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姜黄素诱导前列腺癌细胞毒性中 ERK1/2 依赖性糖酵解抑制作用。

ERK1/2-Dependent Inhibition of Glycolysis in Curcumin-Induced Cytotoxicity of Prostate Carcinoma Cells.

机构信息

Department of Biochemistry, College of Medicine, Soonchunhyang University, Cheonan 31151, Republic of Korea.

出版信息

Biomed Res Int. 2022 Aug 24;2022:7626405. doi: 10.1155/2022/7626405. eCollection 2022.

DOI:10.1155/2022/7626405
PMID:36060138
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC9433281/
Abstract

METHODS

Cell viability, glycolytic activity, Annexin V-PE binding activity, reactive oxygen species levels, mitochondrial membrane potential, ATP content, Western blot analysis, and spheroid viability were measured for this study.

RESULTS

Acidic pH-tolerant prostate cancer cells, PC-3AcT and DU145AcT, increased cytotoxicity with ERK1/2 inhibition in a curcumin concentration-dependent manner at concentrations that resulted in >90% cell viability in normal prostate epithelial HPrEC cells. ERK1/2 inhibition by curcumin and/or PD98059 suppressed cell growth, reduced glucose consumption, and downregulated the expression of key regulatory enzymes in glucose metabolism including hexokinases, phosphofructokinase, and pyruvate dehydrogenase. In addition, these compounds caused loss of mitochondrial membrane potential with increased intracellular ROS levels, decreased levels of complexes I, III, and IV in the mitochondrial electron transport chain, and cellular ATP depletion, leading to upregulation of marker proteins in apoptosis (cleaved caspase-3 and cleaved PARP) and necroptosis (p-MLKL and p-RIP3). The results of curcumin and/or PD98059 treatment in 3D cultures showed similar trends to those in 2D cultures.

CONCLUSION

Taken together, the results provide mechanistic evidence for the antiglycolytic and cytotoxic roles of curcumin through inhibition of the MEK/ERK signaling pathway in prostate carcinoma cells preadapted to acidic conditions.

摘要

方法

本研究测定了细胞活力、糖酵解活性、Annexin V-PE 结合活性、活性氧水平、线粒体膜电位、ATP 含量、Western blot 分析和球体活力。

结果

耐酸性前列腺癌细胞 PC-3AcT 和 DU145AcT 中，ERK1/2 抑制在浓度依赖性方式下增加了细胞毒性，在正常前列腺上皮细胞 HPrEC 中，细胞活力>90%的浓度下，细胞活力>90%。Curcumin 和/或 PD98059 通过 ERK1/2 抑制抑制细胞生长、减少葡萄糖消耗，并下调葡萄糖代谢中的关键调节酶的表达，包括己糖激酶、磷酸果糖激酶和丙酮酸脱氢酶。此外，这些化合物导致线粒体膜电位丧失，细胞内 ROS 水平升高，线粒体电子传递链中复合物 I、III 和 IV 的水平降低，细胞内 ATP 耗竭，导致凋亡（裂解 caspase-3 和裂解 PARP）和坏死性凋亡（p-MLKL 和 p-RIP3）标记蛋白上调。在 3D 培养物中用 curcumin 和/或 PD98059 处理的结果与 2D 培养物中的结果相似。

结论

综上所述，这些结果为 curcumin 通过抑制 MEK/ERK 信号通路在预先适应酸性条件的前列腺癌细胞中发挥抗糖酵解和细胞毒性作用提供了机制证据。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/405b/9433281/24680b3dba44/BMRI2022-7626405.007.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/405b/9433281/6b93bef453b2/BMRI2022-7626405.001.jpg
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https://cdn.ncbi.nlm.nih.gov/pmc/blobs/405b/9433281/6ae5c435f7a5/BMRI2022-7626405.006.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/405b/9433281/24680b3dba44/BMRI2022-7626405.007.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/405b/9433281/6b93bef453b2/BMRI2022-7626405.001.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/405b/9433281/e0a096d61895/BMRI2022-7626405.002.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/405b/9433281/4c043260637e/BMRI2022-7626405.003.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/405b/9433281/b5f016200eb2/BMRI2022-7626405.004.jpg
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https://cdn.ncbi.nlm.nih.gov/pmc/blobs/405b/9433281/6ae5c435f7a5/BMRI2022-7626405.006.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/405b/9433281/24680b3dba44/BMRI2022-7626405.007.jpg

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