Background:
Genistein is one of the other known isoflavones found in different soybeans and soy products. The chemical name for genistein is 4 ‘, 5,7-trihydroxyisoflavone. Genistein has drawn the attention of the scientific community due to its potential beneficial effects on serious human diseases, such as cancer. Mechanistic knowledge of genistein reveals its potential for apoptotic induction, cell cycle arrest, as well as antiangiogenic, antimetastatic, and anti-inflammatory effects.
Objective:
The purpose of this review is to unravel and analyze various molecular mechanisms of genistein in various cancer models.
Data sources:
English literature was searched using various databases, such as PubMed, ScienceDirect, EBSCOhost, Scopus, Web of Science, and Cochrane Library. Keywords used in various combinations included genistein, cancer, anticancer, prevention of molecular mechanisms, treatment, in vivo, in vitro, and clinical studies.
Study selection:
Study selection was carried out strictly in accordance with the preferred reporting elements statement for systematic reviews and meta-analyses.
Data extraction:
Four authors independently performed article extraction.
Data synthesis:
One hundred and one article were considered suitable for use in this review.
Conclusion:
This review covers several molecular interactions of genistein with various cellular targets in cancer models. It will help the scientific community to understand genistein and cancer biology and will encourage them to design novel therapeutic strategies.
Molecular mechanisms of action of genistein
The molecular mechanism of action of genistein as a chemotherapeutic agent has been extensively studied in different types of cancers. Genistein modulates various steps of the cell cycle, apoptosis, angiogenesis, and metastasis. The main molecular targets of genistein include caspases, B-cell lymphoma 2 (Bcl-2), Bcl-2 associated protein X (Bax), nuclear factor-κB (NF-κB), NF-κB inhibitor, phosphoinositide 3 – kinase / Akt (PI3K / Akt), extracellular signal-regulated kinase 1/2 (ERK 1/2), mitogen-activated protein kinase (MAPK) and wingless and integrating signaling 1 / β-catenin (Wnt / β- catenina) route.
In addition to transcription factors, genistein-induced endoplasmic reticulum (ER) stress and its subsequent targets have also been reported to induce apoptosis in cancer. Interestingly, peroxisome proliferator-activated receptors (PPARs) have also emerged as potential therapeutic targets of interest to modulate tumor growth, and genistein has been documented to induce apoptosis in tumor cells through the PPARγ signaling cascade. directed.