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Objective@#To investigate the relationship between the expression of voltage-gated sodium channel subtype Nav1.5 in oral squamous cell carcinoma (OSCC) and the occurrence and lymph node metastasis of OSCC.@*Methods@#Totally 10 samples of normal oral mucosa tissue as control group, 26 samples of OSCC as the experimental group was divided into non-metastatic group (n=16) and metastatic group (n=10) according to the presence or absence of lymph node metastasis. Quantitative real-time PCR (qPCR), Western blotting, immunohistochemistry, and enzyme-linked immunosorbent assay (ELISA) were used to detect the expression of Nav1.5 in control group and experimental groups at mRNA and protein levels. The data were analyzed by one-way analysis.@*Results@#The expression of Nav1.5 mRNA in the experimental group (non-metastatic group: 2.311±0.134, metastatic group: 4.462±0.362) was higher than those in the control group (1.054±0.162) (P=0.037; P=0.029), and the metastasis group was significantly higher than the non-metastasis group (P=0.031). Western blotting showed the expression of Nav1.5 in experimental groups (non-metastatic: 0.143±0.005, metastatic: 0.253±0.015) was up-regulated significantly compared with control group (0.080±0.010) (P=0.034, P=0.026), and the metastasis group was significantly higher than the non-metastasis group (P=0.033). The immunohistochemistry show the positive expression rates of Nav1.5 in normal and OSCC tissues were 1/10 and 92% (24/26). The differences were statistically significant (P=0.016), and the metastasis group was significantly higher than the non-metastasis group (P=0.028). The ELISA results revealed that the level of Nav1.5 in control was control group (0.834±0.103) μg/L, in non-metastasis group was (1.578±0.167) μg/L, in metastasis group was (3.882±0.422) μg/L (P=0.041; P=0.032), and the metastasis group was significantly higher than the non-metastasis group (P=0.030).@*Conclusions@#Nav1.5 was highly expressed in poorly differentiated OSCC and the expression was significantly different with or without lymph node metastasis. Nav1.5 may be involved in the occurrence and metastasis of OSCC.
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Objective:The different subtypes of voltagE-gated sodium channels (VGSCs) are known to correlate with the migration of many malignant cancers. This study was to investigate the significance of functional expression of SCN5A/Nav1.5 in human ovarian cancer and its effects on migration capability of ovarian cancer cells in vitro. Methods: Sodium indicator SBFI and immunofluorescence method were used to detect the distribution of intracellular Na+. Real-time PCR, Western blotting, and immunohistochemistry were used to detect the mRNA and protein expression of SCN5A/Nav1.5. The effect of specific voltagE-gated sodium channels inhibitor tetrodotoxin (TTX) on cell viability was measured by CCK-8 kit. The migration and invasion of ovarian cancer cell lines SKOV-3 were tested by Transwell chamber assay. Results:SCN5A/Nav1.5 were over-expressed in ovarian cancer cell lines SKOV-3 and ovarian cancer specimens at mRNA and protein levels. TTX 30 μmol/L inhibited the intracellular Na+ concentration by (41.51±0.41)%. TTX also suppressed the invasion and migration capacities of SKOV-3 cells by (33.80±1.6)% and (43.60±2.9)%, respectively. The difference was significant (P<0.05). Conclusion:SCN5A/Nav1.5 is involved in the metastasis progression of ovarian cancer in vitro and plays an important role in the initiation and progression of ovarian cancer. It may become a target for ovarian cancer therapy.