[Retracted] lncRNA MSC-AS1/miRNA-429 Axis Mediates Growth and Metastasis of Nasopharyngeal Carcinoma via JAK1/STAT3 Signaling Pathway

Figure 5

miR-429 knockdown promotes the proliferation, migration, and invasion of C666-1 cells through JAK1/STAT3 pathway. (a) The binding site between miR-429 and JAK1 was predicted by starBase. The mutant binding sequence was designed for dual-luciferase report assay. The luciferase signaling was significantly declined in JAK1 wild group transfected with miR-429 mimic. , compared with miRNA-ctrl group. After being transfected with si-JAK1, the mRNA expression (b) and protein expression (c) of JAK1 was detected by RT-PCR analysis and western blot analysis, respectively. Results showed that JAK1 expression significantly declined, suggesting the transcription efficiency was high. NS: no significant difference; ; . (d) Cell colony formation assay was performed to evaluate cell validity. Cell vitality was significantly elevated after being cultured for 24, 48, and 72 h in the miR-429 inhibitor + si-NC group and reversed after being transfected with si-JAK1. . (e) Cell colony formation assay showed that the number of cell colonies was significantly increased in miR-429 knockdown cells and obviously reversed after cotransfected with si-JAK1. NS: no significant difference; . Cell wound scratch (f) and transwell assay (g) were conducted to further investigate the effect of si-JAK1 on cell migration and invasion. The migration and invasion ability of C666-1 cells were significantly elevated in the miR-429 inhibitor + si-NC group. NS: no significant difference; ; .

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