The Synthetic Peptide CIGB-300 Inhibits NF-κB Translocation Affecting the Survival and Chemoresistance of NSCLC Cell Lines

CIRIGLIANO S; DÍAZ BESSONE MI; FLUMIAN C; BERARDI D; PEREA S; DE KIER JOFFÉ EB; FARINA H; TODARO L; URTREGER A

JOURNAL OF THORACIC ONCOLOGY

LIPPINCOTT WILLIAMS & WILKINS

Lugar: Philadelphia; Año: 2016 p. 218 - 219

1556-0864

The CK2 is a Ser/Thr kinase that has been historically associated with cancer. It is involved in cellproliferation, survival and apoptosis by modulating diverse signaling pathways, including Wnt and NF-kBamong the most relevant. CIGB-300 is a synthetic antitumor peptide with a novel mechanism of action, since it is capable of binding to CK2 substrates thus preventing the enzyme activity. NF-kB activation can reducechemotherapy efficiency in lung cancer. We have determined that CIGB-300 inhibits NF-kB (p65) nucleartranslocation. Based on this evidence, we hypothesize that supplementing cisplatin with CIGB-300 wouldimprove the treatment efficiency. Also, CIGB-300 alters the ability of lung cancer cells to grow in a threedimensional spheroid model.