揭示细胞朊蛋白在癌症进展中的致瘤潜能。

IF 4.2 2区生物学 Q2 BIOCHEMISTRY & MOLECULAR BIOLOGY

Biochimica et biophysica acta. Molecular basis of disease Pub Date : 2025-09-09 DOI:10.1016/j.bbadis.2025.168049

Memoona Zahra , Adi Idris , Ming Q. Wei , Nigel A.J. McMillan , Alan L. Munn

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引用次数: 0

摘要

细胞朊蛋白（PrPC）在胃癌、乳腺癌、前列腺癌和结直肠癌中过度表达，其改变形式与神经系统朊蛋白疾病有关。它的过度表达影响细胞增殖、迁移和侵袭，并使其对化疗产生耐药性。PrPC是治疗和生物标志物开发的潜在靶点，对PrPC的研究可能为癌症生物学提供新的理论见解。本文综述了PrPC过表达促进肿瘤发生的分子机制。我们假设PrPC可能在血管生成中起作用。我们也考虑可能使用脂质纳米颗粒作为治疗药物靶向癌症中过度表达的PrPC。对这些分子机制的进一步了解可能会揭示癌症治疗的其他靶点。需要进一步的研究来阐明这些机制并制定有针对性的干预措施。

本文章由计算机程序翻译，如有差异，请以英文原文为准。

Unmasking the tumorigenic potential of cellular prion protein in cancer progression

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Unmasking the tumorigenic potential of cellular prion protein in cancer progression

The cellular prion protein (PrP^C), altered forms of which are associated with neurological prion disorders, is overexpressed in gastric, breast, prostate, and colorectal cancer. Its overexpression affects cell proliferation, migration, and invasion, and confers resistance to chemotherapy. PrP^C is a prospective target for therapeutic and biomarker development and the study of PrP^C may offer new theoretical insights into cancer biology. This review explores the molecular mechanism by which PrP^C overexpression contributes to the promotion of cancer. We hypothesise that PrP^C may have a role in angiogenesis. We also consider the possible use of lipid nanoparticles as the therapeutic agent to target overexpressed PrP^C selectively in cancer. An improved knowledge of these molecular mechanisms may reveal additional targets for cancer treatment. Further research is required to elucidate these mechanisms and to formulate targeted interventions.

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来源期刊

Biochimica et biophysica acta. Molecular basis of disease 生物-生化与分子生物学

CiteScore

12.30

自引率

0.00%

发文量

218

审稿时长

32 days

期刊介绍： BBA Molecular Basis of Disease addresses the biochemistry and molecular genetics of disease processes and models of human disease. This journal covers aspects of aging, cancer, metabolic-, neurological-, and immunological-based disease. Manuscripts focused on using animal models to elucidate biochemical and mechanistic insight in each of these conditions, are particularly encouraged. Manuscripts should emphasize the underlying mechanisms of disease pathways and provide novel contributions to the understanding and/or treatment of these disorders. Highly descriptive and method development submissions may be declined without full review. The submission of uninvited reviews to BBA - Molecular Basis of Disease is strongly discouraged, and any such uninvited review should be accompanied by a coverletter outlining the compelling reasons why the review should be considered.