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长非编码 RNA 01614 通过抑制 GSK-3β 来激活 WNT/β-catenin 信号通路，从而促进胰腺癌的进展。

Long non‑coding RNA 01614 hyperactivates WNT/β‑catenin signaling to promote pancreatic cancer progression by suppressing GSK‑3β.

机构信息

Department of Pancreatic Surgery, Renmin Hospital of Wuhan University, Wuhan, Hubei 430060, P.R. China.

Department of Breast and Τhyroid Surgery, Experiment Center of Medicine, Sinopharm Dongfeng General Hospital, Hubei University of Medicine, Shiyan, Hubei 442008, P.R. China.

出版信息

Int J Oncol. 2022 Oct;61(4). doi: 10.3892/ijo.2022.5406. Epub 2022 Aug 5.

DOI:10.3892/ijo.2022.5406
PMID:35929518
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC9387559/
Abstract

Pancreatic cancer (PC) is a lethal type of cancer for which effective therapies are limited. Long non‑coding RNAs (lncRNAs) represent a critical type of regulator category, mediating the tumorigenesis and development of various tumor types, including PC. However, the expression patterns and functions of numerous lncRNAs in PC remain poorly understood. In the present study, linc01614 was identified as a PC‑related lncRNA. linc01614 was notably upregulated in PC tissues and cell lines and was associated with the poor disease‑free survival of patients with PC according to the analysis of The Cancer Genome Atlas‑derived datasets. Functionally, linc01614 knockdown suppressed PC cell proliferation, migration and invasion , and inhibited tumor proliferation and . Mechanistically, linc01614 overexpression stabilized the level of β‑catenin protein to hyperactivate the WNT/β‑catenin signaling pathway in PC cells. Further analyses revealed that linc01614 bound to GSK‑3β and perturbed the interaction between GSK‑3β and AXIN1, thereby preventing the formation of the β‑catenin degradation complex and reducing the degradation of β‑catenin. In summary, the present findings reveal that linc01614 may function as an oncogene and promote the progression of PC and may thus be considered as a potential therapeutic target in the future.

摘要

胰腺癌（PC）是一种致命的癌症，有效的治疗方法有限。长链非编码 RNA（lncRNA）是一种重要的调控因子类别，介导包括 PC 在内的多种肿瘤类型的发生和发展。然而，许多 lncRNA 在 PC 中的表达模式和功能仍知之甚少。在本研究中，鉴定出 linc01614 是一种与 PC 相关的 lncRNA。lnc01614 在 PC 组织和细胞系中显著上调，并根据癌症基因组图谱衍生数据集的分析与 PC 患者无病生存不良相关。功能上，linc01614 敲低抑制 PC 细胞增殖、迁移和侵袭，并抑制肿瘤增殖和转移。机制上，linc01614 过表达稳定 β-连环蛋白蛋白水平，过度激活 PC 细胞中的 WNT/β-连环蛋白信号通路。进一步分析表明，linc01614 与 GSK-3β 结合，并干扰 GSK-3β 与 AXIN1 之间的相互作用，从而阻止 β-连环蛋白降解复合物的形成并减少 β-连环蛋白的降解。总之，本研究结果表明，linc01614 可能作为一种癌基因发挥作用，促进 PC 的进展，因此可能成为未来潜在的治疗靶点。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/b545/9387559/a800ea3e1a17/IJO-61-4-05406-g07.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/b545/9387559/7b5b7e6e2ef1/IJO-61-4-05406-g00.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/b545/9387559/fd2647727a26/IJO-61-4-05406-g01.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/b545/9387559/bf84f19b909f/IJO-61-4-05406-g02.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/b545/9387559/7878833f6462/IJO-61-4-05406-g03.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/b545/9387559/d5a869a8aa69/IJO-61-4-05406-g04.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/b545/9387559/06da8508acac/IJO-61-4-05406-g05.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/b545/9387559/704cfe899804/IJO-61-4-05406-g06.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/b545/9387559/a800ea3e1a17/IJO-61-4-05406-g07.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/b545/9387559/7b5b7e6e2ef1/IJO-61-4-05406-g00.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/b545/9387559/fd2647727a26/IJO-61-4-05406-g01.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/b545/9387559/bf84f19b909f/IJO-61-4-05406-g02.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/b545/9387559/7878833f6462/IJO-61-4-05406-g03.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/b545/9387559/d5a869a8aa69/IJO-61-4-05406-g04.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/b545/9387559/06da8508acac/IJO-61-4-05406-g05.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/b545/9387559/704cfe899804/IJO-61-4-05406-g06.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/b545/9387559/a800ea3e1a17/IJO-61-4-05406-g07.jpg

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