Sirtuin1 (sirt1) regulates the glycolysis pathway and decreases cisplatin chemotherapeutic sensitivity to esophageal squamous cell carcinoma.

IF 4.4 4区医学 Q2 ONCOLOGY

Cancer Biology & Therapy Pub Date : 2024-12-31 Epub Date: 2024-06-12 DOI:10.1080/15384047.2024.2365449

Xuewen Yang, Shisen Li, Chunsheng Xu, Shushang Liu, Xiang Zhang, Bo Lian, Mengbin Li

引用次数: 0

Abstract

We aimed to evaluate the influence of sirtuin1 (sirt1) on the ESCC chemotherapeutic sensitivity to cisplatin. We used ESCC cell ablation sirt1 for establishing a xenograft mouse tumor model. The tumor volume was then detected. sirt1 was over-expressed significantly in ESCC patients and cells. Moreover, sirt1 knockdown raised ESCC sensitivity to cisplatin. Besides, glycolysis was associated with ESCC cell chemotherapy resistance to cisplatin. Furthermore, sirt1 increased ESCC cells' cisplatin chemosensitivity through HK2. Sirt1 enhanced in vivo ESCC chemosensitivity to cisplatin. Overall, these findings suggested that sirt1 knockdown regulated the glycolysis pathway and raised the ESCC chemotherapeutic sensitivity.

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Sirtuin1（sirt1）调节糖酵解途径并降低顺铂化疗对食管鳞状细胞癌的敏感性。

我们旨在评估sirtuin1（sirt1）对ESCC顺铂化疗敏感性的影响。我们使用 ESCC 细胞消融 sirt1 来建立异种移植小鼠肿瘤模型，然后检测肿瘤体积。sirt1在ESCC患者和细胞中显著过度表达。此外，sirt1的敲除提高了ESCC对顺铂的敏感性。此外，糖酵解与 ESCC 细胞对顺铂的化疗耐药性有关。此外，sirt1通过HK2增加了ESCC细胞对顺铂的化疗敏感性。Sirt1增强了体内ESCC对顺铂的化疗敏感性。总之，这些研究结果表明，sirt1的敲除调节了糖酵解途径，提高了ESCC的化疗敏感性。

本文章由计算机程序翻译，如有差异，请以英文原文为准。

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来源期刊

Cancer Biology & Therapy 医学-肿瘤学

CiteScore

7.00

自引率

0.00%

发文量

审稿时长

2.3 months

期刊介绍： Cancer, the second leading cause of death, is a heterogenous group of over 100 diseases. Cancer is characterized by disordered and deregulated cellular and stromal proliferation accompanied by reduced cell death with the ability to survive under stresses of nutrient and growth factor deprivation, hypoxia, and loss of cell-to-cell contacts. At the molecular level, cancer is a genetic disease that develops due to the accumulation of mutations over time in somatic cells. The phenotype includes genomic instability and chromosomal aneuploidy that allows for acceleration of genetic change. Malignant transformation and tumor progression of any cell requires immortalization, loss of checkpoint control, deregulation of growth, and survival. A tremendous amount has been learned about the numerous cellular and molecular genetic changes and the host-tumor interactions that accompany tumor development and progression. It is the goal of the field of Molecular Oncology to use this knowledge to understand cancer pathogenesis and drug action, as well as to develop more effective diagnostic and therapeutic strategies for cancer. This includes preventative strategies as well as approaches to treat metastases. With the availability of the human genome sequence and genomic and proteomic approaches, a wealth of tools and resources are generating even more information. The challenge will be to make biological sense out of the information, to develop appropriate models and hypotheses and to translate information for the clinicians and the benefit of their patients. Cancer Biology & Therapy aims to publish original research on the molecular basis of cancer, including articles with translational relevance to diagnosis or therapy. We will include timely reviews covering the broad scope of the journal. The journal will also publish op-ed pieces and meeting reports of interest. The goal is to foster communication and rapid exchange of information through timely publication of important results using traditional as well as electronic formats. The journal and the outstanding Editorial Board will strive to maintain the highest standards for excellence in all activities to generate a valuable resource.