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collapsin 反应介质蛋白 2 在合并糖尿病的结直肠癌患者中的肿瘤进展中的特征。

Characterization of Collapsin Response Mediator Protein 2 in Colorectal Cancer Progression in Subjects with Diabetic Comorbidity.

机构信息

Department of Biotechnology and Laboratory Science in Medicine, National Yang Ming Chiao Tung University, Taipei 112, Taiwan.

Department of Medicine, National Yang Ming Chiao Tung University, Taipei 112, Taiwan.

出版信息

Cells. 2022 Feb 18;11(4):727. doi: 10.3390/cells11040727.

DOI:10.3390/cells11040727
PMID:35203376
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC8869905/
Abstract

BACKGROUND

Common demographic risk factors are identified in colorectal cancer (CRC) and type 2 diabetes mellitus (DM), nevertheless, the molecular link and mechanism for CRC-DM comorbidity remain elusive. Dysregulated glycogen synthase kinase-3 beta under metabolic imbalance is suggested to accelerate CRC pathogenesis/progression via regulating collpasin response mediator protein-2 (CRMP2). Accordingly, roles of CRMP2 in CRC and CRC-DM patients were investigated for elucidating the molecular convergence of CRC and DM.

METHODS

CRMP2 profile in tumor tissues from CRC and CRC-DM patients was investigated to explore the link between CRC and DM etiology. Meanwhile, molecular mechanism of glucose to regulate CRMP2 profile and CRC characteristics was examined in vitro and in vivo.

RESULTS

CRMP2 was significantly lower in tumor lesions and associated with advanced tumor stage in CRC-DM patients. Physiological hyperglycemia suppressed CRMP2 expression/activity and augmented malignant characteristics of CRC cells. Hyperglycemia promotes actin de-polymerization, cytoskeleton flexibility and cell proliferation/metastasis by downregulating CRMP2 profile and thus contributes to CRC disease progression.

CONCLUSIONS

This study uncovers molecular evidence to substantiate and elucidate the link between CRC and T2DM, as well as characterizing the roles of CRMP2 in CRC-DM. Accordingly, altered metabolic adaptations are promising targets for anti-diabetic and cancer strategies.

摘要

背景

结直肠癌（CRC）和 2 型糖尿病（DM）存在共同的人口统计学危险因素，但 CRC-DM 合并症的分子联系和机制仍不清楚。代谢失衡下的糖原合酶激酶-3β（GSK-3β）失调被认为通过调节卷曲螺旋结构域蛋白 2（CRMP2）加速 CRC 的发病/进展。因此，研究了 CRMP2 在 CRC 和 CRC-DM 患者中的作用，以阐明 CRC 和 DM 的分子趋同。

方法

研究了 CRC 和 CRC-DM 患者肿瘤组织中的 CRMP2 谱，以探讨 CRC 和 DM 病因之间的联系。同时，在体外和体内研究了葡萄糖调节 CRMP2 谱和 CRC 特征的分子机制。

结果

CRMP2 在 CRC-DM 患者的肿瘤病变中显著降低，并与晚期肿瘤分期相关。生理高血糖抑制 CRMP2 的表达/活性，并增强 CRC 细胞的恶性特征。高血糖通过下调 CRMP2 谱促进肌动蛋白解聚、细胞骨架灵活性和细胞增殖/转移，从而促进 CRC 疾病进展。

结论

本研究提供了分子证据，证实并阐明了 CRC 和 T2DM 之间的联系，并描述了 CRMP2 在 CRC-DM 中的作用。因此，改变代谢适应可能是抗糖尿病和癌症策略的有前途的靶点。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/a5f8/8869905/d168335c4d85/cells-11-00727-g007.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/a5f8/8869905/da2b1e714538/cells-11-00727-g001.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/a5f8/8869905/c8eb166d6b76/cells-11-00727-g002.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/a5f8/8869905/89785f76939c/cells-11-00727-g003.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/a5f8/8869905/9dfe212ec534/cells-11-00727-g004.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/a5f8/8869905/1dc831b66a97/cells-11-00727-g005.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/a5f8/8869905/f1293db11fae/cells-11-00727-g006.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/a5f8/8869905/d168335c4d85/cells-11-00727-g007.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/a5f8/8869905/da2b1e714538/cells-11-00727-g001.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/a5f8/8869905/c8eb166d6b76/cells-11-00727-g002.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/a5f8/8869905/89785f76939c/cells-11-00727-g003.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/a5f8/8869905/9dfe212ec534/cells-11-00727-g004.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/a5f8/8869905/1dc831b66a97/cells-11-00727-g005.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/a5f8/8869905/f1293db11fae/cells-11-00727-g006.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/a5f8/8869905/d168335c4d85/cells-11-00727-g007.jpg

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