Purpose: To investigate the function of long noncoding RNA (lncRNA) FGD5-AS1 in oral cancer (OC) and to further clarify the regulation of FGD5-AS1 on miR-153-3p/MCL1 axis. Results: FGD5-AS1 was significantly increased in OC tissues and cells. Loss of FGD5-AS1 inhibited the proliferation, migration and invasion of OC cells. FGD5-AS1 acted as a sponge of miR-153-3p, and MCL1 was direct target of miR-153-3p. Forced expression of miR-153-3p or inhibition of MCL1 reversed the promoted role of FGD5-AS1 on OC cells’ migration and invasion. The in vivo tumor growth assay showed that FGD5-AS1 promoted OC tumorigenesis by regulating miR-153-3p/MCL1 axis. Conclusions: Our research revealed lncRNA FGD5-AS1 acted as an oncogene by regulating MCL1 via sponging miR-153-3p, thus providing some novel experimental basis for clinical treatment or prevention of OC. Patients and Methods: The mRNA expression of FGD5-AS1, miR-153-3p and MCL1 was detected by qRT-PCR. CCK8 assay, Edu assay, wound healing assay and transwell assay were used to detect the FGD5-AS1/ miR-153-3p/MCL1 axis function on proliferation, migration and invasion in OC cells. Western blot was used to calculate protein level of MCL1. Luciferase assay was used to detect the binding of miR-153-3p and MCL1, FGD5-AS1and miR-153-3p.

Osteogenic differentiation is a complicated process that depends on various regulatory factors and signal pathways. In our research, the osteogenic differentiation capacity was analyzed by alizarin red staining, alkaline phosphatase activity, and protein levels of osteogenic differentiation markers including runt-related transcription factor 2, bone morphogenetic protein 2, and osteocalcin (OCN). We observed a notable decrease of miR-24-3p level in osteogenic-differentiated human periodontal ligament stem cells (hPDLSCs) by microarray analysis. In our gain-and loss-offunction experiments, we discovered that miR-24-3p has a suppression effect on hPDLSCs osteogenic differentiation. Moreover, SMAD family member 5 (Smad5), the critical osteogenic differentiation transcription factors, was predicted to be targets of miR-24-3p. In addition, luciferase reporter assay further proved that miR-24-3p directly targeted the 3′-untranslated region of Smad5. Similarly, we found that the overexpression of miR-24-3p significantly decreased the Smad5 messenger RNA level in hPDLSCs, which was detected by real-time quantitative polymerase chain reaction.Then hPDLSCs were transfected with miR-24-3p mimics to inhibit Smad5 expression; meanwhile, Smad5 RNA interference could significantly reverse the osteogenic differentiation inhibition effect of miR-24-3p. In brief, a series of data showed that miR-24-3p is a regulator of Smad5, playing an important role in osteogenic differentiation. K E Y W O R D Shuman periodontal ligament stem cells (hPDLSCs), miR-24-3p, oral medicine, osteogenic differentiation, SMAD family member 5 (Smad5)

BackgroundPolysulfides are reported to be involved in various important biological processes. N‐acetyl‐l‐cysteine polysulfide with 2 sulfane sulfur atoms (NAC‐S2) regulates diverse toll‐like receptor (TLR) signaling pathways. Here, we aimed to determine the role of NAC‐S2 in periodontitis and explore the potential mechanism.MethodsA periodontitis mouse model was established by ligating the subgingival between the first and second molars in wild‐type, TLR4‐/‐, and Myd88‐/‐ mice.ResultsNAC‐S2 did not affect the proportion of macrophages (CD11b+F4/80+) or neutrophils (CD11b+GR‐1+) in the bone marrow. Mechanically, lipopolysaccharides (LPS), Zymosan A, or poly I: C induced tumor necrosis factor (TNF), interleukin (IL)‐6, and IL‐1β expression in bone marrow‐derived macrophages (BMDMs) could be inhibited by NAC‐S2. On the other hand, NAC‐S2 suppressed the phosphorylation levels of IκB‐α, p65, and IκB kinase (IKK)‐β induced by LPS in BMDMs, while LPS induced phosphorylation of ERK1/2, p38, and transforming growth factor β‐activated kinase 1 (TAK1) could not be affected by NAC‐S2. In wild‐type periodontitis mice, NAC‐S2 administration decreased the cemento‐enamel‐junction–alveolar bone crest (CEJ‐ABC) distance and the relative mRNA expression of TNF, IL‐6, and IL‐1β, while such phenomena could not be observed in TLR4 deficiency or Myd88 deficiency mice.ConclusionsAll of these results indicate that NAC‐S2 ameliorates TLR4/NF‐κB pathway mediated inflammation in mouse periodontitis model.