Colon cancer etiology involves a wide spectrum of genetic and epigenetic alterations, finding it challenging to find effective therapeutic strategies. Quercetin exhibits potent anti-proliferative/apoptotic properties. In the present study, we aimed to elucidate the anti-cancer and anti-aging effect of quercetin in colon cancer cell lines. The anti-proliferative effect of quercetin was assessed in vitro by CCK-8 in normal and colon cancer cell lines. To check the anti-aging potential of quercetin, collagenase, elastase, and hyaluronidase inhibitory activity assays were performed. The epigenetic and DNA damage assays were performed using the human NAD-dependent deacetylase Sirtuin-6, proteasome 20S, Klotho, Cytochrome-C, and telomerase ELISA kits. Furthermore, the aging-associated miRNA expression profiling was performed on colon cancer cells. The treatment with quercetin inhibited cell proliferation of colon cancer cells in a dose-dependent manner. Quercetin arrested colon cancer cell growth by modulating expression of aging proteins including Sirtuin-6 and Klotho and also by inhibiting telomerase activity to restrict the telomere length which is evident from qPCR analysis. Quercetin also exhibited DNA damage protection by reducing proteasome 20S levels. The miRNA expression profiling results displayed differential expression of miRNA in colon cancer cell, and in addition, the highly upregulated miRNA was involved in the regulation of cell cycle, proliferation, and transcription. Our data suggest that quercetin treatment inhibited cell proliferation in colon cancer cells through regulating the anti-aging protein expression and provides better understanding for quercetin’s potential use in colon cancer treatment.
Background: Colon cancer is the third leading cause of cancer-related deaths worldwide. Colon tumorigenesis is a sequential process called “Adenoma-carcinoma sequence”. The alimentary habits, obesity, heavy alcohol consumption, inflammatory bowel diseases, family history of colon cancer, oxidative stress, and cellular senescence are the major risk factor influencing colon cancer development. Senescence contributes to the aging process as well as in the development and progression of colon cancer. However, the precise mechanism underlying the aging-related progress of colon cancer is yet to be answered. Recent studies proposed that the senescent cell secretes Senescence-Associated Secretory Phenotype (SASP) includes pro-inflammatory cytokines, interleukins, growth factors, and proteases actively involved in the creation of pro-tumorigenic microenvironment. Objective: This review aims to provide an overview of ROS influence cellular senescence and colon cancer development and summarize the antioxidant and antiaging activity of natural flavonoids. Many of the studies had reported that pro-aging genes were suppressed cancer, and various ‘markers’ are used to identify senescent cells in vitro and in vivo. The SASP of the cells may act as a link between senescence and cancer. Conclusion: This review facilitates a better understanding and might contribute to diagnostic and prognostic systems and find out the novel and targeted therapeutic approaches. Additionally, we focused on the potential role of natural flavonoids in colon cancer therapies, highlighting the flavonoid-based treatments as innovative immunomodulatory strategies to inhibit the growth of colon cancer.
Background: Gastrointestinal (GI) cancer is associated with a group of cancers affecting the organs in the GI tract, with a high incidence and mortality rate. This type of cancer development involves a series of molecular events that arise by the dysregulation of gene expressions and microRNAs (miRNAs). Objectives: This mini-review focuses on elucidating the mechanism of tumor suppressor miRNA–mediated oncogenic gene silencing, which may contribute to a better understanding of miRNA-mediated gene expression regulation of cell cycle, proliferation, invasion, and apoptosis in GI cancers. In this review, the biological significance of tumor suppressor miRNAs involved in gastrointestinal cancers is briefly explained. Methods: The articles were searched with the keywords ‘miRNA’, ‘gastrointestinal cancers’, ‘esophageal cancer’, ‘gastric cancer’, ‘colorectal cancer’, ‘pancreatic cancer’, ‘liver cancer’ and ‘gall bladder cancer’ from the Google Scholar and PubMed databases. A total of 71 research and review articles have been collected and referred for this study. Results: This review summarises recent research enhancing the effectiveness of miRNAs as novel prognostic,diagnostic and therapeutic markers for GI cancer treatment strategies. The expression pattern of various miRNAs have been dysregulated in GI cancers, that are known to be associated with proliferation, cell cycle regulation, apoptosis, migration, and invasion. Conclusion: The role of tumor suppressor miRNAs in the negative regulation of oncogenic gene expression was thoroughly explained in this review. Its potential role as a microRNA therapeutic candidate is also discussed. Profiling and regulating tumor suppressor miRNA expression in gastrointestinal cancers using miRNA mimics could be used as a prognostic, diagnostic, and therapeutic marker, as well as an elucidating molecular therapeutic approach to tumor suppression.
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