Panoply™ Human HDAC1 Over-expressing Stable Cell Line

Histone deacetylase 1 (HDAC1) plays a crucial role in cancer progression and development. This enzyme has been proven to be a key regulator of tumor biological functions, such as tumor cell proliferation, migration, and invasion. Here, researchers show that both protein and mRNA levels of HDAC1 are elevated in glioma cell lines and glioma tissues compared to normal glial cell lines and non-tumor brain tissue. Furthermore, HDAC1 knockdown reduced the proliferation and invasion capabilities of cells, while HDAC1 overexpression in glioblastoma cells exhibited enhanced proliferation and invasion abilities in vitro. These novel findings indicate that HDAC1 knockdown may suppress the expression of phosphorylated AKT (p-AKT) and phosphorylated ERK (p-ERK) proteins, while HDAC1 overexpression significantly increased the expression of p-AKT and p-ERK proteins in glioblastoma cells. In addition, HDAC1 knockdown inhibited subcutaneous tumor growth in vivo and led to the downregulation of p-AKT and p-ERK proteins in U87 MG xenograft tumors. Therefore, HDAC1 promotes glioblastoma cell proliferation and invasion both in vitro and in vivo by activating the PI3K/AKT and MEK/ERK signaling pathways. These results suggest that HDAC1 may be a novel biomarker and a potential therapeutic target for glioblastoma.

To determine the effect of HDAC1 overexpression on the proliferation and invasion of glioblastoma cells in vitro, researchers constructed HDAC1-overexpressing U87MG cells (Figure 1A, B). The study showed that while no significant changes were observed in the proliferation and invasion abilities of control cells, HDAC1 overexpression significantly increased the proliferation and invasion abilities of U87MG cells (Figure 1C, D), indicating that HDAC1 plays a crucial role in glioblastoma proliferation and invasion. To investigate the signaling pathways mediated by HDAC1 in glioblastoma proliferation and invasion, researchers treated HDAC1-overexpressing U87MG cells with LY294002 or D98059, which specifically inhibit PI3K and MEK, respectively. Compared to untreated cells, treatment with either inhibitor significantly reduced the proliferation and invasion abilities of HDAC1-overexpressing glioblastoma cells (Figure 1C, D). These results suggest that HDAC1 overexpression positively regulates glioblastoma proliferation and invasion in vitro through the PI3K/AKT and MEK/ERK signaling pathways.

Figure 1. Overexpression of HDAC1 promotes U87MG cell proliferation and invasion in vitro, partially reversible with LY294002 and PD98059. (Li S, et al., 2018)