Coronavirus disease 2019 (COVID-19) is a respiratory infectious disease that seriously threatens human life. The clinical manifestations of severe COVID-19 include acute respiratory distress syndrome and multiple organ failure. Severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2), the causal agent of COVID-19, spreads through contaminated droplets. SARS-CoV-2 particles have been detected in the saliva of COVID-19 patients, implying that the virus can infect and damage the oral cavity. The oral manifestations of COVID-19 include xerostomia and gustatory dysfunction. Numerous studies showed that the four structural proteins of SARS-CoV-2 are its potential pathogenic factors, especially the S protein, which binds to human ACE2 receptors facilitating the entry of the virus into the host cells. Usually, upon entry into the host cell, a pathogen triggers the host’s immune response. However, a mount of multi-omics and immunological analyses revealed that COVID-19 is caused by immune dysregulation. A decrease in the number and phenotypes of immune cells, IFN-1 production and excessive release of certain cytokines have also been reported. In conclusion, this review summarizes the oral manifestations of COVID-19 and multi-omics analysis of SARS-CoV-2 infection.

Objective: Tongue squamous cell carcinoma (TSCC) is an oral cancer, with high malignancy and frequent early migration and invasion. Only a few drugs can treat tongue cancer. Ginsenoside Rd is a ginseng extract with anti-cancer effects. Many noncoding RNAs are abnormally expressed in tongue cancer, thus influencing its occurrence and development. H19 and miR-675-5p can promote cancer cell growth. This study aimed to analyze the regulation effect of ginsenoside Rd on H19 and miR-675-5p in tongue cancer.Methodology: We used CCK8 and flow cytometry to study the growth and apoptosis. Transwell assay was used to assess invasion; wound-healing assay to assess migration; and colony formation assays to test the ability of cells to form colonies. H19, miR-675-5p, and CDH1 expressions were analyzed by qPCR. E-cadherin expression was detected using western blot. CRISPR/ cas9 system was used for CDH1 knockout. Results: Ginsenoside Rd inhibited the growth and increased the apoptosis of SCC9 cells. Ginsenoside Rd also inhibited the migration and invasion of SCC9 cells. H19 and miR-675-5p were highly expressed, while CDH1 and E-cadherin expressions were low. H19 and miR-675-5p promoted SCC9 metastasis. In contrast, CDH1 and E-cadherin inhibited the metastasis of SCC9 cells. Bioinformatics analysis showed that miR-675-5p was associated with CDH1. H19 and miR-675-5p expressions decreased after ginsenoside Rd treatment, while CDH1 and E-cadherin expressions increased. Conclusions: Ginsenoside Rd inhibits tongue cancer cell migration and invasion via the H19/miR-675-5p/CDH1 axis.

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Previous report suggested that the expression of ten-eleven translocation (TET) proteins was abnormal in different cancers. Quercetin, has been demonstrated as anti-caner role in cancer development. To analyze the expression of TETs, quercetin treated with uveal melanoma cells in the present study. Our results suggested that the expression of TET1 was increased following treated with quercetin in OCM-1, SK-MEL-1 and B16 cells. In addition, quercetin treatment induced apoptosis and inhibited invasion. To further investigate if the expression of TET1 was associate with cell growth, apoptosis, migration and invasion, knocked down and overexpressing of TET1 was constructed. The results showed that the increased expression of TET1 induced cell apoptosis, increased 5-hydroxymethylcytosine (5hmC) and inhibited cell invasion. TET1 was a target gene of miR-17. Our results showed that inhibited expression of miR-17 increased TET1 expression in OCM-1 cells. To further confirm the effect of TET1 on melanoma tumors, nude mice was used. The results indicated that quercetin treatment increased TET1 expression and inhibited tumor growth. Taken together, these results suggested that quercetin can regulate cell proliferation and apoptosis through TET1 via miR-17 in melanoma cells.