Number of the records: 1

Substituted 2-hydroxy-N-(arylalkyl)benzamide sensitizes cancer cells to metabolic stress by disrupting actin cytoskeleton and inhibiting autophagic flux

SYSNO ASEP	0467237
Document Type	J - Journal Article
R&D Document Type	Journal Article
Subsidiary J	Článek ve WOS
Title	Substituted 2-hydroxy-N-(arylalkyl)benzamide sensitizes cancer cells to metabolic stress by disrupting actin cytoskeleton and inhibiting autophagic flux
Author(s)	Pachnikova, G. (CZ) Uldrijan, S. (CZ) Imramovský, A. (CZ) Kryštof, Vladimír (UEB-Q)_{RID, ORCID} Slaninová, I. (CZ)
Number of authors	5
Source Title	Toxicology in Vitro. - : Elsevier - ISSN 0887-2333 Roč. 37, DEC (2016), s. 70-78
Number of pages	9 s.
Language	eng - English
Country	GB - United Kingdom
Keywords	hepatocellular-carcinoma cells ; sorafenib ; apoptosis ; death ; maturation ; membrane ; melanoma ; Actin ; Autophagy ; Melanoma ; Metabolic stress ; Sorafenib ; Substituted 2-hydroxy-N-(arylalkyl)benzamide
Subject RIV	CE - Biochemistry
Institutional support	UEB-Q - RVO:61389030
UT WOS	000387198300009
DOI	10.1016/j.tiv.2016.09.006
Annotation	N-((R)-1-(4-chlorophenylcarbamoy1)-2-phenylethyl)-5-chloro-2-hydroxybenzamide (Compound 6k), was recently isolated during the preparation of amino adds esters with salicylanilides. We show here that 6k disrupts the dynamics of actin cytoskeleton in human melanoma cells, affecting processes essential for the maintenance and expansion of tumours such as cell adlision, motility, proliferation, vesicular transport, and autophagic flux. We demonstrated that inhibition of autophagy by 6k increased the sensitivity of melanoma cells to metabolic stress induced by rotenone or nutrient starvation and potentiated the anti-proliferative activity of small molecule multikinase inhibitor sorafenib. Since autophagy plays an important role in survival of cancer cells subjected to chemotherapy, the above mentioned properties are interesting from clinical point of view as 6k could promote metabolic stress within the tumour microenvironment and potentiate the effect of cytostatics in combination therapy.
Workplace	Institute of Experimental Botany
Contact	David Klier, knihovna@ueb.cas.cz, Tel.: 220 390 469
Year of Publishing	2017

Number of the records: 1