Fucoxanthin Inactivates the PI3K/Akt Signaling Pathway to Mediate Malignant Biological Behaviors of Non-Small Cell Lung Cancer.

Although lung cancer treatment strategies have improved in recent years, the 5-year overall survival of non-small cell lung cancer (NSCLC) remains less than 15%. Chemotherapy is considered the most promising option in the comprehensive treatment of NSCLC. Fucoxanthin (FX) is a natural product derived from brown algae and has extensive applications in medicine. Previous studies reported that FX effectively inhibits the growth of NSCLC cells in vitro and in vivo. However, the mechanism underlying the anti-NSCLC effect of FX remains unknown. In this study, NSCLC cell lines and a xenograft nude mouse model were used to examine the anti-NSCLC activities of FX in vitro and in vivo. Network pharmacology analysis and inhibitors or activators of the PI3K/Akt signaling pathway were used to explore the anti-NSCLC mechanisms of FX. The results indicated that FX could inhibit proliferation, migration, and invasion, arrest cell cycle at the G0/G1 phase, and induce apoptosis of NSCLC cells in vitro. Additionally, FX suppressed tumor growth in vivo. The PI3K/Akt signaling pathway was found to be involved in the anti-NSCLC activity of FX. In conclusion, FX inhibits malignant biological behaviors of NSCLC by suppressing the phosphorylation of both PI3K and AKT, and subsequently inactivating PI3K/AKT signaling pathway.

DHPW1 attenuation of UVB-induced skin photodamage in human immortalized keratinocytes.

Ultraviolet radiation (UVB) can result in photodamage to the skin and can seriously threaten health, particularly in the elderly. Oxidative stress and the inflammatory response have been shown to play a significant role in the process. In a previous study, we isolated, purified and identified a polysaccharide from the extract of Dendrobium huoshanense (DHPW1). In this study we evaluated the effect of DHPW1 on ameliorating the UVB photodamage of human immortalized keratinocytes (HaCaT). Cell proliferation and cell scratch assays were used to evaluate the viability of the HaCaT treated with DHPW1, and a fluorescent probe and Western blot analysis were used to examine the production of reactive oxygen species (ROS) and the expression of proinflammatory factors IL-1ß, IL-6, and NF-κB(p65). The results show that, compared with the control group (UVB irradiation only), DHPW1 significantly improved the viability of UVB-irradiated HaCaT and enhanced the migration rate of the cell scratch after 24 h. The scratch-healing rate reached 90 % after 36 h. DHPW1 also significantly inhibited UVB-induced oxidative stress and expression of proinflammatory factors . Compared with the control group, the production of ROS decreased by 49.11 %, and the relative protein expression of IL-6 and NF-κB(p65) decreased by up to 13.30 % and 31.02 %, respectively. It is concluded that DHPW1 can significantly improve viability and wound closure rate of UVB-irradiated HaCaT. In addition, it can reduce the expression of IL-1 and IL-6 by inhibiting the transcription of NF-κB(p65), thereby reducing inflammation and oxidative stress in UVB-irradiated HaCaT.