Objective To investigate the level of miR-634 in nasopharyngeal carcinoma and its effects on the cell growth and MEK/ERK signaling pathway in nasopharyngeal carcinoma, and discuss the possible mechanism.
Methods Total 60 specimens of nasopharyngeal carcinoma and 60 specimens of nasopharyngeal non-cancerous tissue were collected. The level of miR-634 in nasopharyngeal carcinoma tissues and nasopharyngeal carcinoma cells were determined by reverse transcription-polymerase chain reaction (RT-PCR). Human nasopharyngeal carcinoma CNE-1 cells were divided into blank control group, negative control group and overexpressed miR-634 group. The cell proliferation was measured by MTT. The cell apoptosis was detected by flow cytometry. The levels of extracellular regulated protein kinase (ERK), phosphorylated extracellular regulated protein kinase (p-ERK), mitogen-activated protein kinase (MEK) and phosphatiated mitogen-activated protein kinase (p-MEK) proteins in nasopharyngeal carcinoma cells were determined by Western blotting.
Results The level of miR-634 in nasopharyngeal carcinoma tissues was lower than that in the adjacent tissues (
P<0.05). The level of miR-634 in nasopharyngeal carcinoma cells was lower than that in normal nasopharyngeal epithelial cells (
P<0.05). Compared with the blank control group and the negative control group, the level of miR-634 and the apoptosis rate in the overexpressed miR-634 group were increased (
P<0.05); the levels of p-ERK, p-MEK mRNA and protein were decreased (
P<0.05). After transfection for 3 d and 5 d, There was significant difference in OD values among the three groups (
P<0.05), compared with the blank control group and the negative control group, the OD value of the overexpress miR-634 group was decreased (
P<0.05).
Conclusion The level of miR-634 is decreased in nasopharyngeal carcinoma, and overexpression of miR-634 can inhibit the proliferation of nasopharyngeal carcinoma and promote apoptosis. The mechanism may be related to MEK/ERK signaling pathway.
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