Browsing by Author "Sally A. Fahim"

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    Hydroxychloroquine modulates the progression of experimentally induced benign prostatic hyperplasia in rats via targeting EGFR/ERK/STAT3 and AR/FOXO1/ TRAIL pathways: computational and in vivo studies
    (Nature Research, 2025-06-20) Walaa H. El-Maadawy; Ehab Hafiz; Samer A.Tadros; Sally A. Fahim; Haidy M. Ebrahim; Marwa A. Fouad; Yasmin M.Attia
    Benign prostatic hyperplasia (BPH) is a prevalent progressive age-related disorder in men, yet its etiopathophysiology remains poorly understood. Current treatments like finasteride (Fin) have limited long-term efficacy, necessitating alternative therapies. Hydroxychloroquine (HCQ), a safe antimalarial agent, possesses anti-inflammatory, immunomodulatory, and antiproliferative activities, however, its therapeutic effect in BPH has not been investigated. Accordingly, we examined its therapeutic potential and underlying mechanisms, alone or combined with Fin, in testosterone-induced BPH in rats. In BPH-induced rats, HCQ markedly reduced prostate weight and index, and PSA, testosterone, dihydrotestosterone, pro-inflammatory cytokines (TNF-α, κ and IL-6), and the transcription factor “NF-κB” levels, while improving histological abnormalities in epithelial and stromal tissues. HCQ reduced the mRNA expression of AR and ERK1/2, and decreased the protein levels of EGFR and STAT3. Additionally, HCQ increased the mRNA expression of FOXO1 and promoted apoptosis through both intrinsic and TRAIL-mediated pathways. This was evidenced by the upregulation of pro-apoptotic Bax and the downregulation of anti-apoptotic Bcl-2 and Bcl-XL levels in the intrinsic pathway, as well as the reduction in mRNA expression of DR4 and DR5 in the TRAIL-mediated pathway. Notably, combining HCQ with Fin enhanced these effects. Molecular docking revealed HCQ’s strong interactions with androgen receptor (AR), EGFR, ERK1/2, FOXO, and TRAIL death receptors (DR4/DR5), comparable to Fin except for STAT3. Our findings suggest that HCQ modulates BPH progression by targeting STAT3/ FOXO1/TRAIL and EGFR/ERK/AR pathways, offering a promising therapeutic strategy for BPH, either alone or in combination with Fin.
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    Role of noncoding RNA as a pacemaker in cancer stem cell regulation: a review article
    (National Cancer Institute, 2025-03-24) Yasmin M. Attia; Samer A. Tadros; Sally A. Fahim; Doaa M. Badr
    Accumulated evidence supported the crucial role of a tiny population of cells within the tumor called cancer stem cells (CSCs) in cancer origination, and proliferation. Additionally, these cells are distinguished by their self-renewal, diferentiation, and therapeutic resistance capabilities. Interestingly, many studies recorded dysregulation of diferent types of noncoding RNAs, such as microRNA (miRNA) and long non-coding RNA (LncRNA), in cancer cells as well as CSCs. Moreover, several studies also supported the regulation of the transcription factors and signaling pathways required for CSC progression by these noncoding RNAs. However, the exact biological functions of all these noncoding RNAs are not well understood yet. These fndings are of great interest, implying usage of noncoding RNA as therapeutic tool to target these cells. In this review, we provide an insight into how noncoding RNAs regulate CSCs and how this correlation is manipulated to develop new therapies to eradicate cancer cells successfully