CircLDLRAD3 inhibits Oral squamous cell carcinoma progression by regulating miR-558/Smad4/TGF-ß.

Oral squamous cell carcinoma (OSCC) is a malignant neoplasm with high mortality and morbidity. The role of circRNA and its molecular mechanism in OSCC remains largely unknown. The study aims to explore the role of a novel circular RNA (circLDLRAD3) in OSCC and its underlying mechanism. PCR and fluorescence in situ hybridization were used to explore the expression features of circLDLRAD3 in OSCC. The effects of circLDLRAD3 on the behaviour of OSCC were investigated using CCK-8, colony formation assay, transwell and animal experiments. Bioinformatics analysis along with dual luciferase reporter assay and RIP assay were used to reveal the interaction between circLDLRAD3, miR-558 and Smad4. It was revealed that circLDLRAD3 exhibited low expression status in OSCC. CircLDLRAD3 inhibits proliferation, migration, and invasion of OSCC cells both in vitro and in vivo. Mechanistically, circLDLRAD3 could bind with miR-558 to positively regulate its target gene Smad4 expression. Rescue experiments further confirmed both miR-558 overexpression and Smad4 knockdown could reverse the influence of circLDLRAD3 on OSCC phenotypes. Moreover, circLDLRAD3 regulate the TGF-ß signalling pathways to influence EMT through miR-558/Smad4 axis. Our study found that circLDLRAD3 is downregulated in OSCC and verified its tumour suppressor function and mechanism in OSCC through sponging miR-558 to regulate miR-558/Smad4/TGF-ß axis. The characterization of such regulating network uncovers an important mechanism underlying OSCC progression, which could provide promising targets targeted therapy strategies for OSCC in the future.

Clinical efficacy of melatonin as adjunctive therapy to non-surgical treatment of periodontitis: a systematic review and meta-analysis.

OBJECTIVE: This study aimed to evaluate the effect of adjunctive melatonin supplementation on clinical outcomes after non-surgical periodontal treatment. METHODS: PubMed, Embase, and Web of Science databases were systematically searched for randomised controlled trials (RCTs) of melatonin adjuvant therapy for periodontitis from inception until May 2021. The systematic review was conducted according to the Preferred Reporting Items for Systematic Reviews and Meta-Analyses guidelines and registered on The International Prospective Register of Systematic Reviews (PROSPERO) (CRD42021250630). The risk of bias of included studies was assessed according to the Cochrane Handbook for Systematic Reviews of Interventions. The pooled effect estimates were calculated by a random-effects model, and results were expressed as weighted mean differences (WMD). RESULTS: Seven RCTs comprising 412 participants were included in the meta-analysis. The pooled results showed that adjuvant use of melatonin for non-surgical periodontal treatment significantly improved the probing depth (PD) [WMD = - 1.18, 95% CI (- 1.75, - 0.62) I2 = 85.7%], clinical attachment loss (CAL) [WMD = - 1.16, 95% CI (- 1.60, - 0.72) I2 = 76.7%] and gingival index (WMD = - 0.29, 95%CI [- 0.48, - 0.11], I2 = 63.6%) compared with non-surgical treatment alone. In addition, subgroup analysis showed that higher doses of melatonin (3-10 mg) significantly improved PD [WMD = - 1.32, 95%CI (- 2.31, - 0.15) I2 = 93%] and CAL [WMD = - 1.30, 95%CI (- 1.80, - 0.81) I2 = 73.7%] compared with lower doses of melatonin (< 3 mg). CONCLUSIONS: We found that adjunctive melatonin supplementation can significantly improve the periodontal status after non-surgical treatment, suggesting that melatonin may be a new adjuvant therapy for periodontitis when non-surgical periodontal treatment alone cannot achieve the desired improvement.

Role of Interleukin-10 Promoter Polymorphisms in Oral Cancer Susceptibility: A Meta-Analysis.

Role of interleukin-10 (IL-10) promoter polymorphisms in the risk of oral cancer (OC) remains controversial. The present study aimed to explore the relation between IL10 promoter polymorphisms and the progression of oral cancer by performing meta-analysis. Seven studies with a total of 2141 controls and 1928 cases were included in our analysis. Overall results showed significant associations between IL-10-1082A/G gene polymorphism and OC susceptibility under all five models. However, OC was not significantly related to the IL-10-592A/C or -819 T/C polymorphism (p > 0.05).

Correlation between hypoxia-inducible factor-1α C1772T/G1790A polymorphisms and head and neck cancer risk: a meta-analysis.

OBJECTIVE: This meta-analysis was implemented to evaluate the association between hypoxia-inducible factor-1α (HIF-1α) C1772T/G1790A polymorphisms and susceptibility to head and neck cancer (HNC). MATERIAL AND METHODS: This meta-analysis has been registered on PROSPERO platform ( CRD42021257309 ). The PubMed, Embase and Web of Science databases were searched to retrieve eligible published papers. STATA software was used to calculate the pooled odds ratios (ORs) and corresponding 95% confidence intervals (CIs) to assess the correlation strength. RESULTS: Our results demonstrated that the HIF-1α C1772T polymorphism was significantly related to an increased HNC risk (OR = 2.27, 95% CI = 1.17-4.42 for the homozygous model; OR = 11.53, 95% CI = 1.11-120.4 for the recessive model), especially in Caucasians (OR = 2.16, 95% CI = 1.09-4.27 for the homozygous model; OR = 2.28, 95% CI = 1.15-5.51 for the recessive model). Similarly, a remarkable correlation was discovered between the G1790A polymorphism and HNC risk (OR = 72.11, 95% CI = 2.08-2502.4 for the homozygous model; OR = 58.05, 95% CI = 1.70-1985.77 for the recessive model). Moreover, in the subgroup analysis by source of controls, a statistically significant correlation was discovered in the population-based (PB) subgroup (OR = 9.43, 95% CI = 1.20-73.9 for allelic model; OR = 72.11, 95% CI = 2.08-2502.4 for the homozygous model; OR = 3.22, 95% CI = 1.28-8.08 for the heterozygous model; OR = 7.83, 95% CI = 1.48-41.37 for the dominant model; OR = 58.05, 95% CI = 1.70-1985.8 for the recessive model) but not in the hospital-based (HB) subgroup. CONCLUSION: Our study found that both HIF-1α C1772T and G1790A polymorphisms might be a higher risk of HNC, especially in the Caucasian group with the C1772T polymorphism.