Fucoidan has received increasing attention in anti-(lung) tumors. However, the effect of fucoidan on the gene changes of lung cancer cells (LCCs) has not been examined systematically. Herein, we investigate the effect of fucoidan on the phenotypes of LCCs and their gene expression by transcriptome sequencing analysis. The phenotypes of LCCs are significantly inhibited by fucoidan. Importantly, compared to LCCs, 1 mg/ml fucoidan has no effect on the phenotypes of normal cells. Further, 6,930 differentially expressed genes (DEGs) in the transcriptome of LCCs (3,501 up-regulated and 3,429 down-regulated genes) are detected via RNA-sequencing between the fucoidan and control groups. Gene Ontology analysis confirms that DEGs are reflected in DNA replication, cell-substrate junction, regulation of cell cycle phase transition, apoptosis, focal adhesion, cadherin binding, and cell adhesion molecule binding. Thus, our findings on the transcriptomic level highlight the therapeutic potential of fucoidan for lung cancer treatment.
Background
Carbon dots (CDs), as excellent antibacterial nanomaterials, have gained great attention in treating infection-induced diseases such as periodontitis and stomatitis. Given the eventual exposure of CDs to the intestine, elucidating the effect of CDs on intestinal health is required for the safety evaluation of CDs.
Results
Herein, CDs extracted from ε-poly-l-lysine (PL) were chosen to explore the modulation effect of CDs on probiotic behavior in vitro and intestinal remodeling in vivo. Results verify that PL-CDs negatively regulate Lactobacillus rhamnosus (L. rhamnosus) growth via increasing reactive oxygen species (ROS) production and reducing the antioxidant activity, which subsequently destroys membrane permeability and integrity. PL-CDs are also inclined to inhibit cell viability and accelerate cell apoptosis. In vivo, the gavage of PL-CDs is verified to induce inflammatory infiltration and barrier damage in mice. Moreover, PL-CDs are found to increase the Firmicutes to Bacteroidota (F/B) ratio and the relative abundance of Lachnospiraceae while decreasing that of Muribaculaceae.
Conclusion
Overall, these evidences indicate that PL-CDs may inevitably result in intestinal flora dysbiosis via inhibiting probiotic growth and simultaneously activating intestinal inflammation, thus causing pathological damage to the intestine, which provides an effective and insightful reference for the potential risk of CDs from the perspective of intestinal remodeling.
Colorectal cancer (CRC) is the second leading cause of cancer death and the third most prevalent malignancy. Colorectal tumors exchange information with the surrounding environment and influence each other, which collectively constitutes the tumor microenvironment (TME) of CRC. Many studies have shown that exosome-derived non-coding RNAs (ncRNAs) play important roles in various pathophysiological processes by regulating the TME of CRC. This review summarizes recent findings on the fundamental roles of exosomal ncRNAs in angiogenesis, vascular permeability, tumor immunity, tumor metabolism and drug resistance. Certainly, the in-depth understanding of exosomal ncRNAs will provide comprehensive insights into the clinical application of these molecules against CRC.
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