Aims: The aim of this study is to explore essential oil from the bark of Cedrus deodara
(CDEO) as an potential anticancer agent.
Background: The frontline drugs against cancer in clinical settings are posing challenges of resistance
and other detrimental side-effects. This has led to the exploration of new anticancer chemical entities
from natural sources, particularly plant-based products such as essential oils that serve as vast repositories
of pharmacologically active substances for combating cancer.
Objective: The objective is to isolate and characterize the essential oil from the bark of Cedrus deodara
(CDEO) and evaluate its potential as an anticancer agent and delineate the possible underlying mechanism
Methods: Cedrus deodara essential oil from bark (CDEO) was obtained by hydro-distillation and analyzed
by GC/MS for vital constituents. Further, in vitro cytotoxic potential was measured by MTT assay
against a panel of cancer cell lines. The apoptosis-inducing potential of CDEO was analyzed by mitochondrial
membrane potential loss (ΔΨm) and nuclear fragmentation assay. Besides, wound healing assay
and colonogenic assay were employed to check the anti-metastatic potential of CDEO. Molecular
docking approaches were employed for target identification, while immuno-blotting was carried out for
Results and Discussion: The major components identified were 2-(tert-Buyl)-6-methyl-3-(2- (trifluoromethyl)
benzyl)imidazo [1,2-a]pyridine (26.32 %);9- Octadecenoic acid (8.015 %); Copaene (5.181
%);2-(4-Methoxy-2,6-dimethylphenyl) -3-methyl-2H- benzo[g]indazole(4.36 %) and 9(E),11(E)-
Conjugated linoleic acid (4.299 %). Further, potent in vitro cytotoxic activity with IC50 values of 11.88
μg/ ml and 14.63 μg/ ml in colon cancer cell lines of HCT-116 and SW-620, respectively. Further, a
significant and dose-dependent decrease in colony formation, cell migration, induction of ROS formation
and loss in ΔΨm was observed. Additionally, major compounds identified were chosen for ligandprotein
binding interaction studies to predict the molecular targets in colon cancer. It was observed that
compounds such as 9-Octadecenoic acid;4H-1- Benzopyran-4-one, 3-(3,4-dimethoxyphenyl)-6,7-
dimethoxy; 2-(4-Methoxy-2,6-dimethylphenyl) -3-methyl-2H-benzo [g]indazole and 2-Bornanol,5-(2,4-
dinitro phenyl) hydrazono have a prominent binding affinity with NF-κB. This was also further validated
by immuno-blotting results wherein CDEO treatment in colon cancer cells led to the abrogation of
NFκB, and the Bcl-2-associated X protein (Bax): B-cell lymphoma (Bcl)-2 ratio was up-regulated leading
to enhanced cleaved caspase 3 formation and subsequent apoptosis.
Conclusion: These results unveil CDEO inhibits cell proliferation and induces apoptosis in colon cancer
cells, which can be attributed to the abrogation of the NFκB signaling pathway.