A concise review on anti-breast cancer effectiveness of s-triazines through EGFR kinase inhibition

• Published in: Medicinal chemistry research Vol. 33; no. 1; pp. 47 - 65
• Main Authors: Tandel, Pooja, Upadhyay, Rachana, Patel, Amit B.
• Format: Journal Article
• Language: English
• Published: New York Springer US 01.01.2024; Springer Nature B.V
• Subjects: 1-Phosphatidylinositol 3-kinase; AKT protein; Anticancer properties; Antineoplastic drugs; Antitumor agents; Apoptosis; Biochemistry; Biomedical and Life Sciences; Biomedicine; Bioorganic Chemistry; Breast cancer; Cell death; Cell proliferation; Drugs; Enzymatic activity; Epidermal growth factor receptors; Inorganic Chemistry; Kinases; Malignancy; Medicinal Chemistry; Pharmacology/Toxicology; Review Article; s-triazines; Signal transduction; Structure-activity relationships; TOR protein; Triazine; Structure-activity relationships (SAR); Signaling pathway; Anti-breast cancer; MCF-7; EGFR; triazine
• ISSN: 1054-2523; 1554-8120
• DOI: 10.1007/s00044-023-03180-1

Today, one of the most common malignancies in women is breast cancer. Despite the large number of commercially available anticancer drugs, cancer cannot be cured without leaving adverse effects. The MCF-7, a human breast cancer cell line, has been the subject of the most research globally. Similarly, overexpression of the EGFR protein increases cell proliferation and decreases cell death or apoptosis. This can stimulate several downstream signaling pathways. Therefore, novel drugs against cancer with improved selectivity and specificity are required to overcome the limitations of present therapy. The s -triazine derivatives have been designed and developed to exhibit excellent anticancer effects on the MCF-7 cell line and demonstrate enzymatic activity by blocking the EGFR via the PI3K/AKT/mTOR signaling pathways. Therefore, the major goal of this in-depth study is to analyze and summarize the literature on recent developments in s -triazine-based heterocycles and their anti-breast cancer potential with structure-activity relationships (SAR).