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Epiplakin1 通过激活 PI3K-AKT 信号通路促进食管鳞状细胞癌的进展。

Epiplakin1 promotes the progression of esophageal squamous cell carcinoma by activating the PI3K-AKT signaling pathway.

机构信息

Cancer Center, The Affiliated Qingdao Central Hospital of Qingdao University, The Second Affiliated Hospital of Medical College of Qingdao University, Qingdao, Shandong, China.

出版信息

Thorac Cancer. 2022 Apr;13(8):1117-1125. doi: 10.1111/1759-7714.14366. Epub 2022 Mar 3.

DOI:10.1111/1759-7714.14366
PMID:35238170
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC9013648/
Abstract

BACKGROUND

Epiplakin1 (EPPK1) has been associated with disease progression and unfavorable prognosis of many cancers, but its functional involvement in esophageal squamous cell carcinoma (ESCC) remains to be uncovered.

METHODS

The Quantitative Real-time PCR (qPCR) assay was employed to determine the expression of EPPK1 in ESCC tissues and cells. CCK-8 assay, colony forming assay, wound healing assay, and transwell invasion assay were utilized to evaluate the effects of EPPK1 on cell proliferation, migration, and invasion capacity in ESCC cells using small interfering ribonucleic acids. Flow cytometry was performed to estimate the cell apoptotic rate caused by silencing of EPPK1. The proteins related to epithelial-to-mesenchymal transition (EMT), apoptosis, and activation of the phosphatidylinositol 3-kinase/serine threonine protein kinase 1 (PI3K/AKT) signaling pathway were measured by western blot.

RESULTS

The expression of EPPK1 was dramatically increased in ESCC tissues and cells compared to that in relative controls. Additionally, silencing of EPPK1 suppressed ESCC cell growth, colony formation, migration, invasion, and EMT, while promoting ESCC cell apoptosis. Furthermore, EPPK1 induced ESCC cell progression via mediating the PI3K/AKT signaling pathway.

CONCLUSION

EPPK1 promotes ESCC progression by modulating the PI3K/AKT signaling pathway and could serve as a potential target for ESCC treatment.

摘要

背景

Epiplakin1（EPPK1）与许多癌症的疾病进展和不良预后有关，但它在食管鳞状细胞癌（ESCC）中的功能作用仍有待揭示。

方法

采用实时定量聚合酶链反应（qPCR）检测 EPPK1 在 ESCC 组织和细胞中的表达。利用小干扰核糖核酸（siRNA）沉默 EPPK1 后，通过 CCK-8 检测、集落形成检测、划痕愈合检测和 Transwell 侵袭检测，评估 EPPK1 对 ESCC 细胞增殖、迁移和侵袭能力的影响。采用流式细胞术估计 EPPK1 沉默引起的细胞凋亡率。通过 Western blot 检测上皮间质转化（EMT）、细胞凋亡和磷脂酰肌醇 3-激酶/丝氨酸苏氨酸蛋白激酶 1（PI3K/AKT）信号通路激活相关蛋白。

结果

与相对对照相比，EPPK1 在 ESCC 组织和细胞中的表达显著增加。此外，沉默 EPPK1 抑制 ESCC 细胞生长、集落形成、迁移、侵袭和 EMT，同时促进 ESCC 细胞凋亡。此外，EPPK1 通过介导 PI3K/AKT 信号通路诱导 ESCC 细胞进展。

结论

EPPK1 通过调节 PI3K/AKT 信号通路促进 ESCC 的进展，可作为 ESCC 治疗的潜在靶点。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/6600/9013648/75ae607c0005/TCA-13-1117-g004.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/6600/9013648/cafc72ae1e8c/TCA-13-1117-g005.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/6600/9013648/37091d738a82/TCA-13-1117-g001.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/6600/9013648/78c4bd9880ff/TCA-13-1117-g006.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/6600/9013648/c1da6643ab60/TCA-13-1117-g002.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/6600/9013648/75ae607c0005/TCA-13-1117-g004.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/6600/9013648/cafc72ae1e8c/TCA-13-1117-g005.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/6600/9013648/37091d738a82/TCA-13-1117-g001.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/6600/9013648/78c4bd9880ff/TCA-13-1117-g006.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/6600/9013648/c1da6643ab60/TCA-13-1117-g002.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/6600/9013648/75ae607c0005/TCA-13-1117-g004.jpg

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