ABSTRACT
MicroRNA-145-5p (miR-145-5p) is expressed in a variety of tumors, but the mechanism underlying miR-145-5p in tongue squamous cell carcinoma (TSCC) is not fully understood. Therefore, the present study investigated the role of miR-145-5p in TSCC. miR-145-5p expression levels in TSCC tissues were analyzed via reverse transcription-quantitative PCR. miR-145-5p mimics and inhibitors were transfected into SCC9 and Cal27 cells. The stability and invasion of SCC9 and Cal27 cells were analyzed by performing Transwell assays, while PI and Annexin V were used to detect cell apoptosis. Oxidative stress levels of superoxide dismutase, malondialdehyde and glutathione peroxidase were measured via ELISA. PI3K/AKT signaling pathway-associated protein expression levels were evaluated using western blotting. miR-145-5p was consistently downregulated in TSCC tissues compared with healthy tissues. miR-145-5p overexpression decreased cell stability and invasion, but promoted cell apoptosis and oxidative stress. In addition, PI3K, AKT and phosphorylated-AKT expression levels were significantly diminished. The results indicated that miR-145-5p overexpression inhibited SCC9 and Cal27 cell stability and invasion, promoted SCC9 and Cal27 cell apoptosis and oxidative stress, and inhibited the PI3K/AKT signaling pathway. The results of the present study suggested that miR-145 may serve as a molecular marker of TSCC.
ABSTRACT
The aim of the present study was to analyze the role of microRNA (miRNA)-21-5p in tongue squamous cell carcinoma (TSCC), predict the target gene of miR-21-5p and provide novel strategies for gene therapy in TSCC treatment. The expression levels of miRNA-21-5p in TSCC tissues were analyzed using reverse transcription quantitative polymerase chain reaction, and the effects of miRNA-21-5p on cell proliferation, invasion and apoptosis and the expression levels of target protein PDCD4 in the Cal 27 and SCC9 cell lines were determined. PI3K/AKT/Forkhead Box O1 (FOXO1) pathway-associated protein expression levels were evaluated by western blot analysis. miRNA-21-5p was consistently upregulated in TSCC tissues compared with normal tissues. Inhibition of miR-21-5p inhibited cell proliferation and invasion, and promoted cell apoptosis. A luciferase reporter assay confirmed that PDCD4 was the target of miR-21-5p. Inhibition of miRNA21-5p suppressed the PI3K/Akt/FOXO1 signaling pathway. The results from the present study indicated that miR-21-5p-targeting PDCD4 suppresses apoptosis in human TSCC cell lines. This anti-apoptotic effect was achieved by regulating the PI3K/Akt/FOXO1 signaling pathway. These data represent the basis for a promising novel strategy for the treatment of TSCC.
ABSTRACT
The aim of the present study was to analyze the percentage of regulatory T cells (Treg) and T helper cell 17 (Th17) cells in the peripheral blood of patients with tongue squamous cell carcinoma (TSCC) to provide novel insight into the development of immune-targeting therapies for TSCC. Peripheral blood samples were collected from 40 patients with TSCC then the peripheral blood mononuclear cells (PBMCs) and plasma were isolated for flow cytometry, cytometric bead array and reverse transcription-quantitative PCR. Results demonstrated that the percentage of cluster of differentiation (CD)4+ T cells in the peripheral blood of patients with TSCC decreased significantly compared with the control. However, the percentage of Treg and Th17 cells increased significantly compared with the control. The levels of interleukin (IL)-10 and IL-17a increased significantly in patients with TSCC. Expression of IL-10 and IL-17 in the advanced stages of cancer (stage III or IV) were significantly higher compared with the early stages (I and II). The mRNA expression levels of the transcription factors forkhead box protein 3 and RAR-related orphan receptor-γ increased significantly with stage of cancer. The percentage of Treg cells and Th17 cells increased significantly in patients with TSCC suggesting that there was an imbalance between Treg and Th17 cells. In conclusion, altered Treg/Th17 balance in TSCC may promote the disease progression and these results provide a theoretical basis for the development of immunomodulators targeting Treg/Th17.
ABSTRACT
BACKGROUND: Vascular endothelial growth factor (VEGF), matrix metallopeptidase-9 (MMP-9) and tissue inhibitor of metalloproteinase-2 (TIMP-2) are potential markers of oral and maxillofacial squamous cell carcinoma (SCC). OBJECTIVES: To explore the association between expression of VEGF, MMP-9 and TIMP-2 in oral and maxillofacial SCC and clinicopathological factors. PATIENTS AND METHODS: Immunohistochemical Envision method was used to analyze the expression of VEGF, MMP-9 and TIMP-2 in 54 cases of oral and maxillofacial SCC and the association with clinicopathological factors such as clinical staging and lymphatic metastasis. RESULTS: Brownish-yellow staining is correlated with positive expression of VEGF, MMP-9 and TIMP-2. Positive expression of VEGF and MMP-9 was correlated with lymphatic metastasis, and their positive expression rates were significantly higher in patients with lymphatic metastasis than those without it (VEGF: χ(2) = 30.00; P = 0.001; MMP-9: χ(2) = 18.27, P = 0.001). The positive expression rate of MMP-9 decreased at earlier clinical stages (P < 0.05). Positive expression of TIMP-2 was correlated with lymphatic metastasis, clinical staging and T classification. The positive rate of TIMP-2 expression in patients with lymphatic metastasis was significantly lower than those without it (χ(2) = 26.74, P = 0.002), which significantly reduced with increasing clinical stage and T classification (P < 0.05). CONCLUSIONS: Lymphatic metastasis in patients with oral and maxillofacial SCC is closely related to the positive expression of VEGF, MMP-9 and TIMP-2. MMP-9 and TIMP-2 can affect the progression of cancer, which is valuable for studies on oral and maxillofacial SCC genes.
