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确定一种创新的自噬特征作为结直肠癌的预后和诊断生物标志物。

Pinpointing an innovative autophagic signature as a prognostic and diagnostic biomarkers in colorectal carcinoma.

作者信息

Kadry Mai O, Abdel-Megeed Rehab M

机构信息

National Research Center, Therapeutic Chemistry Department, Cairo, Egypt.

出版信息

Future Sci OA. 2025 Dec;11(1):2526989. doi: 10.1080/20565623.2025.2526989. Epub 2025 Jul 3.

DOI:10.1080/20565623.2025.2526989
PMID:40607700
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC12233870/
Abstract

BACKGROUND

Autophagy is balanced machinery that supports anti-malignant mechanism via the removal of dysfunctional proteins, ROS and DNA abnormalities. Appropriate autophagic machinery is fundamental for mutant eradication and suitable genomic constancy thus it prevents the genetic faults aggregation which contributes to malignant conversion. This article focuses on the application of liposomal-formulated Nano-medicine as prospective therapy for colon carcinoma and the complemented autophagic deviation.

RESEARCH DESIGN AND METHODS

Colon carcinoma was induced experimentally in rat model via 3-Methyl cholantherene (3-MCA) for 6 months proceeded with liposomal Isethione, Turmeric and Adriamycin treatment for 1 month and was further compared with their non-liposomal analogue. Concomitant supplementation with the aforementioned liposomal-formulated Nano-medicine influence on the gene expression of autophagy biomarkers including X-box binding protein 1 (XBP), C/EBP homologous protein (CHOP), activating transcription factor 4 (ATF-4) and Beclin in addition to, angiogenic biomarker (NOX) and oxidative stress biomarker (Butryl cholinesterase was investigated.

RESULTS

Liposomal-formulated Nano-medicine modulated the deviated autophagy biomarkers and oxidative and nitosative stress biomarkers in addition to, modulating histomorphological changes induced post 3-MCA colorectal cancer induction. Autophagy was involved in all steps of colon cancer progression and apoptosis.

CONCLUSION

liposomal-formulated Nano-medicine might be a prospective candidate for colorectal carcinoma treatment via modulating autophagy XBP/ATF4/Beclin/CHOP.

摘要

背景

自噬是一种平衡机制，通过清除功能失调的蛋白质、活性氧和DNA异常来支持抗恶性机制。适当的自噬机制对于清除突变体和维持合适的基因组稳定性至关重要，因此它可以防止导致恶性转化的遗传缺陷聚集。本文重点关注脂质体配方纳米药物作为结肠癌前瞻性治疗方法的应用以及与之互补的自噬偏差。

研究设计与方法

通过3-甲基胆蒽（3-MCA）在大鼠模型中诱导结肠癌6个月，然后用脂质体异丙硫醇、姜黄和阿霉素治疗1个月，并将其与非脂质体类似物进行进一步比较。同时补充上述脂质体配方纳米药物对自噬生物标志物（包括X盒结合蛋白1（XBP）、C/EBP同源蛋白（CHOP）、激活转录因子4（ATF-4）和Beclin）以及血管生成生物标志物（NOX）和氧化应激生物标志物（丁酰胆碱酯酶）的基因表达的影响进行了研究。

结果

脂质体配方纳米药物除了调节3-MCA诱导结直肠癌后引起的组织形态学变化外，还调节了偏离的自噬生物标志物以及氧化和亚硝化应激生物标志物。自噬参与了结肠癌进展和凋亡的所有步骤。

结论

脂质体配方纳米药物可能是通过调节自噬XBP/ATF4/Beclin/CHOP治疗结直肠癌的一种前瞻性候选药物。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/f294/12233870/33e04ed36bc4/IFSO_A_2526989_F0005_C.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/f294/12233870/935fc68d60ff/IFSO_A_2526989_UF0001_C.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/f294/12233870/02cbc4b4d1e2/IFSO_A_2526989_F0001_C.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/f294/12233870/9aacdc7b0cd7/IFSO_A_2526989_F0002_C.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/f294/12233870/1a1f39b666bc/IFSO_A_2526989_F0003_C.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/f294/12233870/52b49db76ded/IFSO_A_2526989_F0004_C.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/f294/12233870/33e04ed36bc4/IFSO_A_2526989_F0005_C.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/f294/12233870/935fc68d60ff/IFSO_A_2526989_UF0001_C.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/f294/12233870/02cbc4b4d1e2/IFSO_A_2526989_F0001_C.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/f294/12233870/9aacdc7b0cd7/IFSO_A_2526989_F0002_C.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/f294/12233870/1a1f39b666bc/IFSO_A_2526989_F0003_C.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/f294/12233870/52b49db76ded/IFSO_A_2526989_F0004_C.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/f294/12233870/33e04ed36bc4/IFSO_A_2526989_F0005_C.jpg

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