Downregulation of lncRNA CCHE1 inhibits cell proliferation, migration and invasion by suppressing MEK/ERK/c-MYC pathway in nasopharyngeal carcinoma.

OBJECTIVE: The current study was designed to investigate the functionality of lncRNA CCHE1 in nasopharyngeal carcinoma. MATERIALS AND METHODS: MiRNA levels of lncRNA CCHE1 were examined by RT-qPCR. CCK8 assay and colony formation assay were together performed to detect cell proliferation viability. Furthermore, wound healing assay and transwell assay were respectively conducted to assess cell migration and invasion. In addition, proteins related to MEK/ERK/c-MYC pathway were detected by Western blot. RESULTS: Elevated levels of CCHE1 were verified in NPC cell lines. Downregulation of CCHE1 significantly inhibited tumor growth and suppressed A549 cell proliferation, migration and invasion. MEK/ERK/c-MYC pathway was activated in nasopharyngeal carcinoma. Treatment of PD98059 (MEK inhibitor) or SCH772984 (ERK inhibitor) reversed the effects of CCHE1 on cell proliferation, migration and invasion in NPC. CONCLUSIONS: The present study suggested that downregulation of lncRNA CCHE1 could inhibit cell proliferation, migration and invasion by suppressing MEK/ERK/c-MYC pathway in nasopharyngeal carcinoma.

Effects of lncRNA gm4419 on rats with hypertensive cerebral atherosclerosis through NF-κB pathway.

OBJECTIVE: To explore the effects of long non-coding ribonucleic acid (lncRNA) Gm4419 on rats with hypertensive cerebral atherosclerosis through the nuclear factor-kappa B (NF-κB) pathway. MATERIALS AND METHODS: Healthy male rats were selected and randomly divided into control group, model group (hypertensive cerebral atherosclerosis model), and lncRNA group (hypertensive cerebral atherosclerosis model + lncRNA injection). Neurological deficit scoring criteria, flow cytometry, Western blotting, and staining method were adopted to measure the differences in the neurological function score, NF-κB activity, and chemerin level of rats in the three groups. RESULTS: The neurological scores revealed that the neurological function of rats was not damaged in control group, while it was severely damaged in model group. However, the neurological function of rats was more severely damaged in lncRNA group than that in control group and model group, while the neurological function deficits were slighter in model group. In terms of NF-κB expression activity in mononuclear cells, the serum activity of NF-κB in control group appeared the lowest among the three groups and was significantly higher in lncRNA group than in model group. The serum chemerin level was evidently increased in model group compared with control group, while it was significantly decreased in lncRNA group compared with model group and control group. Moreover, the levels of NF-κB and chemerin were most evidently influenced in lncRNA group. CONCLUSIONS: Activating the NF-κB signal, lncRNA Gm4419 promotes the expression of chemerin signal, accelerates the apoptosis of nerve cells, and motivates the deterioration of hypertensive cerebral arteriosclerosis.