Fig. 2: Targeting USP24 induces the expression of ULK1, LC3 and p62 in lung cancer cells. | Cell Death & Differentiation

Fig. 2: Targeting USP24 induces the expression of ULK1, LC3 and p62 in lung cancer cells.

From: USP24-i-101 targeting of USP24 activates autophagy to inhibit drug resistance acquired during cancer therapy

Fig. 2

A549 cells were treated with USP24-i (5 μM and 10 μM) for 24 h, the protein (A) and mRNA (B) levels of ULK1, LC3 and p62 were studied by IB (A (a)) and qPCR (B), and the levels of protein, ULK1 (A(b)) and p62 (A(c)), and mRNA, ULK1 (B(a)), LC3 (B(b)) and p62 (B(c)), were quantitated. USP24 was silenced with sh-USP24 or inhibited with 5 μM USP24-i in A549-T24 (C (a)) and PC9-GR (D (a)) cells, and then, the levels of LC3-II (C(b), (D(b)), USP24 (C (c), (D (c)) and E2F4 (C(d), (D(d)) were studied by IB. The levels were quantitated after three independent experiments. E (a) E2F1 was silenced by sh-E2F1 (#1 and #2) in PC9-GR cells with or without USP24-i treatment. The levels of E2F1 (E (b)) and LC3-II (E (c)) were studied by IB. After three independent experiments, the data were quantitated. F A549 and A549-T24 cells were treated with USP24-i and Rapamycin. The samples were collected to measure the levels of phosphor-ULK, ULK, LC3-II and actin by IB. All quantitation data were analyzed by statistical analysis with a t test; *p < 0.05, **p < 0.01, ***p < 0.005.

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