miR-503 targeting RECK regulates the proliferation, invasion and apoptosis of oral squamous cells carcinoma cells
[Objective:] To study the role of miR-503 targeting reversion inducing cysteine rich protein with Kazal motifs (RECK) in the progression of oral squamous cell carcinoma (OSCC). [Methods:] Human OSCC cells SCC-4 were divided into NC inhibitor group (transfected with miR-503 inhibitor negative control...
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| Main Authors: | , , |
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| Format: | Article |
| Language: | zho |
| Published: |
Editorial Office of Journal of Oral and Maxillofacial Surgery
2023-10-01
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| Series: | Kouqiang hemian waike zazhi |
| Subjects: | |
| Online Access: | https://journal06.magtech.org.cn/Jweb_joms/EN/10.12439/kqhm.1005-4979.2023.05.005 |
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| Summary: | [Objective:] To study the role of miR-503 targeting reversion inducing cysteine rich protein with Kazal motifs (RECK) in the progression of oral squamous cell carcinoma (OSCC). [Methods:] Human OSCC cells SCC-4 were divided into NC inhibitor group (transfected with miR-503 inhibitor negative control sequence), miR-503 inhibitor group (transfected with miR-503 inhibitor), si-NC group (transfected with RECK siRNA negative control sequence), si-RECK group (transfected with RECK siRNA) and miR-503 inhibitor+si-NC group (co-transfected with miR-503 inhibitor and RECK siRNA negative control sequence) and miR-503 inhibitor+si-RECK group (co-transfected with miR-503 inhibitor and RECK siRNA); real-time quantitative polymerase chain reaction (RT-qPCR) was used to detect the expression level of miR-503 and RECK in immortalized human oral keratinocytes RT7 and SCC-4 cells in each group; Western blotting was used to detect the protein expression level of RECK. TargetScan was used to predict the target gene of miR-503 and dual luciferase reporter gene detection was used to verify the targeting relationship between miR-503 and RECK; CCK-8 and EdU staining were used to detect cell proliferation ability in each group; Transwell chamber was used to detect cell invasion ability; flow cytometry was used to detect cell apoptosis in each transfected group. [Results:] Compared with RT7 cells, the expression level of miR-503 in SCC-4 cells was increased (P<0.05), while the expression level of RECK was decreased (P<0.05); Compared with NC inhibitor group, the mRNA expression level of RECK and the protein expression level of RECK in the miR-503 inhibitor group were significantly increased (P<0.05). In addition, TargetScan database and luciferase reporter gene analysis showed a targeting relationship between RECK and miR-503 (P<0.01), suggesting that miR-503 could target the expression of RECK; compared with NC inhibitor group, the proliferation ability and invasion ability of SCC-4 cells in miR-503 inhibitor group were significantly decreased (P<0.05), while cell apoptosis ability was significantly increased (P<0.01), which indicated that the inhibition of miR-503 expression decreased proliferation, invasion ability and accelerated apoptosis ability of OSCC cells. Compared with si-NC group, the cell proliferation and invasion ability of si-RECK group were significantly increased (P<0.05), while cell apoptosis ability was significantly decreased (P<0.05), which indicated that the knockdown of RECK increased the proliferation, invasion ability and reduced the apoptosis ability of OSCC cells; compared with the miR-503 inhibitor+si-NC group, the expression level of RECK mRNA and the apoptotic ability in the miR-503 inhibitor+si-RECK group were significantly decreased (P<0.05), while the cell proliferation and invasion ability was significantly increased (P<0.05), which indicated that the knockdown of RECK weakened the inhibitory effect of miR-503 inhibitor on biological behavior of OSCC cells. [Conclusion:] The expression of miR-503 is up-regulated in OSCC cells. Inhibition of miR-503 can weaken its down-regulation of the target gene RECK, thereby reducing the proliferation and invasion of tumor cells and promoting cell apoptosis. |
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| ISSN: | 1005-4979 |