Abstract
AbstractThere is increasing evidence that the secretory/excretory antigens of the larval stage ofEchinococcus granulosus(hydatid cyst fluid; HCF) can induce both anticancer and oncogenesis effects between parasite-derived metabolites and various cancer lines. The dual role of miR-145 as a tumor suppressor or oncogene has been previously reported in cancers. Nevertheless, it remains unknown, how miR-145 induces apoptosis in HCF-treated lung cancer cells. The fertile HCF was obtained from sheep and subjected to purification and lyophilization. H1299 human lung cancer cells were cultured into two groups: HCF-treated H1299 lung cancer cells and control cells. To evaluate the effects of HCF on the H1299 cells, cell viability was performed by MTT assay. The caspase-3 activity was assessed using fluorometric assay. Furthermore, the mRNA expression of VGEF, Vimentin, caspase-3, miRNA-145, Bax and Bcl-2 genes were characterized by Real-time PCR. A scratch test was done to assess the effects of HCF on cell mobility. MTT assay revealed that there is an increasing slope in the growth of H1299 cells when treated with 60 μg/mL of fertile HCF for 24 h. The fold change of caspase-3, miRNA-145, Bax/Bcl-2 ratio and caspase-3 activity was lower in the HCF-treated H1299 cells than in the control cell. The fold change of VGEF and Vimentin genes in the HCF-treated H1299 cells was higher than that in the control cell. The scratch outcome demonstrated that the mobility of H1299 cells was increased at 24 and 48 hours of scratched time after exposure to HCF. Our results suggest that induction of low expression of miR-145 in patients with hydatid cysts could be a possible oncogenic regulator of lung cancer growth. We conclude that miR-145 may be a promising marker for the diagnosis of lung cancer patients co-infected with pulmonary hydatid cysts. To validate this assumption, further study is needed to assess microRNA profile and potent oncogenesin vivosetting.
Publisher
Cold Spring Harbor Laboratory