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<p>Micro-RNAs (mi-RNAs) can regulate various tumor suppressor genes or oncogenes thus they were monitored in various types of cell carcinoma. Lung cancer extensive progress has led not only to understanding the molecular pathways governing human lung cancer, but it has also created a vast reservoir for alternative development of novel liposomal Nano-medicines counteracting this malignancy. Liposomal drug delivery system can passively accrue in cancer cells via the retention phenomenon and enhanced permeability. This article highlighted liposomal-loaded nano-medicine as a potential treatment for lung cancer and clarifies the correlated miRNA and mRNA gene profile. Lung cancer was induced experimentally in rats via 3-methylcholanthrene (3-MCA) in a dose of 40 mg IV for 4 months followed by treatment via certain liposomal-loaded compounds, namely, liposomal doxorubicin (LIP-DOX), curcumin (LIP-CUR) and glutathione (LIP-GSH) in a dose of 5mg/kg IP daily for 1 month and were compared with their non-liposomal analogue. Concomitant supplementation with the aforementioned liposomal-loaded compounds impact on lung cancer was estimated via monitoring microRNA biomarkers including miR-122-5P and SNORD-78, pro-inflammatory biomarker Survivin, apoptotic and cell survival biomarkers including fms-related tyrosine kinase 3 (FLT-3), jasnus Janus kinase-2 (JAK-2), Phosphatidylinositol-3-kinase (PI3K), serine–threonine protein kinase (AKT) and tumor suppressor protein (P53). Liposomal-loaded doxorubicin, curcumin and glutathione significantly modulated these previously deviated genes as compared with their non-liposomal analogue, in addition to modulating lipid peroxide (LPOO) and total antioxidant capacity (TAC). MiR-122-5P and SNORD-78 were also amended reflecting the prospective impact of liposomal-loaded-nano-medicine on lung cancer treatment via up regulating P53 and down regulating PI3K/AKT/JAK2/FLT3 signaling pathway. </p>

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Novel insights into SNORD-78 and miR-122-5P the predicted diagnostic indexes of lung cancer: drug-loaded liposome formulations competing methylcholanthrene-induced lung cancer

  • 期刊论文

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  • 发表日期：

    2025年6月20日

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  • Mai O. Kadry,
  • Rehab M. Abdel-Megeed

摘要

Micro-RNAs (mi-RNAs) can regulate various tumor suppressor genes or oncogenes thus they were monitored in various types of cell carcinoma. Lung cancer extensive progress has led not only to understanding the molecular pathways governing human lung cancer, but it has also created a vast reservoir for alternative development of novel liposomal Nano-medicines counteracting this malignancy. Liposomal drug delivery system can passively accrue in cancer cells via the retention phenomenon and enhanced permeability. This article highlighted liposomal-loaded nano-medicine as a potential treatment for lung cancer and clarifies the correlated miRNA and mRNA gene profile. Lung cancer was induced experimentally in rats via 3-methylcholanthrene (3-MCA) in a dose of 40 mg IV for 4 months followed by treatment via certain liposomal-loaded compounds, namely, liposomal doxorubicin (LIP-DOX), curcumin (LIP-CUR) and glutathione (LIP-GSH) in a dose of 5mg/kg IP daily for 1 month and were compared with their non-liposomal analogue. Concomitant supplementation with the aforementioned liposomal-loaded compounds impact on lung cancer was estimated via monitoring microRNA biomarkers including miR-122-5P and SNORD-78, pro-inflammatory biomarker Survivin, apoptotic and cell survival biomarkers including fms-related tyrosine kinase 3 (FLT-3), jasnus Janus kinase-2 (JAK-2), Phosphatidylinositol-3-kinase (PI3K), serine–threonine protein kinase (AKT) and tumor suppressor protein (P53). Liposomal-loaded doxorubicin, curcumin and glutathione significantly modulated these previously deviated genes as compared with their non-liposomal analogue, in addition to modulating lipid peroxide (LPOO) and total antioxidant capacity (TAC). MiR-122-5P and SNORD-78 were also amended reflecting the prospective impact of liposomal-loaded-nano-medicine on lung cancer treatment via up regulating P53 and down regulating PI3K/AKT/JAK2/FLT3 signaling pathway.