Fig. 7: Inhibition of PTEN promoted cisplatin (CP)-induced apoptosis and DDR, and conversely, alleviated by overexpression of PTEN in TKPTs.
From: SET8 inhibition preserves PTEN to attenuate kidney cell apoptosis in cisplatin nephrotoxicity

TKPTs were treated with CP for 24 h in the presence or absence of UNC and Bpv as indicated (A) or after transfection of siRNA targeting PTEN (siPTEN) or control siRNA (siCON) for 24 h (H). Cell lysates were prepared and subjected to immunoblot analysis with antibodies as indicated. Expression levels of all the proteins were quantified by densitometry, and PTEN (B, I), SET8 (C, J), Cleaved cas3 (E, L) and p53 (G, N) were normalized with GAPDH, H4K20me1 (D, K) was normalized with H4, and p-p53 (F, M) was normalized with p53. TKPTs were transfected with PTEN plasmid (PTEN-OE) or empty vector (Vector-NC) and then exposed to CP for an additional 24 h. Cell lysates were prepared and subjected to immunoblot analysis with antibodies as indicated (O). Expression levels of all the proteins were quantified by densitometry, and PTEN (P), Cleaved cas3 (T), SET8 (U), p53 (S) and H4 (W) were normalized with GAPDH; γ-H2A (Q), p-p53 (R), and H4K20me1 (V) were normalized with H2A, p53, and H4, respectively. Data are represented as the mean ± SEM of at least three experiments. *P < 0.05, **P < 0.01, ***P < 0.001.