Glyoxal-induced disruption of tumor cell progression in breast cancer.

IF 1.4 Q4 ONCOLOGY Molecular and clinical oncology Pub Date : 2023-04-01 DOI:10.3892/mco.2023.2622
Pu Rong, Li Yanchu, Guo Nianchun, Li Qi, Li Xianyong
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Abstract

Breast cancer is the most common malignant tumor in women and remains a major global challenge, with ~1.4 million cases per year, worldwide. Numerous studies have shown that changes in cell metabolism are associated with the regulation of tumor progression. In the present study, the anti-cancer properties of glyoxal (GO), which is the smallest dialdehyde formed in the oxidation-reduction reaction and involved in electron transfer and energy metabolism, in breast cancer was investigated. The biological functions and molecular mechanisms of GO were investigated in breast cancer cell lines using MTT and crystal violet assays, flow cytometry, western blot analysis, 3D laser scanning confocal microscopy and transmission electron microscopy. The results showed that GO strongly inhibited cell proliferation, promoted cell apoptosis and cell cycle G2/M arrest, induced the disappearance of cellular microvilli, and enlarged mitochondria. In addition, the protein expression level of AKT, mTOR and p70-S6K decreased in the AKT-mTOR pathway, accompanied by an increase in p-ERK and p-MEK in the MAPK pathway. The results from the present study indicate that GO suppressed breast cancer progression via the MAPK and AKT-mTOR pathways. Taken together, these results provide the basis for a potential therapeutic strategy for breast cancer.

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乙二醛诱导的乳腺癌肿瘤细胞进展中断。
乳腺癌是女性中最常见的恶性肿瘤,仍然是一个重大的全球挑战,全世界每年约有140万例。大量研究表明,细胞代谢的变化与肿瘤进展的调控有关。在本研究中,我们研究了氧化还原反应中形成的最小的双醛(GO)在乳腺癌中的抗癌特性。采用MTT、结晶紫、流式细胞术、western blot、三维激光扫描共聚焦显微镜和透射电镜等方法研究氧化石墨烯在乳腺癌细胞株中的生物学功能和分子机制。结果表明,氧化石墨烯能强烈抑制细胞增殖,促进细胞凋亡和细胞周期G2/M阻滞,诱导细胞微绒毛消失,线粒体增大。此外,AKT-mTOR通路中AKT、mTOR和p70-S6K蛋白表达水平降低,MAPK通路中p-ERK和p-MEK蛋白表达水平升高。本研究的结果表明氧化石墨烯通过MAPK和AKT-mTOR途径抑制乳腺癌的进展。综上所述,这些结果为乳腺癌的潜在治疗策略提供了基础。
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CiteScore
2.80
自引率
0.00%
发文量
108
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