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CircRHOT1 通过海绵吸附 miR-125a-3p 促进胰腺癌细胞的增殖、凋亡和侵袭。

CircRHOT1 mediated cell proliferation, apoptosis and invasion of pancreatic cancer cells by sponging miR-125a-3p.

机构信息

Medical School of Southeast University, Nanjing, Jiangsu, China.

Pancreas Center, The First Affiliated Hospital with Nanjing Medical University, Nanjing, Jiangsu, China.

出版信息

J Cell Mol Med. 2020 Sep;24(17):9881-9889. doi: 10.1111/jcmm.15572. Epub 2020 Jul 22.

DOI:10.1111/jcmm.15572
PMID:32697386
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC7520287/
Abstract

Pancreatic cancer patients are asymptomatic at early stages and leading to late diagnoses. Additionally, pancreatic cancer easily metastasizes and is resistant to radiotherapy and chemotherapy. Therefore, it is critical to understand the underlying molecular mechanisms involved in pancreatic cancer to develop more efficient diagnostic and treatment strategies. In this study, we demonstrated that circRHOT1 was overexpressed in pancreatic cancer tissues and cell lines, and it was found to directly bind to miR-125a-3p, acting as an endogenous sponge to inhibit its activity. Knockdown of circRHOT1 expression significantly inhibited proliferation as well as invasion, and it promoted apoptosis of pancreatic cancer cells via the regulation of E2F3 through the targeting of miR-125a-3p. Taken together, our results showed that circRHOT1 plays critical roles in regulating the biological functions of pancreatic cancer cells, suggesting that circRHOT1 may serve as a potential diagnostic marker and therapeutic target for patients with pancreatic cancer.

摘要

胰腺癌患者在早期阶段无症状，导致诊断较晚。此外，胰腺癌易发生转移，对放疗和化疗具有抗性。因此，了解胰腺癌相关的潜在分子机制对于开发更有效的诊断和治疗策略至关重要。在本研究中，我们证明 circRHOT1 在胰腺癌组织和细胞系中过表达，并发现其可直接与 miR-125a-3p 结合，作为内源性海绵体抑制其活性。circRHOT1 表达的敲低显著抑制了胰腺癌细胞的增殖和侵袭，并通过 miR-125a-3p 的靶向作用调节 E2F3 促进了胰腺癌细胞的凋亡。综上所述，我们的研究结果表明 circRHOT1 在调节胰腺癌细胞的生物学功能中发挥着关键作用，提示 circRHOT1 可能成为胰腺癌患者的潜在诊断标志物和治疗靶点。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/1f53/7520287/eb240ce4c772/JCMM-24-9881-g005.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/1f53/7520287/0a6c4d7a6473/JCMM-24-9881-g001.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/1f53/7520287/a7e5aa9e4e72/JCMM-24-9881-g002.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/1f53/7520287/bfd9505e27c7/JCMM-24-9881-g003.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/1f53/7520287/304b4dc44cfc/JCMM-24-9881-g004.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/1f53/7520287/eb240ce4c772/JCMM-24-9881-g005.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/1f53/7520287/0a6c4d7a6473/JCMM-24-9881-g001.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/1f53/7520287/a7e5aa9e4e72/JCMM-24-9881-g002.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/1f53/7520287/bfd9505e27c7/JCMM-24-9881-g003.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/1f53/7520287/304b4dc44cfc/JCMM-24-9881-g004.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/1f53/7520287/eb240ce4c772/JCMM-24-9881-g005.jpg

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