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迈克尔受体作为抗癌化合物:巧合还是必然?

Michael Acceptors as Anti-Cancer Compounds: Coincidence or Causality?

机构信息

Hospital Clínico Universitario of Valladolid, Avenida de Ramón y Cajal, 3, 47003 Valladolid, Spain.

Institute of Natural Products and Agrobiology, CSIC-Spanish Research Council, Avda. Astrofísico Fco. Sánchez, 3, 38206 La Laguna, Spain.

出版信息

Int J Mol Sci. 2024 Jun 1;25(11):6099. doi: 10.3390/ijms25116099.

DOI:10.3390/ijms25116099
PMID:38892287
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC11172677/
Abstract

Michael acceptors represent a class of compounds with potential anti-cancer properties. They act by binding to nucleophilic sites in biological molecules, thereby disrupting cancer cell function and inducing cell death. This mode of action, as well as their ability to be modified and targeted, makes them a promising avenue for advancing cancer therapy. We are investigating the molecular mechanisms underlying Michael acceptors and their interactions with cancer cells, in particular their ability to interfere with cellular processes and induce apoptosis. The anti-cancer properties of Michael acceptors are not accidental but are due to their chemical structure and reactivity. The electrophilic nature of these compounds allows them to selectively target nucleophilic residues on disease-associated proteins, resulting in significant therapeutic benefits and minimal toxicity in various diseases. This opens up new perspectives for the development of more effective and precise cancer drugs. Nevertheless, further studies are essential to fully understand the impact of our discoveries and translate them into clinical practice.

摘要

迈克尔受体是一类具有潜在抗癌特性的化合物。它们通过与生物分子中的亲核位点结合而起作用,从而破坏癌细胞功能并诱导细胞死亡。这种作用模式以及它们能够被修饰和靶向的能力,使它们成为推进癌症治疗的有前途的途径。我们正在研究迈克尔受体的分子机制及其与癌细胞的相互作用,特别是它们干扰细胞过程和诱导细胞凋亡的能力。迈克尔受体的抗癌特性并非偶然,而是由于它们的化学结构和反应性。这些化合物的亲电性使它们能够选择性地靶向与疾病相关的蛋白质上的亲核残基,从而在各种疾病中产生显著的治疗益处和最小的毒性。这为开发更有效和精确的癌症药物开辟了新的前景。然而,进一步的研究对于充分了解我们的发现的影响并将其转化为临床实践是必不可少的。

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9
Xanthohumol hinders invasion and cell cycle progression in cancer cells through targeting MMP2, MMP9, FAK and P53 genes in three-dimensional breast and lung cancer cells culture.在三维乳腺癌和肺癌细胞培养中,黄腐酚通过靶向基质金属蛋白酶2(MMP2)、基质金属蛋白酶9(MMP9)、粘着斑激酶(FAK)和P53基因来阻碍癌细胞的侵袭和细胞周期进程。
Cancer Cell Int. 2023 Aug 2;23(1):153. doi: 10.1186/s12935-023-03009-2.
10
Caffeic acid phenethyl ester suppresses metastasis of breast cancer cells by inactivating FGFR1 via MD2.阿魏酸苯乙酯通过 MD2 使 FGFR1 失活来抑制乳腺癌细胞的转移。
PLoS One. 2023 Jul 25;18(7):e0289031. doi: 10.1371/journal.pone.0289031. eCollection 2023.