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14-3-3 的过表达通过 PI3K/Akt 信号调节胆管癌细胞的存活。

Overexpression of 14-3-3 Modulates Cholangiocarcinoma Cell Survival by PI3K/Akt Signaling.

机构信息

Department of Hepatobiliary Surgery, Beijing Chao Yang Hospital, Capital Medical University, Beijing 100020, China.

出版信息

Biomed Res Int. 2020 Jun 22;2020:3740418. doi: 10.1155/2020/3740418. eCollection 2020.

DOI:10.1155/2020/3740418
PMID:32685476
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC7330627/
Abstract

The protein 14-3-3 is involved in numerous cellular processes through its ability to bind phosphorylated serine/threonine residues. It is a key regulator of the cell cycle involving in G2 arrest by p53. Deregulation of 14-3-3 expression has been associated with a large variety of human cancers. However, its physiological function and therapeutic significance have rarely been investigated in cholangiocarcinoma. Using immunohistochemistry (IHC), we evaluated 14-3-3 expression in 65 human extrahepatic cholangiocarcinomas. As a result, we found that 14-3-3 is expressed in the tissue of 56 patients (86.2%), and its expression is positively correlated with tumor size, lymph node metastasis, and tumor stage. We also explored the significance of 14-3-3 and found that 14-3-3 exerts cell type-dependent effects on cell proliferation through PI3K/Akt signaling in both and xenograft models. These results suggest that 14-3-3 assumes a constitutive role in tumorigenesis rather than acting as a cell cycle regulator in cholangiocarcinoma, which makes 14-3-3 a new potential target for therapeutic intervention.

摘要

蛋白质 14-3-3 通过与磷酸化丝氨酸/苏氨酸残基结合，参与多种细胞过程。它是细胞周期的关键调节剂，通过 p53 参与 G2 期阻滞。14-3-3 表达失调与多种人类癌症有关。然而，其生理功能和治疗意义在胆管癌中很少被研究。我们使用免疫组织化学（IHC）评估了 65 例人肝外胆管癌中 14-3-3 的表达。结果发现，14-3-3 在 56 例患者（86.2%）的组织中表达，其表达与肿瘤大小、淋巴结转移和肿瘤分期呈正相关。我们还探讨了 14-3-3 的意义，发现 14-3-3 通过 PI3K/Akt 信号通路在 和 异种移植模型中对细胞增殖产生细胞类型依赖性影响。这些结果表明，14-3-3 在胆管癌中发挥致癌作用，而不是作为细胞周期调节剂，这使其成为治疗干预的新潜在靶点。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/acdd/7330627/79d529b992ae/BMRI2020-3740418.007.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/acdd/7330627/0dd2912d684f/BMRI2020-3740418.001.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/acdd/7330627/01a07d78bc48/BMRI2020-3740418.002.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/acdd/7330627/08b1138aa9b1/BMRI2020-3740418.003.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/acdd/7330627/9655501bae02/BMRI2020-3740418.004.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/acdd/7330627/dd891036f0d3/BMRI2020-3740418.005.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/acdd/7330627/012fbf38ccf1/BMRI2020-3740418.006.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/acdd/7330627/79d529b992ae/BMRI2020-3740418.007.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/acdd/7330627/0dd2912d684f/BMRI2020-3740418.001.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/acdd/7330627/01a07d78bc48/BMRI2020-3740418.002.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/acdd/7330627/08b1138aa9b1/BMRI2020-3740418.003.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/acdd/7330627/9655501bae02/BMRI2020-3740418.004.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/acdd/7330627/dd891036f0d3/BMRI2020-3740418.005.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/acdd/7330627/012fbf38ccf1/BMRI2020-3740418.006.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/acdd/7330627/79d529b992ae/BMRI2020-3740418.007.jpg

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