Ursolic and oleanolic acids are natural isomeric triterpenes known for their anticancer activity. Here, we investigated the effect of triterpenes on the viability of A549 human lung cancer cells and the role of autophagy in their activity. The induction of autophagy, the mitochondrial changes and signaling pathway stimulated by triterpenes were systematically explored by confocal microscopy and western blotting. Ursolic and oleanolic acids induce autophagy in A549 cells. Ursolic acid activates AKT/mTOR pathways and oleanolic acid triggers a pathway independent on AKT. Both acids promote many mitochondrial changes, suggesting that mitochondria are targets of autophagy in a process known as mitophagy. The PINK1/Parkin axis is a pathway usually associated with mitophagy, however, the mitophagy induced by ursolic or oleanolic acid is just dependent on PINK1. Moreover, both acids induce an ROS production. The blockage of autophagy with wortmannin is responsible for a decrease of mitochondrial membrane potential (Δψ) and cell death. The wortmannin treatment causes an over-increase of p62 and Nrf2 proteins promote a detoxifying effect to rescue cells from the death conducted by ROS. In conclusion, the mitophagy and p62 protein play an important function as a survival mechanism in A549 cells and could be target to therapeutic control.

Background: Plants and algae harbor diverse molecules with antioxidant activity and have been demonstrated to directly inhibit cancer cell growth and mitigate the oxidative damage associated with certain antitumor therapies. While antioxidant supplementation, either alone or in combination with chemotherapy, has shown promise in improving quality of life, further research is needed to explore the effects of antioxidant combinations on specific cancer cell lines. Methods: In this study, the in vitro cytotoxic and apoptotic properties of natural compounds derived from plants and algae, as well as certain dietary supplements, were investigated against various human cancer cell lines, including bone, leukemia, colorectal, breast, and prostate cancers. Results: Apple polyphenols, fucoxanthin, and plant-derived tocotrienols exhibited cytotoxic effects across all lines; however, tocotrienols demonstrated the most potent, time-dependent cytotoxic activity, with a half-inhibitory concentration (IC₅₀) of 4.3 μg/mL in bone cancer cells. Analysis of dietary supplements 2.1, 4.0, and 10.0 revealed that supplement 10.0 exhibited specific cytotoxic activity against bone cancer line TIB-223 and colorectal cancer cell line Caco2, with IC₅₀ values of 126 μg/mL and 158 μg/mL, respectively. Both tocotrienols and supplement 10.0 induced morphological changes in TIB-223 cells, inhibited cell migration (anti-metastatic activity), and promoted apoptosis, as evidenced by caspase 3/7 activation in both bone and colorectal cancer cells. Conclusions: These findings provide valuable insights for the development of targeted dietary supplements to enhance the anticancer effect of conventional chemotherapy in specific cancer types.

Age-related macular degeneration (AMD) is the leading cause of central vision loss and severe blindness among the elderly population. Recently, we reported on the association of the SGCD gene (encoding for δ-sarcoglycan) polymorphisms with AMD. However, the functional consequence of Sgcd alterations in retinal degeneration is not known. Herein, we characterized changes in the retina of the Sgcd knocked-out mouse (KO, Sgcd^−/−). At baseline, we analyzed the retina structure of three-month-old wild-type (WT, Sgcd^+/+) and Sgcd^−/− mice by hematoxylin and eosin (H&E) staining, assessed the Sgcd–protein complex (α-, β-, γ-, and ε-sarcoglycan, and sarcospan) by immunofluorescence (IF) and Western blot (WB), and performed electroretinography. Compared to the WT, Sgcd^−/− mice are five times more likely to have retinal ruptures. Additionally, all the retinal layers are significantly thinner, more so in the inner plexiform layer (IPL). In addition, the number of nuclei in the KO versus the WT is ever so slightly increased. WT mice express Sgcd-protein partners in specific retinal layers, and as expected, KO mice have decreased or no protein expression, with a significant increase in the α subunit. At three months of age, there were no significant differences in the scotopic electroretinographic responses, regarding both a- and b-waves. According to our data, Sgcd^−/− has a phenotype that is compatible with retinal degeneration.

The role of the gut microbiota in obesity has been extensively studied worldwide, but research in Mexican populations is still limited. This is particularly important given the high obesity rates in Mexico, despite a traditional diet rich in diverse, plant-based foods. We conducted a systematic review of studies examining the gut microbiota in obese Mexican children and adults. The literature search was conducted in the Medline, CINAHL, SciELO, Redalyc and Web of Science databases. The included studies addressed topics such as obesity in different Mexican subgroups (e.g., adults, children, rural communities), dietary behaviors and interventions, traditional dietary patterns, and gut microbiota composition. Of the 2332 datasets, 19 studies met the inclusion criteria. These studies indicated that obesity in Mexican individuals is associated with specific changes in the gut microbiota, including decreased bacterial diversity and shifts in the abundance of key microbial genera. Differences were found between age groups and regions. This review highlights a clear association between gut microbiota composition and obesity in the Mexican population. Further research is essential to investigate how the traditional Mexican diet may influence gut health and serve as a potential tool to treat obesity.

Plants and algae harbor diverse molecules with antioxidant activity that have been demonstrated to directly inhibit the growth of cancer cells and alleviate the oxidative damage side effects of certain antitumor therapies. Although supplementation with antioxidants alone or in combination with chemotherapy has shown promise in improving quality of life, further investigation is needed into the effects of antioxidant combinations on specific cancer cell lines. In this study, the in vitro cytotoxic and apoptotic properties of plant/algae natural compounds and dietary supplements were investigated on various human cancer cell lines, including bone, leukemia, colorectal, breast and prostatic cancers. Apple polyphenols, fucoxanthin, and plant tocotrienols exhibited cytotoxic effects across all lines, with tocotrienols particularly potent, showing a low half- inhibitory concentration (IC50) in bone cancer cells (4.3 μg/mL). Analysis of dietary supplements 2.1, 4.0 and 10.0, revealed that supplement 10.0 exhibited specific cytotoxic activity against the TIB-223 bone cancer line, with an IC50 of 126 μg/mL. Both tocotrienols and supplement 10.0, induced morphological changes, inhibited cell migration (anti-metastatic activity), and promoted apoptosis in TIB-223 cells, as demonstrated by caspase 3/7 activation. These findings provide valuable insights for the development of specific dietary supplements to enhance the anticancer effect of traditional chemotherapies for certain cancer types.

The pulmonary parenchyma is the primary site of metastasis for giant cell tumor (GCT) of bone, a benign yet aggressive musculoskeletal tumor. Current treatments, including surgery and antibody therapy, are only partially effective and often lead to significant side effects. This study aimed to evaluate the apoptotic activity of quercetin, a naturally occurring flavonoid with anticancer properties, on metastatic GCT lung cells (TIB-223). The immunophenotype of the TIB-223 cell line was characterized using flow cytometry, revealing positivity for CD166 and CD47 markers and negativity for CD34, CD73, CD117, CD45, and fibroblast markers. The IC50 of quercetin was determined at 91.1 µM through MTT assays, demonstrating its cytotoxic effect in a dose-dependent manner. Apoptosis was confirmed via flow cytometry and Western blotting, showing increased caspase-3 expression after 24 hours of treatment. These findings indicate that quercetin induces apoptosis in metastatic GCT cells and could serve as a basis for developing phytopharmaceutical therapies targeting this pathology.