Guangdong Province Key Laboratory of Pharmaceutical Bioactive Substances

Guangzhou, China

Guangdong Province Key Laboratory of Pharmaceutical Bioactive Substances

Guangzhou, China
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Jin X.-B.,Guangdong Pharmaceutical University | Jin X.-B.,Guangdong Province Key Laboratory of Pharmaceutical Bioactive Substances | Mei H.-F.,Guangdong Pharmaceutical University | Mei H.-F.,Guangdong Province Key Laboratory of Pharmaceutical Bioactive Substances | And 10 more authors.
Biological and Pharmaceutical Bulletin | Year: 2013

This study was designed to explore the effects of Musca domestica antimicrobial peptides cecropin on the adhesion and migration of human hepatocellular carcinoma BEL-7402 cells. The adhesive and migratory capacities were determined by adhesion assay and transwell assay, respectively. The changes in microvilli of tumor cells were determined by scanning electron microscopy (SEM). Western blotting and quantitative polymerase chain reaction (qPCR) were carried out to determine the expression levels of proteins related to adhesion and migration, such as matrix metalloproteinase-2 (MMP2), tissue inhibitors of metalloproteinase-2 (TIMP2), and epithelial cadherin (E-cadherin). We found that Musca domestica cecropin inhibited the adhesion and migration of BEL-7402 cells, which also displayed curling microvilli, increased ball structures on cell surface, gradually broken connections between tumor cells, and even disappeared microvilli on some cells. The expression of MMP2 was significantly reduced after cecropin treatment, while the levels of TIMP2 and E-cadherin were significantly increased. These results suggest that Musca domestica cecropin inhibits the adhesion and migration of human hepatocellular carcinoma BEL-7402 cells by destroying the microvilli of tumor cells and changing the expression of MMP2, TIMP2 and E-cadherin. © 2013 The Pharmaceutical Society of Japan.


Jin X.-B.,Guangdong Pharmaceutical University | Jin X.-B.,Guangdong Province Key Laboratory of Pharmaceutical Bioactive Substances | Wang Y.-J.,Guangdong Pharmaceutical University | Wang Y.-J.,Guangdong Province Key Laboratory of Pharmaceutical Bioactive Substances | And 12 more authors.
Asian Pacific Journal of Cancer Prevention | Year: 2014

Conventional chemotherapy against hepatocellular carcinoma typically causes various side effects. Our previous study showed that cecropin of Musca domestica can induce apoptosis in human hepatocellular carcinoma BEL-7402 cells in vitro. However, whether cecropin inhibits BEL-7402 cell in vivo and the question of possible side effects remained undentified. The present study confirmed tumor-inhibitory effects of cecropin in vivo, and furthermore strongly suggested that cecropin cytotoxicity in BEL-7402 cells in vivo may be mainly derived from its pro-apoptotic action. Specifically, we found that cecropin exerted no obvious side effects in tumor-bearing mice as it had no significant hematoxicity as well as visceral toxicity. Therefore, cecropin may be a potential candidate for further investigation as an antitumor agent against hepatocellular carcinoma.


Wang W.-Z.,Guangdong Province Key Laboratory of Pharmaceutical Bioactive Substances | Wang W.-Z.,Guangdong Pharmaceutical University | Pu Q.-H.,Guangdong Province Key Laboratory of Pharmaceutical Bioactive Substances | Pu Q.-H.,Guangdong Pharmaceutical University | And 11 more authors.
Leukemia Research | Year: 2015

BCR-ABL tyrosine kinase inhibitor imatinib fails to eradicate leukemia stem cells (LSCs), the underlying mechanisms maintaining CML LSCs remain poorly understood. Here, we showed that transient inhibition of miR-21 by antagomiR-21 markedly increased imatinib-induced apoptosis in CML, but not normal CD34+ stem/progenitor cells. Furthermore, PI3K inhibitors also significantly sensitized CML CD34+ cells to imatinib-induced apoptosis. MiR-21 or PI3K inhibitor in combination with imatinib treatment significantly decreased AKT phosphorylation and c-Myc expression than either agent did alone, but did not affect Bim and Bcl-6 expresssion. These findings indicate that miR-21 is required for maintaining the imatinib-resistant phenotype of CML CD34+ cells through PI3K/AKT signaling pathway, thus providing the basis for a promising therapeutic approach to eliminate CML LSCs. © 2015 Elsevier Ltd.


PubMed | Sun Yat Sen University, Guangdong Pharmaceutical University and Guangdong Province Key Laboratory of Pharmaceutical Bioactive Substances
Type: Journal Article | Journal: Leukemia research | Year: 2015

BCR-ABL tyrosine kinase inhibitor imatinib fails to eradicate leukemia stem cells (LSCs), the underlying mechanisms maintaining CML LSCs remain poorly understood. Here, we showed that transient inhibition of miR-21 by antagomiR-21 markedly increased imatinib-induced apoptosis in CML, but not normal CD34+ stem/progenitor cells. Furthermore, PI3K inhibitors also significantly sensitized CML CD34+ cells to imatinib-induced apoptosis. MiR-21 or PI3K inhibitor in combination with imatinib treatment significantly decreased AKT phosphorylation and c-Myc expression than either agent did alone, but did not affect Bim and Bcl-6 expresssion. These findings indicate that miR-21 is required for maintaining the imatinib-resistant phenotype of CML CD34+ cells through PI3K/AKT signaling pathway, thus providing the basis for a promising therapeutic approach to eliminate CML LSCs.

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