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氧化应激依赖的 C/EBPβ 表达在 CAF 转化诱导 HCT116 结直肠癌细胞进展、迁移和侵袭中的作用。

Role of Oxidative Stress-Dependent C/EBPβ Expression on CAF Transformation Inducing HCT116 Colorectal Cancer Cell Progression; Migration and Invasion.

机构信息

Department of Pathobiology, Faculty of Science, Mahidol University, Bangkok 10400, Thailand.

Department of Pathology, Faculty of Medicine, Ramathibodi Hospital, Mahidol University, Bangkok 10400, Thailand.

出版信息

Asian Pac J Cancer Prev. 2023 Nov 1;24(11):3825-3835. doi: 10.31557/APJCP.2023.24.11.3825.

DOI:10.31557/APJCP.2023.24.11.3825
PMID:38019240
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC10772768/
Abstract

OBJECTIVE

To investigate oxidative stress-related CAF transformation through C/EBPβ, which affects CRC progression and may have a potential implication for CRC treatment.

METHODS

The conditioned media (CM) from HCT116, CRC cells, was used to activate CCD-18Co, colon fibroblasts, then the ability of activated FBs to induce HCT116 growth and progression was assessed using MTT assay, transwell migration, and matrix invasion assay. Alteration of the cytokine profile and oxidative stress of the activated FBs were studied with cytokine arrays and DCFH-DA assay, respectively. The protein expressions of the CAF markers (α-SMA and FAP) and C/EBPβ were investigated with immunofluorescence and western blotting.

RESULT

It was found that CM from HCT116 cells induced oxidative stress, change of cytokine profile, CAF markers, and the C/EBPβ expression of activated FBs. Furthermore, when the oxidative stress of the activated FBs was suppressed, FAP and C/EBPβ expression were downregulated, correlating with the disabling of their capability to support the cancer progression. The C/EBPβ and prognosis for CRC patients were accessed using the GEPIA dataset, in which high C/EBPβ expression was associated with a poor prognosis.

CONCLUSION

These findings suggest that C/EBPβ expression has a role in CAF transformation in an oxidative stress-related manner and might be used as a target to improve aggressive CRC treatment outcomes.

摘要

目的

通过 C/EBPβ 研究与氧化应激相关的 CAF 转化，这影响 CRC 的进展，并且可能对 CRC 的治疗具有潜在意义。

方法

使用 HCT116、CRC 细胞的条件培养基 (CM) 激活 CCD-18Co、结肠成纤维细胞，然后使用 MTT 测定法、Transwell 迁移和基质侵袭测定法评估激活的 FBs 诱导 HCT116 生长和进展的能力。通过细胞因子阵列和 DCFH-DA 测定法分别研究激活的 FBs 的细胞因子谱和氧化应激的改变。用免疫荧光和 Western blot 研究 CAF 标志物（α-SMA 和 FAP）和 C/EBPβ 的蛋白表达。

结果

发现 HCT116 细胞的 CM 诱导了氧化应激、细胞因子谱的变化、CAF 标志物和激活的 FBs 中的 C/EBPβ 表达。此外，当抑制激活的 FBs 的氧化应激时，FAP 和 C/EBPβ 的表达下调，与它们支持癌症进展的能力丧失相关。使用 GEPIA 数据集评估 C/EBPβ 和 CRC 患者的预后，其中 C/EBPβ 高表达与预后不良相关。

结论

这些发现表明，C/EBPβ 表达以与氧化应激相关的方式在 CAF 转化中起作用，并且可以用作改善侵袭性 CRC 治疗结果的靶点。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/6eea/10772768/bec1fb49561e/APJCP-24-3825-g010.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/6eea/10772768/d89d465f2d99/APJCP-24-3825-g002.jpg
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https://cdn.ncbi.nlm.nih.gov/pmc/blobs/6eea/10772768/b6dac3fa43e0/APJCP-24-3825-g007.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/6eea/10772768/16123b14a5bd/APJCP-24-3825-g008.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/6eea/10772768/4e664c103ca3/APJCP-24-3825-g009.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/6eea/10772768/bec1fb49561e/APJCP-24-3825-g010.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/6eea/10772768/d89d465f2d99/APJCP-24-3825-g002.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/6eea/10772768/904afda586e3/APJCP-24-3825-g003.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/6eea/10772768/aa2917ad5f5a/APJCP-24-3825-g004.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/6eea/10772768/668223388454/APJCP-24-3825-g005.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/6eea/10772768/b73fba99bb9f/APJCP-24-3825-g006.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/6eea/10772768/b6dac3fa43e0/APJCP-24-3825-g007.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/6eea/10772768/16123b14a5bd/APJCP-24-3825-g008.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/6eea/10772768/4e664c103ca3/APJCP-24-3825-g009.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/6eea/10772768/bec1fb49561e/APJCP-24-3825-g010.jpg

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