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溶质载体家族12成员8（SLC12A8）的上调促进结直肠癌进展和化疗耐药。

SLC12A8 upregulation promotes colorectal cancer progression and chemoresistance.

作者信息

Sun Zhe, Nie Zhiyan, Xu Yao, Cui Yingshun, Ma Wenjian, Zhang Tongcun

机构信息

College of Biotechnology, Tianjin University of Science and Technology, Tianjin, China.

Institute of Biology and Medicine, College of Life Sciences and Health, Wuhan University of Science and Technology, Wuhan, China.

出版信息

Transl Cancer Res. 2024 Jul 31;13(7):3446-3464. doi: 10.21037/tcr-24-87. Epub 2024 Jul 24.

DOI:10.21037/tcr-24-87
PMID:39145047
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC11319960/
Abstract

BACKGROUND

Colorectal cancer (CRC), a prevalent gastrointestinal malignant disease, causes substantial morbidity and mortality. Identification of novel prognostic biomarkers and therapeutic targets is critically needed to improve patient outcomes. Although solute carrier family 12 member 8 (SLC12A8) has high expression in various tumors and affects tumor progression, its role in CRC remains unclear. The aim of this study was to investigate the functions of SLC12A8 in CRC.

METHODS

SLC12A8 expression and its association with clinical significance in CRC patients were explored via multiple public databases, including The Cancer Genome Atlas (TCGA), Genotype-Tissue Expression (GTEx), The Human Protein Atlas (HPA), The University of ALabama at Birmingham CANcer data analysis Portal (UALCAN), and Kaplan-Meier plotter. The effects of SLC12A8 on the CRC cell apoptosis, epithelial-mesenchymal transition (EMT), reactive oxygen species (ROS) production, and sensitivity to oxaliplatin were verified by experiments.

RESULTS

SLC12A8 expression was upregulated in CRC tissues compared with normal colorectal tissues. Furthermore, high expression of SLC12A8 was associated with poorer prognosis in CRC patients. Pathway enrichment analyses revealed SLC12A8 involvement in oxidative stress and transforming growth factor-beta (TGF-β) signaling. Experiments in CRC cells showed that SLC12A8 upregulation promoted apoptosis resistance, EMT, and inhibited ROS production. Moreover, SLC12A8 knockdown enhanced the sensitivity of CRC cells to oxaliplatin chemotherapy.

CONCLUSIONS

Our integrative analyses identify SLC12A8 as a candidate biomarker for CRC progression. Targeting SLC12A8 may improve patient responses to oxaliplatin-based treatment regimens.

摘要

背景

结直肠癌（CRC）是一种常见的胃肠道恶性疾病，会导致较高的发病率和死亡率。迫切需要鉴定新的预后生物标志物和治疗靶点，以改善患者预后。尽管溶质载体家族12成员8（SLC12A8）在各种肿瘤中高表达并影响肿瘤进展，但其在结直肠癌中的作用仍不清楚。本研究的目的是探讨SLC12A8在结直肠癌中的功能。

方法

通过多个公共数据库，包括癌症基因组图谱（TCGA）、基因型-组织表达（GTEx）、人类蛋白质图谱（HPA）、阿拉巴马大学伯明翰分校癌症数据分析门户（UALCAN）和Kaplan-Meier绘图仪，探讨SLC12A8在结直肠癌患者中的表达及其与临床意义的关联。通过实验验证SLC12A8对结直肠癌细胞凋亡、上皮-间质转化（EMT）、活性氧（ROS）产生以及对奥沙利铂敏感性的影响。

结果

与正常结直肠组织相比，结直肠癌组织中SLC12A8表达上调。此外，SLC12A8高表达与结直肠癌患者较差的预后相关。通路富集分析显示SLC12A8参与氧化应激和转化生长因子-β（TGF-β）信号传导。结直肠癌细胞实验表明，SLC12A8上调促进细胞凋亡抵抗、EMT并抑制ROS产生。此外，敲低SLC12A8增强了结直肠癌细胞对奥沙利铂化疗的敏感性。

结论

我们的综合分析确定SLC12A8是结直肠癌进展的候选生物标志物。靶向SLC12A8可能改善患者对基于奥沙利铂的治疗方案的反应。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/6576/11319960/ba4928a450d8/tcr-13-07-3446-f9.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/6576/11319960/2ea215885175/tcr-13-07-3446-f1.jpg
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https://cdn.ncbi.nlm.nih.gov/pmc/blobs/6576/11319960/c46d4146df2c/tcr-13-07-3446-f5.jpg
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https://cdn.ncbi.nlm.nih.gov/pmc/blobs/6576/11319960/5a6f29e26bf7/tcr-13-07-3446-f7.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/6576/11319960/a6c4705147f3/tcr-13-07-3446-f8.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/6576/11319960/ba4928a450d8/tcr-13-07-3446-f9.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/6576/11319960/2ea215885175/tcr-13-07-3446-f1.jpg
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https://cdn.ncbi.nlm.nih.gov/pmc/blobs/6576/11319960/9e183323d15c/tcr-13-07-3446-f3.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/6576/11319960/b4d14a437e26/tcr-13-07-3446-f4.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/6576/11319960/c46d4146df2c/tcr-13-07-3446-f5.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/6576/11319960/e2fe7b551305/tcr-13-07-3446-f6.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/6576/11319960/5a6f29e26bf7/tcr-13-07-3446-f7.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/6576/11319960/a6c4705147f3/tcr-13-07-3446-f8.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/6576/11319960/ba4928a450d8/tcr-13-07-3446-f9.jpg

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