NCAPD2通过wnt5a依赖性Notch激活刺激糖酵解和食管癌转移。

IF 3.7 2区 生物学 Q2 CELL BIOLOGY
Qian Xu , Sheng Yang
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引用次数: 0

摘要

背景:尽管非smc凝血素I复合体D2亚基(NCAPD2)在多种肿瘤中发挥重要作用,但其在食管癌(EC)中的作用仍不明确。本研究旨在探讨NCAPD2影响EC转移的分子机制。方法:通过转录组测序分析NCAPD2在EC细胞中的作用机制。采用检测试剂盒测定细胞外酸化率(ECAR)、耗氧量(OCR)、乳酸生成和葡萄糖消耗,以评估糖酵解代谢水平。Western blot验证了关键糖酵解酶、EMT标记物和Notch信号成分的表达。通过划痕和Transwell实验评估细胞迁移和侵袭。体内实验包括在BALB/c裸鼠皮下建立肿瘤,通过H&E染色监测肿瘤生长并评估其侵袭性。免疫组化检测NCAPD2、Wnt5A、Notch通路及emt相关蛋白的表达。结果:NCAPD2在EC细胞中的过表达通过促进糖酵解增强其迁移和侵袭能力,这一过程与Wnt5A的激活密切相关。具体来说,NCAPD2提高了Wnt5A水平,从而提高了糖酵解通量。这种代谢转变依赖于Wnt5A对Notch通路的激活,最终促进了EC的转移潜力。结论:NCAPD2通过wnt5a介导的Notch通路激活促进糖酵解,从而促进EC细胞的增殖和转移。这一发现不仅揭示了NCAPD2/Wnt5A轴在EC中的关键作用,也为EC的治疗提供了潜在的治疗靶点。
本文章由计算机程序翻译,如有差异,请以英文原文为准。
NCAPD2 stimulates glycolysis and esophageal cancer metastasis through Wnt5A-dependent Notch activation

Background

Although non-SMC condensin I complex subunit D2 (NCAPD2) is a significant player in multiple tumors, its role in esophageal cancer (EC) remains poorly defined. This study aimed to investigate the molecular mechanisms by which NCAPD2 influenced EC metastasis.

Methods

The mechanism of NCAPD2 in EC cells was analyzed through transcriptome sequencing. The extracellular acidification rate (ECAR), oxygen consumption rate (OCR), lactate production, and glucose consumption were measured using assay kits to evaluate the level of glycolytic metabolism. Western blot was used to validate the expression of critical glycolytic enzymes, EMT markers, and Notch signaling components. Cell migration and invasion were assessed through scratch and Transwell assays. In vivo experiments included the establishment of subcutaneous tumors in BALB/c nude mice to monitor tumor growth and assess invasiveness via H&E staining. The expression of NCAPD2, Wnt5A, Notch pathway, and EMT-related proteins was detected by immunohistochemistry.

Results

NCAPD2 overexpression in EC cells enhanced their ability to migrate and invade by promoting glycolysis—a process tightly linked to the activation of Wnt5A. Specifically, NCAPD2 drove up Wnt5A levels, which in turn boosted glycolytic flux. This metabolic shift relied on the activation of the Notch pathway by Wnt5A, ultimately fueling the metastatic potential of EC.

Conclusion

NCAPD2 enhanced the proliferation and metastasis of EC cells by promoting glycolysis through Wnt5A-mediated activation of the Notch pathway. This finding not only revealed the critical role of the NCAPD2/Wnt5A axis in EC but also provided a potential therapeutic target for EC treatment.
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来源期刊
Cellular signalling
Cellular signalling 生物-细胞生物学
CiteScore
8.40
自引率
0.00%
发文量
250
审稿时长
27 days
期刊介绍: Cellular Signalling publishes original research describing fundamental and clinical findings on the mechanisms, actions and structural components of cellular signalling systems in vitro and in vivo. Cellular Signalling aims at full length research papers defining signalling systems ranging from microorganisms to cells, tissues and higher organisms.
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