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lncRNA FLVCR1-AS1 与 KLF10 之间的正反馈可能通过 PTEN/AKT 通路抑制胰腺癌的进展。

Positive feedback between lncRNA FLVCR1-AS1 and KLF10 may inhibit pancreatic cancer progression via the PTEN/AKT pathway.

机构信息

Department of General Surgery, Pancreatic Disease Center, Research Institute of Pancreatic Diseases, Ruijin Hospital, Shanghai Jiao Tong University School of Medicine, Shanghai, China.

Research Institute of Pancreatic Diseases, Shanghai Jiao Tong University School of Medicine, Shanghai, China.

出版信息

J Exp Clin Cancer Res. 2021 Oct 11;40(1):316. doi: 10.1186/s13046-021-02097-0.

DOI:10.1186/s13046-021-02097-0
PMID:34635142
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC8507233/
Abstract

BACKGROUND

FLVCR1-AS1 is a key regulator of cancer progression. However, the biological functions and underlying molecular mechanisms of pancreatic cancer (PC) remain unknown.

METHODS

FLVCR1-AS1 expression levels in 77 PC tissues and matched non-tumor tissues were analyzed by qRT-PCR. Moreover, the role of FLVCR1-AS1 in PC cell proliferation, cell cycle, and migration was verified via functional in vitro and in vivo experiments. Further, the potential competitive endogenous RNA (ceRNA) network between FLVCR1-AS1 and KLF10, as well as FLVCR1-AS1 transcription levels, were investigated.

RESULTS

FLVCR1-AS1 expression was low in both PC tissues and PC cell lines, and FLVCR1-AS1 downregulation was associated with a worse prognosis in patients with PC. Functional experiments demonstrated that FLVCR1-AS1 overexpression significantly suppressed PC cell proliferation, cell cycle, and migration both in vitro and in vivo. Mechanistic investigations revealed that FLVCR1-AS1 acts as a ceRNA to sequester miR-513c-5p or miR-514b-5p from the sponging KLF10 mRNA, thereby relieving their suppressive effects on KLF10 expression. Additionally, FLVCR1-AS1 was shown to be a direct transcriptional target of KLF10.

CONCLUSIONS

Our research suggests that FLVCR1-AS1 plays a tumor-suppressive role in PC by inhibiting proliferation, cell cycle, and migration through a positive feedback loop with KLF10, thereby providing a novel therapeutic strategy for PC treatment.

摘要

背景

FLVCR1-AS1 是癌症进展的关键调节因子。然而，胰腺癌（PC）的生物学功能和潜在分子机制仍不清楚。

方法

通过 qRT-PCR 分析 77 例 PC 组织和配对非肿瘤组织中的 FLVCR1-AS1 表达水平。此外，通过体外和体内功能实验验证了 FLVCR1-AS1 在 PC 细胞增殖、细胞周期和迁移中的作用。进一步研究了 FLVCR1-AS1 与 KLF10 之间的潜在竞争性内源 RNA（ceRNA）网络以及 FLVCR1-AS1 的转录水平。

结果

FLVCR1-AS1 在 PC 组织和 PC 细胞系中表达水平较低，FLVCR1-AS1 下调与 PC 患者预后不良相关。功能实验表明，FLVCR1-AS1 过表达可显著抑制 PC 细胞在体外和体内的增殖、细胞周期和迁移。机制研究表明，FLVCR1-AS1 作为 ceRNA 从海绵状 KLF10 mRNA 中分离 miR-513c-5p 或 miR-514b-5p，从而解除其对 KLF10 表达的抑制作用。此外，FLVCR1-AS1 被证明是 KLF10 的直接转录靶标。

结论

我们的研究表明，FLVCR1-AS1 通过与 KLF10 形成正反馈环抑制增殖、细胞周期和迁移，从而在 PC 中发挥肿瘤抑制作用，为 PC 的治疗提供了一种新的治疗策略。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/2794/8507233/a7f5df52370d/13046_2021_2097_Fig7_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/2794/8507233/dedecf19cd32/13046_2021_2097_Fig1_HTML.jpg
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https://cdn.ncbi.nlm.nih.gov/pmc/blobs/2794/8507233/c27ab531fa16/13046_2021_2097_Fig4_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/2794/8507233/f1df3e7046f8/13046_2021_2097_Fig5_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/2794/8507233/547ded099774/13046_2021_2097_Fig6_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/2794/8507233/a7f5df52370d/13046_2021_2097_Fig7_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/2794/8507233/dedecf19cd32/13046_2021_2097_Fig1_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/2794/8507233/a6cc8979c2eb/13046_2021_2097_Fig2_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/2794/8507233/ea54e09a6cd1/13046_2021_2097_Fig3_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/2794/8507233/c27ab531fa16/13046_2021_2097_Fig4_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/2794/8507233/f1df3e7046f8/13046_2021_2097_Fig5_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/2794/8507233/547ded099774/13046_2021_2097_Fig6_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/2794/8507233/a7f5df52370d/13046_2021_2097_Fig7_HTML.jpg

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