Quinolines compounds are toxic pollutants. Their biodegradation by microbes represents a tool
for bioremediation. The growth of Klebsiella penumoniae on 2-methylquinoline shows typical
sigmoidal bacterial growth curves. Since there exists a variety of models for describing the
growth profile of microorganism such as logistic, Gompertz, Richards, Schnute, Baranyi-
Roberts, Von Bertalanffy, Buchanan three-phase and more recently Huang models, the growth
curves exhibit under such conditions would be an excellent study for finding the best model.
The Huang model was chosen as the best model based on statistical tests such as root-meansquare
error (RMSE), adjusted coefficient of determination (R2), bias factor (BF), accuracy
factor (AF) and corrected AICc (Akaike Information Criterion). Novel constants obtained from
the modelling exercise would be used for further secondary modelling.
Dihydroorotate dehydrogenase (DHODH) inhibitors have recently gained increasing research interest owing to their potential for treating breast cancers. We explored their effects in different breast cancer subtypes, focusing on mitochondrial dysfunction. The sensitivity of different subtypes to the inhibitors was investigated with respect to DHODH expression, tumorigenic, and receptor status. Analysis of respiratory complexes, cell cycle, reactive oxygen species (ROS), and cell differentiation were performed. Four cell lines with different receptor status were included, namely MCF-7, MDAMB-231, SKBR-3, and MCF-10A. We showed that MCF-7 and MDAMB-231 cells of the subtypes (ER+/PR+/HER2-) and (ER-/PR-/HER2-), respectively, were responsive to brequinar. Brequinar (BQR) caused cell cycle arrest in the S-phase in sensitive subtypes of breast cells but induced cell differentiation only in poorly differentiated breast cells. All cell subtypes showed increased generation of ROS, both intracellular and mitochondrial ROS with a greater increase seen in mitochondrial ROS in response to DHODH inhibitor, subsequently contributing to mitochondrial dysfunction. BQR also disrupts the function of complex III in ER+/PR+ and triple negative breast cancer (TNBC) subtypes. Collectively, we have found that MDAMB-231 TNBC cell was the most affected by DHODH inhibition in terms of sensitivity, cell cycle arrest, induction of cell differentiation, production of ROS, and mitochondrial complexes disruption. In conclusion, these findings suggest that DHODH inhibitors can potentially become a valuable targeted therapy for TNBC subtype and further consolidates its therapeutic potential as part of the combinatorial therapy against this resilient breast cancer subtype.