Abstract
The oral cancer cell line OC3-I5 with a highly invasive ability was selected and derived from an established OSCC line OC3. In this study, we demonstrated that matrix metalloproteinases protein MMP-13 was up-regulated in OC3-I5 than in OC3 cells. We also observed that expression of epithelial–mesenchymal transition (EMT) markers including Twist, p-Src, Snail1, SIP1, JAM-A, and vinculin were increased in OC3-I5 compared to OC3 cells, whereas E-cadherin expression was decreased in the OC3-I5 cells. Using siMMP-13 knockdown techniques, we showed that siMMP-13 not only reduced the invasion and migration, but also the adhesion abilities of oral cancer cells. In support of the role of MMP-13 in metastasis, we used MMP-13 expressing plasmid-transfected 293T cells to enhance MMP-13 expression in the OC3 cells, transplanting the MMP-13 over expressing OC3 cells into nude mice led to enhanced lung metastasis. In summary, our findings show that MMP-13 promotes invasion and metastasis in oral cancer cells, suggesting altered expression of MMP-13 may be utilized to impede the process of metastasis.
Highlights
Oral cancer occurring often in oral cavity belongs to head and neck cancer; tumors at these sites typically cause eating, drinking, and speech difficulties as well as facial malformation resulting from treatment
In the less invasive OC3 cell line, after downregulation by siMMP-13, the G1 phase decreased by approximately 19.9%, the S phase increased by approximately 3.7%, and the G2/M phase increased by approximately 11.2%
In transwell invasion and migration assays, the shMMP-13 knockdown, the transwell invasion ability of transwell membrane is a cell membrane simulator, and the the OC3 and OC3-I5 cells decreased by 50% and 70%, aggressive cancer cell enhances the invasion ability because respectively. (Figure 7) These results indicate that longof the high expression of metastasis-related proteins such as term shMMP-13 can be used in animal tests
Summary
The oral cancer cell line OC3-I5 with a highly invasive ability was selected and derived from an established OSCC line OC3. R matrix metalloproteinases protein MMP-13 was up-regulated in OC3-I5 than in OC3 cells. Using siMMP-13 knockdown techniques, we showed that siMMP-13 reduced the invasion and migration, and the adhesion abilities of oral cancer cells. In support of the role of MMP-13 in metastasis, we used MMP-13 expressing. E plasmid-transfected 293T cells to enhance MMP-13 expression in the OC3 cells, transplanting the MMP-13 over expressing OC3 cells into nude mice led to enhanced lung metastasis. Our findings show that MMP-13 promotes invasion. Rand metastasis in oral cancer cells, suggesting altered expression of MMP-13 may be utilized to impede the process of metastasis
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