RESUMO
Objective@#To explore the effect of circ_0001273 on the proliferation, migration and invasion of oral squamous cell carcinoma（OSCC） cells and to provide a relevant research basis for the use of targeted therapy in OSCC. @*Methods@#Data from twelve patients with a clinical diagnosis of OSCC were collected from tumor specimens and adjacent tissues. qRT-PCR was used to detect the expression levels of circ_0001273, circ_0018569, circ_0027152, and circ_0001273 which had the highest difference in expression in cancer and adjacent tissues was selected. siRNA was used for the knockdown of circ_0001273 in two types of OSCC cell lines, UM1 and CAL27, and the effects on the proliferation, migration, and invasion of UM1 and CAL27 cells were measured by MTS and Transwell experiments, respectively. @*Results@#The expression of circ_0001273 was abnormally increased in the 12 OSCC tissues (P < 0.05). After knocking down circ_0001273 in UM1 and CAL27 cells, the proliferation, migration and invasion abilities of UM1 and CAL27 cells were significantly reduced (P < 0.05).@*Conclusion@#The knockdown of circ_0001273 can inhibit the proliferation, migration and invasion of OSCC cells.
RESUMO
PURPOSE: Oral squamous carcinoma (OSCC) cells exhibit resistance to chemotherapeutic agent-mediated apoptosis in the late stage of malignancy. Increased levels of heat shock proteins 70 (HSP70) in cancer cells are known to confer resistance to apoptosis. Since recent advances in the understanding of bacterial toxins have produced new strategies for the treatment of cancers, we investigated the effect of Pseudomonas aeruginosa exotoxin A (PEA) on HSP70 expression and induction of apoptosis in chemoresistant OSCC cell line (YD-9). MATERIALS AND METHODS: The apoptotic effect of PEA on chemoresistant YD-9 cells was confirmed by MTT, Hoechst and TUNEL stains, DNA electrophoresis, and Western blot analysis. RESULTS: While YD-9 cells showed high resistance to chemotherapeutic agents such as etoposide and 5-fluorouraci (5-FU), HSP70 antisense oligonucelotides sensitized chemoresistant YD-9 cells to etoposide and 5-FU. On the other hand, PEA significantly decreased the viability of YD-9 cells by deteriorating the HSP70-relating protecting system through inhibition of HSP70 expression and inducing apoptosis in YD-9 cells. Apoptotic manifestations were evidenced by changes in nuclear morphology, generation of DNA fragmentation, and activation of caspases. While p53, p21, and E2F-1 were upregulated, cdk2 and cyclin B were downregulated by PEA treatment, suggesting that PEA caused cell cycle arrest at the G2/M checkpoint. CONCLUSION: Therefore, these results indicate that PEA reduced the chemoresistance through inhibition of HSP70 expression and also induced apoptosis in chemoresistant YD-9 cells.