Abstract
Progress in our understanding of molecular oncology has started to shed light on dysregulation of spatio-temporally controlled signaling pathways, inactivation of tumor suppressor genes, tumour and normal stem cell quiescence, overexpression of oncogenes, extracellular and stromal microenvironments, epigenetics and autophagy. Sequentially and characteristically it has been shown that cancer cells acquire the ability to escape from apoptotic cell death, proliferate uncontrollably, sustain angiogenesis and tactfully reconstitute intracellular pathways to avoid immune surveillance. We have attempted to provide a recent snapshot of most recent progress with emphasis on how rutin modulates wide ranging intracellular signaling cascades as evidenced by in-vitro and in-vivo research. It is worth describing that 'single-cell proteomics' analysis has further improved our understanding regarding intracellular signaling pathways frequently activated in cancer cells resistant to therapeutics and can provide biomarkers for cancer diagnosis and prognosis. Data obtained from preclinical studies will prove to be helpful for scientists to bridge basic and translational studies.
Highlights
Decades of research have using high-throughput technologies have sequentially revealed that cancer is a multifaceted and genomically complex disease
Rutin has been noted to directly bind with EGFR as evidenced by pull-down assay which indicated that EGFR protein was pulled down with rutin–Sepharose 4B beads [18]. This finding needs additional verification in different cancer cell lines to know if Rutin can effectively inhibit EGFR induced signaling in HER2-overexpressing breast cancer
The results revealed that macrophages infiltrating tumor dramatically reduced peritoneal colorectal carcinoma metastases rutin significantly inhibited infiltration of macrophages [35]
Summary
Decades of research have using high-throughput technologies have sequentially revealed that cancer is a multifaceted and genomically complex disease. There is a list of newly emerging scientific evidence highlighting molecular mechanisms reported to be modulated by rutin to induce apoptosis in cancer cells. We divide this multi-component discussion into how rutin modulates, Wnt signaling, JAKSTAT signaling, EGF signaling, AP-1, NF-κB and Akt. We discuss how ER stress induced response is targeted by rutin to induce apoptosis in cancer cells. Rutin did not target Wnt/β-catenin signaling in an experimental model of Xenopus embryos [10], it still needs research in different cancer cell lines.
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