Natural compounds targeting cancer-associated genes: Multi-omics mechanisms and therapeutic potential

Cancer is caused by excessive expression of oncogenic proteins as well as inactivity of tumor suppressor proteins. In this way, complex gene regulatory processes are altered, leading to uncontrolled proliferation, chromosomal instability, and metastasis. Furthermore, conventional cancer therapy encounters severe challenges associated with drug cytotoxicity and multidrug resistance, as it focuses on a single drug target mechanism. It can be seen that there is a need to find targeted drugs to correct disrupted gene expression without harmful side effects. This review examines how phytochemicals have high potential for action due to their selective modulation of gene regulatory complexes. Herein, we provide a comprehensive overview of key gene interactions involved in cancer, including fundamental oncogenic proteins such as RAS, MYC, and EGFR, as well as key tumor suppressors such as TP53. Moreover, mechanisms of multi-omic action of phytochemicals are examined at the genotypic, transcriptional, and epigenetic levels. Importantly, gene regulation-based therapeutic targets are identified, including apoptosis induction, cell cycle regulation, DNA damage responses, and metastasis. Furthermore, this review examines barriers to clinical translation, advances in improving the bioavailability of phytochemicals, and the potential applications of AI and multi-omics in drug discovery and development.