Regulation of gene expression by modulating microRNAs through Epigallocatechin-3-gallate in cancer.

Cancer is an intricate ailment that has a higher death rate globally and is characterized by aberrant cell proliferation and metastasis in nature. Since the beginning of healthcare, natural products, especially those derived from plants, have been utilized to support human health. Green tea contains an essential catechin called epigallocatechin gallate, which has anti-proliferative, anti-mutagenic, anti-inflammatory, and antioxidative properties. The anticancer properties of EGCG have been extensively studied using pre-clinical cell culture and animal model systems. Dysregulated miRNA may be a biomarker since it influences the different characteristics of cancer like upholding proliferative signaling, cell death, invasiveness, metastasis, and angiogenesis. EGCG either elevates or lowers the expression of dysregulated miRNAs in cancer. Nonetheless, due to its anticancer properties, greater attention has been paid towards the development of efficient strategies for utilizing EGCG in cancer chemotherapy. This review summarizes the modifying effect of EGCG on miRNAs in cancer after briefly discussing the anticancer mechanisms of EGCG and the function of miRNAs in cancer.

Regulatory Components of Oxidative Stress and Inflammation and Their Complex Interplay in Carcinogenesis.

Cancer progression is closely linked to oxidative stress (OS) inflammation. OS is caused by an imbalance between the amount of reactive oxygen species produced and antioxidants present in the body. Excess ROS either oxidizes biomolecules or activates the signaling cascade, resulting in inflammation. Immune cells secrete cytokines and chemokines when inflammation is activated. These signaling molecules attract a wide range of immune cells to the site of infection or oxidative stress. Similarly, increased ROS production by immune cells at the inflamed site causes oxidative stress in the affected area. A review on the role of oxidative stress and inflammation in cancer-related literature was conducted to obtain data. All of the information gathered was focused on the current state of oxidative stress and inflammation in various cancers. After gathering all relevant information, a narrative review was created to provide a detailed note on oxidative stress and inflammation in cancer. Proliferation, differentiation, angiogenesis, migration, invasion, metabolic changes, and evasion of programmed cell death are all aided by OS and inflammation in cancer. Imbalance between reactive oxygen species (ROS) and antioxidants lead to oxidative stress that damages macromolecules (nucleic acids, lipids and proteins). It causes breakdown of the biological signaling cascade. Prolonged oxidative stress causes inflammation by activating transcription factors (NF-κB, p53, HIF-1α, PPAR-γ, Nrf2, AP-1) that alter the expression of many other genes and proteins, including growth factors, tumor-suppressor genes, oncogenes, and pro-inflammatory cytokines, resulting in cancer cell survival. The present review article examines the complex relationship between OS and inflammation in certain types of cancer (colorectal, breast, lung, bladder, and gastric cancer).