Long noncoding RNAs play essential roles in cancer development and progression. Here, we tried to investigate the role of GIHCG in the progression and metastasis of tongue squamous cell carcinoma (TSCC). In our study, we showed that that the expression level of GIHCG was upregulated in TSCC tissues and cell lines. In addition, we indicated that high GIHCG expression was positively associated with poor overall survival. Moreover, ectopic expression of GIHCG enhanced TSCC cell cycle, proliferation, and migration. Elevated expression of GIHCG inhibited the miR-429 expression in TSCC cells. We demonstrated that the expression level of miR-429 was lower in TSCC tissues and cell lines. Low miR-429 expression was positively associated with poor overall survival. We then determined the correlation between miR-429 and GIHCG expression levels. A statistically significantly inverse correlation was observed between miR-429 and GIHCG expression levels in TSCC tissues. In addition, overexpression of miR-429 suppressed the TSCC cell cycle, proliferation, and migration. Elevated expression of GIHCG promoted TSCC cell cycle, proliferation, and migration through regulating miR-429 expression. These results suggested that GIHCG increased TSCC progression through negative modulation of miR-429. Our results suggested that GIHCG/miR-429 might play a vital role in TSCC progression.
Veratric acid, one of the major benzoic acid isolated from vegetables and fruits, has been reported to have anti-inflammatory activity. The purpose of this study was to investigate the anti-inflammatory effects of veratric acid on lipopolysaccharide (LPS)-induced inflammatory response in human gingival fibroblasts (HGFs). HGFs were pretreated with veratric acid 1 h before LPS stimulation. The productions of IL-6 and IL-8 were detected by ELISA. The expression of iNOS, COX-2, PI3K, AKT, and NF-κB were detected by western blotting. The results showed that veratric acid inhibited LPS-induced IL-6 and IL-8 production, as well as iNOS and COX-2 expression. Veratric acid also inhibited LPS-induced NF-κB activation. In addition, veratric acid was found to suppress LPS-induced PI3K and AKT phosphorylation. In conclusion, the anti-inflammatory mechanism of veratric acid is due to its ability to inhibit PI3K/Akt/NF-κB signaling pathway.
Long non-coding RNAs (lncRNAs) have gained a lot of attention because they participate in several human disorders, including tumors. This study determined the role of LncRNA CASC15 (cancer susceptibility candidate 15) in the development of tongue squamous cell carcinoma (TSCC). Here, we identified that CASC15 expression was upregulated in TSCC samples and cell lines. We showed that overexpression of CASC15 promoted cell proliferation, cycle, and migration in TSCC. In addition, we revealed that miR-33a-5p expression was downregulated in TSCC tissues and cell lines. Moreover, we showed that the expression of CASC15 was negatively related with miR-33a-5p expression in TSCC tissues. Ectopic expression of miR-33a-5p suppressed cell proliferation, cycle, and migration in TSCC. Elevated expression of CASC15 suppressed miR-33a-5p expression and promoted ZEB1 expression in SCC4 cell. Ectopic expression of CASC15 promoted TSCC cell proliferation, cycle, and migration through targeting miR-33a-5p. These results suggested that lncRNA CASC15 and miR-33a-5p might be exploited as new markers of TSCC and were potential treatment targets for TSCC patients.
Denervation effectively aggravates ligature-induced rat periodontitis by the NF-κB signaling pathway for excessive production of IL-1β and TNF-α and increased osteoclasts for decreased OPG/RANKL ratio. The rat model of inferior alveolar nerve transection that combined ligature-induced periodontitis provides an animal model to observe further the change of nerve-related factors in the occurrence and development of periodontitis, so as to select positive nerve-related factors to regulate inflammation and promote periodontal regeneration in the future.
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