The potential mechanism of WT1-associated protein-induced N-6-methyladenosine modification of colony-stimulating factor 2 in the progression of oral squamous cell carcinoma by JAK/STAT3 pathway regulation.

Colony-stimulating factor 2 (CSF2) plays a regulatory role in numerous cancers. However, there is needed to investigate the role of CSF2 in oral squamous cell carcinoma (OSCC) malignant phenotype and the specific mechanisms of CSF2 N-6-methyladenosine (m6A) modification. Therefore, we investigated the regulatory mechanism of m6A-modified CSF2 by WT1-associated protein (WTAP) in OSCC via qRT-PCR, western blot, WTAP and CSF2 overexpression in OSCC. In a panel of OSCCs, Kaplan-Meier plot analysis indicated that high expression of CSF2 was associated with poorer prognosis. Cell functional experiments revealed that enrichment of CSF2 promoted the proliferation and migration of OSCC cells by activating the JAK/STAT3 pathway, whereas the reduced expression of CSF2 resulted in the malignant decline of OSCC cells by blocking the JAK/STAT3 pathway. This study also confirmed that WTAP enhanced the m6A level of CSF2 and facilitated the expression of CSF2 and that CSF2 silencing blocked the invasive phenotype of OSCC cells and reversed the malignancy induced by WTAP overexpression. Overall, this study demonstrated that WTAP mediates the m6A modification of CSF2 and the JAK/STAT3 pathway, which plays an oncogenic role in the development of OSCC and can be a target for the treatment of patients with OSCC.

Long non-coding RNA TTN-AS1/microRNA-199a-3p/runt-related transcription factor 1 gene axis regulates the progression of oral squamous cell carcinoma.

Oral squamous cell carcinoma (OSCC) has a high degree of malignancy, which affects the quality of life and prognosis of patients with OSCC. Our study aimed to reveal the function of long non-coding RNA TTN-AS1/microRNA-199a-3p (miR-199a-3p)/runt-related transcription factor 1 (RUNX1) axis in OSCC progression, thereby providing a novel OSCC effective strategy. Real-time quantitative polymerase chain reaction and western blotting were performed to detect the expression of TTN-AS1, miR-199a-3p, and RUNX1 in OSCC. Several cell functional experiments, including Cell Counting Kit-8, flow cytometry, and cell adhesion assays, were used to assess cell proliferation, apoptosis, adhesion, and migration. A luciferase assay was performed to confirm the interaction between TTN-AS1, miR-199a-3p, and RUNX1. Our results revealed that TTN-AS1 and RUNX1 were upregulated in OSCC tissues and cells, whereas miR-199a-3p expression was downregulated. Knockdown of TTN-AS1 or RUNX1 suppressed cell proliferation, adhesion, and migration but induced apoptosis. Additionally, miR-199a-3p inhibitor partly relieved the effects of silencing TTN-AS1 and RUNX1 in OSCC cells due to their targeting relationship. In conclusion, TTN-AS1 and RUNX1 could promote OSCC progression and miR-199a-3p partly relieved the effects of TTN-AS1 and RUNX1.

Expression of Dickkopf-related Protein 1 in Patients with Temporomandibular Osteoarthritis after Treatment with Hyaluronic Acid.

We previously reported that the increased expression of Dickkopf-related protein 1 (DKK1) is positively related to vascular endothelial growth factor in the synovial fluid from patients with temporomandibular joint disorders (TMDs). DKK1 is involved in angiogenic activities in the TMD synovium in vitro, but the expression of DKK1 after treatment of TMD-osteoarthritis (TMD-OA) with hyaluronic acid (HA) remains unknown. In this study, we assessed the expression of DKK1 in the synovial fluid of TMD-OA patients before and after treatment with HA via enzyme-linked immunosorbent assay. We also investigated the role of DKK1 in TMD-OA via immunohistochemical staining. The relationship between the expression of DKK1 and the clinicopathological characteristics was determined by Pearson analysis. The results showed that the expression of DKK1 was significantly decreased after treatment with HA. Correlation analyses indicated that the expression of DKK1 in the TMD-OA samples was closely correlated with mouth opening and pain. These findings suggest that DKK1 could play an important role in the pathogenesis and treatment of TMD. Reduction of the pain by HA treatment may be correlated with the decreased expression of DKK1.

Long noncoding RNA MORT overexpression inhibits cancer cell proliferation in oral squamous cell carcinoma by downregulating ROCK1.

Long noncoding RNA (lncRNA) mortal obligate RNA transcript (MORT) was downregulated many types of cancer tissues, while its functionality in cancer biology is unclear. In the present study, we systemically investigated the involvement of lncRNA MORT in oral squamous cell carcinoma (OSCC). In the present study, we found that lncRNA MORT was downregulated, while rho-associated coiled-coil containing protein kinase 1 (ROCK1) messenger RNA was upregulated in cancer tissues than in adjacent healthy tissues of OSCC patients. In addition, expression levels of lncRNA MORT and ROCK1 were inversely correlated in both tumor tissues and healthy tissues. Follow-up study showed that low MORT level was significantly correlated with poor survival. Overexpression of lncRNA MORT inhibited the proliferation of OSCC cells and downregulated ROCK1. ROCK1 overexpression led to significantly promoted cell proliferation but showed no significant effect on MORT expression. In addition, ROCK1 overexpression attenuated the inhibitory effects of lncRNA MORT overexpression on the proliferation of OSCC cells. Therefore, lncRNA MORT overexpression may inhibit cancer cell proliferation in OSCC cells by downregulating ROCK1.