Panoply™ Human SMARCA4 Over-expressing Stable Cell Line

SWI/SNF-associated matrix-associated actin-dependent chromatin regulator subfamily a member 4 (SMARCA4, also known as BRG1), is the ATPase subunit of the SWI/SNF chromatin remodeling complex and plays an important regulatory role in many cytogenetic and cellular processes during cancer development. However, the biological function and mechanism of SMARCA4 in oral squamous cell carcinoma (OSCC) remain unclear. Here, researchers explored the role of SMARCA4 in OSCC and its potential mechanisms. Using tissue microarray technology, they found that SMARCA4 is highly expressed in OSCC tissues. Furthermore, high expression of SMARCA4 promotes the in vitro migration and invasion of OSCC cells, as well as tumor growth and invasion in vivo. These phenomena are associated with the promoting effect of epithelial-mesenchymal transition (EMT). Bioinformatics analysis and luciferase reporter gene assays confirmed that SMARCA4 is a target gene of microRNA miR-199a-5p. Further mechanistic studies showed that miR-199a-5p-regulated SMARCA4 can promote tumor cell invasion and metastasis through EMT. These findings indicate that the miR-199a-5p-SMARCA4 axis plays a role in tumorigenesis by promoting the invasion and metastasis of OSCC cells through the regulation of EMT. These results reveal the role and mechanism of SMARCA4 in OSCC, which may have significant implications for the treatment of OSCC.

Since tumor invasion and metastasis are closely associated with the progression of oral squamous cell carcinoma (OSCC), researchers investigated whether SMARCA4 is involved in the migration and invasion of OSCC cells. Scratch assays showed that SMARCA4 overexpression significantly enhanced the migration ability of SAS and CAL-27 cells (Figure 1A, B). Transwell migration assays showed that, compared with the corresponding NC group, SMARCA4-overexpressing SAS and CAL-27 cells exhibited significantly enhanced migration and invasion abilities (Figure 1C, D). Cancer cell invasion and eventual metastasis require epithelial cells to undergo a dedifferentiation process, namely epithelial-mesenchymal transition (EMT). The loss of E-cadherin and the upregulation of mesenchymal markers (such as vimentin) are considered key events in EMT. Immunofluorescence assays showed that E-cadherin expression was significantly attenuated in SMARCA4-overexpressing OSCC cells, while vimentin expression was upregulated (Figure 1E, F). Western blot analysis further confirmed these results (Figure 1G, H).

Figure 1. SMARCA4 promotes OSCC cell migration and invasion. (Xu, Mingyan, et al., 2023)