Panoply™ Human HDAC1 Knockdown Stable Cell Line

Glioma is the most common malignant tumor of the central nervous system, with a low five-year survival rate worldwide. Although recent studies have reported that histone deacetylase 1 (HDAC1) is highly expressed in various human tumors and has prognostic value, the molecular mechanisms by which HDAC1 exerts its biological functions in glioma remain unclear. Here, researchers found that HDAC1 expression was elevated in glioma tissues and cell lines. HDAC1 expression was closely associated with the pathological grade and overall survival of glioma patients. Downregulation of HDAC1 expression inhibited glioma cell proliferation, prevented cell invasion, and induced apoptosis. The expression of apoptosis and metastasis-related molecules in U251 and T98G cells after HDAC1 knockdown was detected using RT-PCR and Western blot methods. The results showed that in HDAC1-knockdown U251 and T98G cells, the expression of BIM, BAX, cleaved CASPASE3, and E-CADHERIN was upregulated, while the expression of TWIST1, SNAIL, and MMP9 was downregulated. In vivo experiments showed that HDAC1 knockdown inhibited tumor growth in nude mice. In summary, HDAC1 can be considered an indicator of poor prognosis in glioma patients and may serve as a potential therapeutic target.

To investigate the role of HDAC1 in cell migration, researchers cultured HDAC1 knockdown cells, control cells, and NC cells in Boyden chambers. After 48 hours of incubation, the migration ability of HDAC1 knockdown U251 and HDAC1 knockdown T98G glioblastoma cells was significantly reduced compared to NC cells (Figure 1A and 1B). The researchers used Transwell chambers coated with Matrigel to measure the effect of HDAC1 on cell invasion ability. After 48 hours of incubation, the number of invading NC-infected cells was similar to the control group, while the invasion ability of HDAC1 knockdown cells was significantly reduced (Figure 1C and 1D). To explore the effect of HDAC1 on cell-matrix adhesion, the researchers performed cell adhesion experiments on culture plates coated with fibronectin. Compared to NC cells, the adhesion ability of HDAC1 knockdown U251 and HDAC1 knockdown T98G glioblastoma cells was significantly reduced (Figure 1E and 1F). These results indicate that HDAC1 plays an important role in promoting glioblastoma invasion.

Figure 1. Knockdown of HDAC1 inhibits migration, invasion and adhesion in glioma cell lines. (Wang X Q, et al., 2017)