Objective To explore the anti-tumor effects of Egr-IFNγ gene therapy combined with 125I-UdR radionuclide therapy in mice bearing H22 hepatocarcinoma and its mechanism. Methods The recombinant plasmid pcDNAEgr-IFNγ mixed with liposome was injected into tumor. 48 h later, 370 kBq 125I-UdR was injected into tumor. The tumor growth rates at different times were observed. After 3 d gene-radionuclide therapy, the concentration of IFNγ in cytoplasm of H22 cells and cytotoxic activities of splenic CTL of the mice in different groups were examined. Results The tumor growth rates of pcDNAEgr-IFNγ +125 I-UdR group were obviously lower than those of control group, 125I-UdR group and pcDNAEgr-1 +125I-UdR group 6-15 d after gene-radionuclide therapy. IFNγ protein was found in cytoplasm of H22 cells in PcDNAEgr-1FNγ+125I-UdR group after 3 d gene-radionuclide therapy. Cytotoxic activity of splenic CTL in pcDNAEgr-IFN7 + 125I-UdR group was significantly higher than that in the other groups (P<0.01). Conclusions The anti-tumor effects in vivo of pcDNAEgr-IFNγ gene therapy combined with 125I-UdR radionuclide therapy are better than those of 125I-UdR therapy.

Signal transducer and activator of transcription 3 (STAT3) is a signal transcription protein that exists in the cytoplasm. The abnormal activation of STAT3 is closely related to cell proliferation, differentiation, and canceration. It has abnormal expression in cancer stem cells such as breast cancer, pancreatic cancer, lymphoma, and lung cancer. Therefore, inhibiting the abnormal expression of STAT3 has become a new approach for antitumor therapy.

Objective To establish the chemical synthesis of the active ingredient rosavin of Rhodiola rosea. Methods β-D-pentaacetylglucose, 1-hydroxy-2,3,4-triacetylarabinose and cinnamyl alcohol were used as starting materials. The target compound was prepared by 1-position selective of β-D-pentaacetylglucose deacetylation, glycosylation reaction, glucose 6-OH selective protection and deprotection and other 8-step reactions. Results The target product, rosavage, was successfully obtained with high yield. The structure was confirmed by ESI-MS, ¹H-NMR and ¹³C-NMR. The protection of 6-OH with high selectivity and high yield of tert-butyldiphenyl chlorosilane played a vital role in the synthesis process,. Conclusion The synthetic route has the advantages of simple operation, high yield, and good safety.

PURPOSE: Although the effect of lysosome-associated protein transmembrane 4 beta (LAPTM4B) on the proliferation, migration, and invasion of breast cancer (BC) cells has already been studied, its specific role in BC progression is still elusive. Here, we evaluated the effect of different levels of LAPTM4B expression on the proliferation, invasion, adhesion, and tumor formation abilities of BC cells in vitro, as well as on breast tumor progression in vivo. METHODS: We investigated the influence of LAPTM4B expression on MCF-7 cell proliferation, invasion, adhesion, and tube formation abilities in vitro through its overexpression or knockdown and on breast tumor progression in vivo. RESULTS: Cell growth curves and colony formation assays showed that LAPTM4B promoted the proliferation of breast tumor cells. Cell cycle analysis results revealed that LAPTM4B promoted the entry of cells from the G1 into the S phase. Transwell invasion and cell extracellular matrix adhesion assays showed that LAPTM4B overexpression increased the invasion and adhesion capabilities of MCF-7 cells. More branches were observed in MCF-7 cells overexpressing LAPTM4B under an electron microscope. In comparison with LAPTM4B overexpression, LAPTM4B knockdown decreased the expression of vascular endothelial growth factor-A and significantly inhibited the vasculogenic tube formation ability of tumors. These results were also verified with western blot analysis. CONCLUSION: LAPTM4B promoted the proliferation of MCF-7 cells through the downregulation of p21 (WAF1/CIP1) and caspase-3, and induced cell invasion, adhesion, and angiogenesis through the upregulation of hypoxia-inducible factor 1 alpha, matrix metalloproteinase 2 (MMP2), and MMP9 expression. This specific role deems LAPTM4B as a potential therapeutic target for BC treatment.
Blotting, Western ; Breast Neoplasms ; Breast ; Caspase 3 ; Cell Cycle ; Disease Progression ; Down-Regulation ; Extracellular Matrix ; Hypoxia-Inducible Factor 1 ; In Vitro Techniques ; Matrix Metalloproteinase 2 ; MCF-7 Cells ; S Phase ; Up-Regulation ; Vascular Endothelial Growth Factor A