Xenografts