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One of the central signaling pathways with a regulatory effect on cell proliferation and survival is Akt/mTOR. In many human cancer types, for instance, lung cancer, the overexpression of Akt/mTOR has been reported. For this reason, either targeting cancer cells by synthetic or natural products affecting the Akt/mTOR pathway down-regulation is a useful strategy in cancer therapy. Direct inhibition of the signaling pathway or modulation of each related molecule could have significant feedback on the growth and proliferation of cancer cells. A variety of secondary metabolites has been identified to directly inhibit the AKT/mTOR signaling, which is important in the field of drug discovery. Naturally occurring nitrogenous and phenolic compounds can emerge as two pivotal classes of natural products possessing anticancer abilities. Herein, we have summarized the alkaloids and flavonoids for lung cancer treatment together with all the possible mechanisms of action relying on the Akt/mTOR pathway down-regulation. This review suggested that in search of new drugs, phytochemicals could be considered as promising scaffolds to be developed into efficient drugs for the treatment of cancer. In this review, the terms "Akt/mTOR", "alkaloid", "flavonoid", and "lung cancer" were searched without any limitation in search criteria in Scopus, PubMed, Web of Science, and Google scholar engines. [ABSTRACT FROM AUTHOR]

Sesquiterpene lactones (SLs) are a typical group of secondary metabolites in asteraceae family and well-known for their biologically potential in treatment of various diseases such as cancer and inflammation. Glioblastoma (GBM) is a most common brain malignancy in adults with poor prognosis. Finding phytochemicals with potential targeting mitochondria has been suggested as an important approach for many malignancies. In this study, we purified three guaianolide-type SLs, including 8-deacyloxy-8α-(methylacryloxy)-subluteolide (A), subluteolide (B) and janerin (C) from Jurinea gabrieliae Bornm by chromatography methods. Then, mitochondrial toxicity parameters were evaluated. All three SLs selectively inhibited SDH activity in mitochondria from U87 cells but not mitochondria from normal rat brain. In addition these SLs increased ROS formation and cytochrome c release and MMP collapse only in mitochondria from U87 cells but not normal rat neurons. Our results suggest that all three SLs may act as potential agents for future development in anti-glioma therapy. [ABSTRACT FROM AUTHOR]