USP2 Inhibits Lung Cancer Pathogenesis by Reducing ARID2 Protein Degradation via Ubiquitination

Figure 2

The expression and gene regulation features of USP2 in lung cancer; H1299 cells were transfected with Sh USP2#1, Sh USP2#2, or negative control vector. A549 cells were transfected with USP2 overexpression vector or negative control vector. (a) Modulative effects of USP2-specific shRNAs and overexpression vectors on the mRNA expression level of USP2 and ARID2 detected by qRT-PCR ( indicates compared with group control; # indicates no statistical significance). (b, c) Modulative effects of USP2-specific shRNAs and overexpression vectors on the protein expression level of wild-type USP2 and C276R loss-of-function mutated USP2 ( indicates compared with negative control vector; # indicates no statistical significance). (d, e) Exogenously transfected USP2 regulated ARID2 protein level in a dose-dependent manner in HEK-29T and A549 cells (“++” sign indicated twice the amount of HA-USP2 vector; indicates compared with negative control vector). (f, g) ARID2 protein level detection in A549 cells transfected with USP2 overexpression vectors; each group was treated with or without proteasome inhibitor MG132 ( indicates compared with negative control vector; # indicates no statistical significance). (h, i) ARID2 protein level detection in H1299 cells transfected with USP-specific shRNAs; each group of cells was treated with or without proteasome inhibitor ( indicates compared with negative control vector; # indicates no statistical significance).

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