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Madhavan, B.K.* ; Han, Z.* ; Singh, B.* ; Bordt, N.* ; Kaymak, S.* ; Bandapalli, O.R.* ; Kihm, L.* ; Shahzad, K.* ; Isermann, B.* ; Herzig, S. ; Nawroth, P.P.* ; Kumar, V.*

Elevated expression of the rage variant-v in sclc mitigates the effect of chemotherapeutic drugs.

Cancers 13:2843 (2021)
Verlagsversion Forschungsdaten DOI
Open Access Gold
Creative Commons Lizenzvertrag
Small cell lung carcinoma (SCLC) is a highly aggressive malignancy with a very high mortality rate. A prominent part of this is because these carcinomas are refractory to chemotherapies, such as etoposide or cisplatin, making effective treatment almost impossible. Here, we report that elevated expression of the RAGE variant-V in SCLC promotes homology-directed DNA DSBs repair when challenged with anti-cancer drugs. This variant exclusively localizes to the nucleus, interacts with members of the double-strand break (DSB) repair machinery and thus promotes the recruitment of DSBs repair factors at the site of damage. Increased expression of this variant thus, promotes timely DNA repair. Congruently, the tumor cells expressing high levels of variant-V can tolerate chemotherapeutic drug treatment better than the RAGE depleted cells. Our findings reveal a yet undisclosed role of the RAGE variant-V in the homology-directed DNA repair. This variant thus can be a potential target to be considered for future therapeutic approaches in advanced SSLC.
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Publikationstyp Artikel: Journalartikel
Dokumenttyp Wissenschaftlicher Artikel
Schlagwörter Dna Repair ; Invasion ; Laser Induced Dna Damage ; Migration ; Rage ; Small Cell Lung Carcinoma ; Wound Healing; Glycation End-products; Cell Lung-cancer; Targeting Dna-damage; Web Server; Subcellular-localization; Splice Variants; Receptor; Protein; Apoptosis; Biology
ISSN (print) / ISBN 2072-6694
Zeitschrift Cancers
Quellenangaben Band: 13, Heft: 11, Seiten: , Artikelnummer: 2843 Supplement: ,
Verlag MDPI
Verlagsort St Alban-anlage 66, Ch-4052 Basel, Switzerland
Begutachtungsstatus Peer reviewed
Förderungen Foundation for Diabetes Research
Helmholtz Cross Program Topic Metabolic Dysfunction
DZD
Deutsche Forschungsgemeinschaft