Open AccessThe anticancer molecular mechanism of Carnosol in human cervical cancer cells: An in vitro study
Author(s) -
Rand R. Hafidh,
Ahmed Sahib Abdulamir
Publication year - 2020
Publication title -
asia-pacific journal of molecular biology and biotechnology/asia pacific journal of molecular biology and biotechnology
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 0.137
H-Index - 19
eISSN - 2521-9839
pISSN - 0128-7451
DOI - 10.35118/apjmbb.2020.028.3.09
Subject(s) - apoptosis , cell cycle , biology , carcinogenesis , hela , cell cycle checkpoint , cancer research , cell growth , cancer , cell , biochemistry , genetics
Carnosol, a phenolic diterpene, is one of the effective anticancer agents naturally occurring in rosemary, sage, parsley, and oregano. The chemoresistance problem increased with the routinely used chemotherapy. Therefore, the efforts to find a substitute with safe and low cost have become crucial worldwide. The current study attempts to inspect the anticancer molecular mechanisms of Carnosol on modulating up- and down- regulation of multiple genetic carcinogenesis pathways. The cytotoxicity of Carnosol on Hela cells was evaluated by MTS assay. Flow cytometry was used to assess apoptosis and cell cycle arrest. The apoptotic morphological changes were obvious by dual apoptosis assay. The differential gene expression after treatment with Carnosol was investigated by qRT-PCR. Up to 80% of the treated cells with Carnosol IC50 underwent apoptosis. Apoptosis together with cell cycle arrest in G0/G1 phase were induced significantly after treatment with Carnosol IC50. Fifteen out of nineteen genes studied were found to be remarkably up- or down- regulated after treatment with Carnosol. Six up-regulated genes (EREG, FOS-2, ID2, CRYAB, DUSP5, and TICAM2) and nine down-regulated genes (FN1, KRAS2, CCNB1-1, FEN1, MCM4, MCM5, GTSE1, CXCL1, and RALA) were recorded. These genes are candidates for future research for elucidating anticancer molecular targeted therapies, cancerous signaling and cancer development pathways in cervical cancer; moreover, elucidating the role of apoptosis, inflammation, cell proliferation, and cell differentiation in the development of cervical cancer.