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Fig. 1 | Journal of Experimental & Clinical Cancer Research

Fig. 1

From: Loss of RPS27a expression regulates the cell cycle, apoptosis, and proliferation via the RPL11-MDM2-p53 pathway in lung adenocarcinoma cells

Fig. 1

Identification of RPs interacting with RPL11 in A549 cells. A The endogenous RPL11-interacting proteins were pulled down by anti-RPL11 antibody. The immunoprecipitates were separated by SDS-PAGE, then silver stained. The band (approximately 18 kDa) containing proteins strongly bound to RPL11 was digested with trypsin and analyzed with LC-MS/MS. B Interaction network of RPs with RPL11, on the basis of the STRING database. C and D The expression of RPS27a was analyzed by IB in BEAS-2B, A549 and H460 cells. The expression of RPS27a was quantified (RPS27a/β-actin), the normalized RPS27a in BEAS-2B cells was set at 1.0, and **p < 0.01 was calculated with ANOVA (n = 3) (D). E and F Apoptosis of A549 cells was analyzed by flow cytometry at 12, 24 and 48 h after CIR. R1, main population; R2, necrotic cells; R3, late apoptotic cells; R4, early apoptotic cells. Total apoptotic cells = R3 + R4. The percentages of apoptosis after CIR. *p < 0.05, **p < 0.01 were calculated with t-test (n = 3) (F). G IB analysis of RPS27a expression in A549 cells after CIR. H The expression of RPS27a was quantified (RPS27a/β-actin), and the normalized RPS27a in control cells at 12, 24 and 48 h after CIR was set at 1.0. ***p < 0.001 were calculated with the t-test (n = 3). CK, control; CIR, carbon ion radiation; IB, immunoblotting; 2B, BEAS-2B

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