Rawan Mohamed’s research while affiliated with Mansoura University and other places

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Publications (1)

(a) Chemical structure of genistein. (B–F) depict schematic representations of the synthesis pathways for various structurally modified genistein derivatives, including MA-6, MA-8, MA-11, MA-19, MA-20, MA-21, MA-22, and MA-23. These derivatives are displayed to highlight the specific chemical modifications introduced to enhance their biological activity (Marik et al. 2011b)
Genistein modulates several critical cancer cell signaling pathways to exert its anticancer effects. It inhibits the PI3K/AKT/mTOR pathway, leading to the suppression of anti-apoptotic proteins such as Bcl-2 and Bcl-XL, while promoting the activation of pro-apoptotic proteins like Bax and cytochrome c (Cyt C), which in turn activate caspase-9 and caspase-3, inducing apoptosis. Genistein also disrupts the NF-κB signaling pathway by preventing IκB degradation, thereby reducing the nuclear translocation of the p65/p50 complex, which limits cell survival and inflammatory responses. In the MAPK pathway, genistein suppresses JNK and P38 signaling, reducing cell proliferation via P21 activation and mTOR inhibition, further enhancing apoptosis. Additionally, genistein inhibits COX-2 and MMP2, which lowers PGE2 production, thereby impairing angiogenesis and metastasis. Through modulation of the ER-α/c-Src pathway, genistein also influences Ca2 + signaling and cAMP production, ultimately affecting gene transcription related to cell survival. Collectively, these actions of genistein highlight its potent ability to inhibit cancer cell proliferation, survival, metastasis, and angiogenesis, while promoting apoptotic cell death
Unleashing the potential of Genistein and its derivatives as effective therapeutic agents for breast cancer treatment
  • Literature Review
  • Publisher preview available

November 2024

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23 Reads

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1 Citation

Naunyn-Schmiedeberg's Archives of Pharmacology

Eskandar Qaed

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Wu Liu

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Zeyao Tang

Breast cancer remains one of the leading causes of cancer-related deaths among women worldwide. Genistein (Gen), a phytoestrogen soy isoflavone, has emerged as a promising agent in the prevention and treatment of breast cancer due to its ability to function as a natural selective estrogen receptor modulator (SERM). This review explores the multifaceted mechanisms through which Gen and its derivatives exert their anticancer effects, including modulation of the PI3K/Akt signaling pathway, regulation of apoptosis, inhibition of angiogenesis, and impacts on DNA methylation and enzyme functions. We discuss the dual roles of Gen in both enhancing and inhibiting estrogen receptor (ER)-dependent pathways., highlighting its complex interactions with ERα and ERβ. Furthermore, the review examines the synergistic effect of combining Gen with conventional chemotherapeutic agents such as doxorubicin, cisplatin, and selenium, as well as other natural compounds like lycopene. Clinical studies suggest that while isoflavones may not significantly influence breast cancer progression in general, the high consumption of soy isoflavones is associated with reduced recurrence rates in breast cancer survivors. Importantly, Gen’s ability to modulate key signaling pathways and enhance the efficacy of existing treatments improves its potential as a valuable adjunct in breast cancer therapy. In conclusion, Gen and its derivatives offer a novel and promising approach for treatment of breast cancer. Continued research into their mechanisms of action and clinical applications will be essential in optimizing their therapeutic potential and translating these findings into effective clinical interventions.

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