prikaz prve stranice dokumenta Carvacrol induces cytotoxicity in human cervical cancer cells but causes cisplatin resistance: involvement of MEK-ERK activation
Access restricted to all Croatian higher education institution's students and staff
Scientific paper - Original scientific paper
Carvacrol induces cytotoxicity in human cervical cancer cells but causes cisplatin resistance: involvement of MEK-ERK activation
Phytotherapy research, 32 (2018), 6; 1090-1097. urn:nbn:hr:184:306189
Potočnjak, Iva; Gobin, Ivana; Domitrović, Robert

Institutional repository: Repository of the University of Rijeka, Faculty of Medicine

Cite this document

Potočnjak, I., Gobin, I. & Domitrović, R. (2018). Carvacrol induces cytotoxicity in human cervical cancer cells but causes cisplatin resistance: involvement of MEK-ERK activation. Phytotherapy research, 32. (6), 1090-1097. Retrieved from https://urn.nsk.hr/urn:nbn:hr:184:306189

Potočnjak, Iva, et al. "Carvacrol induces cytotoxicity in human cervical cancer cells but causes cisplatin resistance: involvement of MEK-ERK activation." Phytotherapy research, vol. 32, no. 6, 2018, pp. 1090-1097. https://urn.nsk.hr/urn:nbn:hr:184:306189

Potočnjak, Iva, Ivana Gobin and Robert Domitrović. "Carvacrol induces cytotoxicity in human cervical cancer cells but causes cisplatin resistance: involvement of MEK-ERK activation." Phytotherapy research 32, no. 6 (2018): 1090-1097. https://urn.nsk.hr/urn:nbn:hr:184:306189

Potočnjak, I., Gobin, I. and Domitrović, R. (2018) 'Carvacrol induces cytotoxicity in human cervical cancer cells but causes cisplatin resistance: involvement of MEK-ERK activation', Phytotherapy research, 32(6), pp. 1090-1097. Available at: https://urn.nsk.hr/urn:nbn:hr:184:306189 (Accessed 03 May 2024)

Potočnjak I, Gobin I, Domitrović R. Carvacrol induces cytotoxicity in human cervical cancer cells but causes cisplatin resistance: involvement of MEK-ERK activation. Phytotherapy research [Internet]. 2018 [cited 2024 May 03];32(6):1090-1097. Available at: https://urn.nsk.hr/urn:nbn:hr:184:306189

I. Potočnjak, I. Gobin and R. Domitrović, "Carvacrol induces cytotoxicity in human cervical cancer cells but causes cisplatin resistance: involvement of MEK-ERK activation", Phytotherapy research, vol. 32, no. 6, pp. 1090-1097, 2018. [Online]. Available at: https://urn.nsk.hr/urn:nbn:hr:184:306189. [Accessed: 03 May 2024]

Metadata
Title (english)Carvacrol induces cytotoxicity in human cervical cancer cells but causes cisplatin resistance: involvement of MEK-ERK activation
AuthorIva Potočnjak
AuthorIvana Gobin
AuthorRobert Domitrović
Author's institutionUniversity of Rijeka
Faculty of Medicine
(Department of Chemistry and Biochemistry)
Author's institutionUniversity of Rijeka
Faculty of Medicine
(Department of Microbiology and Parasitology)
Scientific / art field,
discipline and subdiscipline		BIOMEDICINE AND HEALTHCARE
Basic Medical Sciences
Abstract (english)
Carvacrol has been shown to possess anticancer activity but the mechanism is unknown, as well as the possibility of interaction with anticancer drugs. The aim of this study was to investigate the role of mitogen-activated protein kinase kinase (MEK)/extracellular signal-regulated kinase (ERK) signaling in carvacrol-induced human cervical cancer HeLa cell cytotoxicity. In addition, we studied sensitization of HeLa cells to cisplatin (CP) by carvacrol. Both carvacrol and CP showed dose-dependent cytotoxicity against HeLa cells and activated ERK1/2. The MEK inhibitor PD325901 suppressed ERK expression and further increased cytotoxicity of carvacrol but increased viability of CP-treated cells by modulating apoptosis. The MEK inhibitor also increased microtubule-associated protein 1A/1B- light chain 3 (LC3B) expression in CP treatment. Co-treatment with CP and carvacrol resulted in increased viability of the cancer cells compared to CP treatment, which was associated with the suppression of apoptosis. MEK inhibition decreased the cell viability, without changes in apoptosis. Concomitantly, carvacrol increased CP-induced expression of LC3B, which was enhanced by MEK inhibition. The results of the current study suggest the opposite role of ERK1/2 in carvacrol and CP- induced HeLa cell cytotoxicity. Interestingly, carvacrol induced CP resistance in HeLa cells through ERK1/2-independent suppression of apoptosis and ERK1/2-dependent modulation of autophagy.
Keywords (english)
Languageenglish
Publication typeScientific paper - Original scientific paper
Publication statusPublished
Peer reviewPeer review
Publication versionPublished version
Journal titlePhytotherapy research
Numberingvol. 32, no. 6, pp. 1090-1097
p-ISSN0951-418X
URN:NBNurn:nbn:hr:184:306189
Publication2018
Document URLhttp://bib.irb.hr/918181
Type of resourceText
Access conditionsRestricted access
Terms of useLicence In copyright icon
Created on2022-02-09 15:57:46