Recombinant IFN-α2b treatment activates poly (ADPR) polymerase-1 (PARP-1) in KB cancer cells

• Published in: European journal of cancer (1990) Vol. 39; no. 14; pp. 2103 - 2109
• Main Authors: Quesada, P, Malanga, M, Di Meglio, S, De Lorenzo, S, Fabbrocini, A, Garbi, C, Bianco, A.R, Pepe, S
• Format: Journal Article
• Language: English
• Published: Oxford Elsevier Ltd 01-09-2003; Elsevier
• Subjects: 3-Aminobenzamide; Apoptosis; Biological and medical sciences; IFN-α; KB cells; Medical sciences; Other treatments; PARP-1; Treatment. General aspects; Tumors; IFN-α; KB cells; PARP-1; 3-Aminobenzamide; Apoptosis; Human; Cell proliferation; Cell culture; Flow cytometry; Squamous cell carcinoma; Alpha interferon; Malignant tumor; Experimental study; Signal transduction; Enzymatic activity; Cell cycle; Biological effect; Therapeutic protocol; Medical application
• ISSN: 0959-8049; 1879-0852
• DOI: 10.1016/S0959-8049(03)00433-7

In the present paper, we investigated the relationship between the growth inhibitory effects of recombinant interferon-α2b (rIFN-α2b) and poly (ADPR) polymerase-1 (PARP-1) activity in the human squamous KB cancer cell line. Growth inhibition of the KB cells mediated by 1000 IU/ml of rIFN-α2b was accompanied by a transient rise in PARP-1 specific activity 24 h after rIFN-α2b treatment, confirmed by both the increase of intracellular poly (ADP-ribose) content and the PARP-1 auto-modification level. At longer times of incubation, the onset of apoptosis accompanied KB cell growth inhibition, as demonstrated by both flow cytometry and western-blotting analysis showing an 89 kDa apoptotic fragment of PARP-1. Moreover, pretreatment of the cells with the PARP-1 inhibitor, 3-aminobenzamide (3-ABA), at non-cytotoxic concentrations (1 mM), reduced the cell-growth inhibition, cell-cycle perturbation and apoptosis caused by rIFN-α2b. Taken together, these results strongly suggest that PARP-1 may be directly involved in the effects of rIFN-α2b in the KB cancer cell line.