Aims: The aim of the current study was to identify active compound(s) responsible
for the antiproliferative effects of O. basilicum and explore their underlying mechanism/s.
Background: Plants have been the source of medicines for the treatment of various diseases
since ancient times. Ocimum basilicum (Sweet Basil, Bobai Tulsi) has been used in the folk
medicine for the treatment of human liver, spleen and stomach cancers.
Objective: To emphasize the importance of O. basilicum as a potential novel non-toxic alternative
to the conventional anticancer therapy.
Methods: O. basilicum (aerial parts) methanolic extract and fractions were screened against
HT-144, MCF-7, NCI-H460 and SF-268 human cancer cell lines using sulforhodamine B
assay. The more active Petroleum Ether Insoluble (PEI) fraction was fractionated into six
sub-fractions (OB-1 to OB-6). Four pure compounds (3-O-methyl ursolic acid, oleanolic acid,
3-epi-ursolic acid and ursolic acid) were isolated from the more potent sub-fraction OB-
6. Triple channel immunofluorescence microscopy was employed to observe the effects of
methanolic extract, PEI fraction, sub-fractions OB-5 and OB-6, 3-epi-ursolic acid and
oleanolic acid on the cytoskeleton and nuclei of MCF-7 cells.
Results: The methanolic extract and the PEI fraction exhibited selectively greater growth inhibition
against MCF-7 cell line (TGI: 56 and 36.2 µg/ml, respectively). By using triple
channel immunofluorescence microscopy, it was observed that the methanolic extract, PEI
fraction, sub-fraction OB-5 and 3-epi-ursolic acid induced irregular mitotic spindle formation
and slowing of mitotic progression in MCF-7 cells while sub-fraction OB-6 induced
mitotic arrest in the prophase stage. F-actin aggregation was also visible in PEI fraction, subfraction
OB-5 and 3-epi-ursolic acid treated MCF-7 cells.
Conclusion: These results emphasize the importance of O. basilicum as a potential novel
non-toxic alternative to the conventional anticancer therapy and suggest that it inhibits the
growth of MCF-7 cancer cells via multiple mechanisms such as interaction with the microtubules
and mitotic spindle apparatus, and F-actin aggregation.