AKT mTOR Inhibition - DOAJ

Sinomenine inhibits the growth of melanoma by enhancement of autophagy via PI3K/AKT/mTOR inhibition

In addition to discovering the underlying mechanism, this research sought to investigate the effects of SIN on melanoma in vitro and in vivo. Methods: Mouse melanoma cell B16-F10 treated by SIN was tested by CCK8 assay and flow cytometry. SIN dose-dependently reduced proliferation of B16-F10 cells in vitro and attenuated melanoma growth in vivo, according to our findings. In addition, SIN treatment promoted B16-F10 cells' apoptosis in a dose-dependent manner, as shown by the rise in apoptotic cells, Bax/Bcl-2 ratio, and caspase-3 activity. Furthermore, preconditioning with SIN greatly enhanced autophagy production by raising Beclin-1 and LC3II/LC3I expression, in addition to decreasing p62 expression and increasing the number of LC3 puncta in B16-F10 cells. Conclusion: Our research has identified a novel function of SIN and provided a molecular basis for future uses of SIN in the treatment of melanoma and other cancers.

Source link: https://doaj.org/article/4e105eb508c744c098f979bb09fb3073

Haprolid Inhibits Tumor Growth of Hepatocellular Carcinoma through Rb/E2F and Akt/mTOR Inhibition

In recent research, including HCC cells, Haprolid has been reported as a potent selective cytotoxin against a panel of tumor cells. The aim of this research is to examine the antitumor activity of haprolid in HCC and to find its underlying molecular mechanisms. Methods: Haprolid's efficacy was determined in human HCC cell lines and xenograft tumors. The WST-1 and crystal violet assay determined haprolid's cytotoxic activity. Immunoblotting and immunohistochemistry investigated the effects of haprolid on the Rb/E2F and Akt/mTOR pathway. In vivo nude mice experiments, however, there was a significant decrease in tumor formation after haprolid therapy. Conclusion: Our findings show that haprolid inhibits HCC formation by dual inhibition of Rb/E2F and Akt/mTOR pathways. Hence, haprolid may be regarded as a new and promising candidate for HCC's palliative therapy.

Source link: https://doi.org/10.3390/cancers12030615

Inhibition of Adipogenesis by Oligonol through Akt-mTOR Inhibition in 3T3-L1 Adipocytes

Oligonol is an oligomerized polyphenol that is mainly composed of catechin-type polyphenols from a variety of fruit and has been found to have greater bioavailability and bioreactivity than natural polyphenols. Oligonol's anti-adipogenic activity may have arisen from its ability to reduce the phosphorylation of ribosomal protein S6 kinase, a downstream target of mTOR and forkhead box protein O1, which can be traced back to the mTOR and mammalian target of rapamycin signaling pathway.

Source link: https://doi.org/10.1155/2014/895272

Effects of Chronic Akt/mTOR Inhibition by Rapamycin on Mechanical Overload–Induced Hypertrophy and Myosin Heavy Chain Transition in Masseter Muscle

We investigated the effects of bite-opening on masseter muscle hypertrophy and myosin heavy chain failure in response to mechanical overload in mice, rats treated or not treated with rapamycin, a selective mTOR inhibitor, in order to investigate the effects of biological overload. BO-rats' masseter muscle mass was significantly higher than that in controls, and RAPA therapy reduced the increase. Expression of slow-twitch MHC isoforms in BO-rats with/without RAPA treatment was significantly elevated in BO-rats with/without RAPA treatment, but the magnitude of the rise in RAPA-treated BO-rats was much smaller. Calcineurin signaling is known as vital for mass muscle hypertrophy and fast-to-slow MHC isoform transition, according to the RAPA study, but expression of known calcineurin activity modulators was unaffected by RAPA therapy.

Source link: https://doi.org/10.1254/jphs.12195FP

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