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TCF-3 介导的长链非编码 RNA HNF1A-AS1 转录靶向抑瘤素 M 表达通过 TGFβ 信号抑制胃肠胰神经内分泌肿瘤的上皮-间充质转化。

TCF-3-mediated transcription of lncRNA HNF1A-AS1 targeting oncostatin M expression inhibits epithelial-mesenchymal transition via TGFβ signaling in gastroenteropancreatic neuroendocrine neoplasms.

机构信息

Department of Geriatric Gastroenterology, Jiangsu People's Hospital, Nanjing Medical University, Nanjing, China.

Department of Gastroenterology, Shaoxing Central Hospital, Shaoxing, China.

出版信息

Aging (Albany NY). 2021 May 25;13(10):14065-14077. doi: 10.18632/aging.203024.

DOI:10.18632/aging.203024
PMID:34037532
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC8202880/
Abstract

Long noncoding RNAs play key roles in several cancers, but their potential functions in gastroenteropancreatic neuroendocrine neoplasms remain to be investigated. We performed GeneChip assay to explore differentiated lncRNAs in gastric NENs and peri-cancerous tissues. The regulation of HNF1A-AS1 on biological behavior of GEP-NENs cells and xenograft model was confirmed by CCK8, colony formation assay, transwell, western blot and qRT-PCR. We next detected the potential transcription factors and the binding sites between them with bioinformatic analysis. qRT-PCR was performed to analyze the exact relationship between them. HNF1A-AS1 expression was decreased in gastric NENs tissues ( < 0.01). Over-expression of HNF1A-AS1 suppressed cellular proliferation, migration and invasion. Knockdown of transcription factor 3 inhibited the expression of HNF1A-AS1 and promoted cellular migration and invasion. Oncostatin M was identified as the downstream target of HNF1A-AS1. Inhibition of transforming growth factor-β activity inhibited HNF1A-AS1/Oncostatin M-mediated epithelial-mesenchymal transition. Our data suggest that transcription factor 3/HNF1A-AS1/Oncostatin M axis inhibits the tumorigenesis and metastasis of gastroenteropancreatic neuroendocrine neoplasms via transforming growth factor-β signaling.

摘要

长链非编码 RNA 在多种癌症中发挥着关键作用，但它们在胃肠胰神经内分泌肿瘤中的潜在功能仍有待研究。我们进行了基因芯片检测，以探索胃 NEN 及其癌旁组织中差异表达的长链非编码 RNA。通过 CCK8、集落形成实验、Transwell、Western blot 和 qRT-PCR 实验，证实了 HNF1A-AS1 对 GEP-NENs 细胞和异种移植模型的生物学行为的调控作用。接下来，我们通过生物信息学分析检测了潜在的转录因子及其结合位点。通过 qRT-PCR 分析了它们之间的确切关系。HNF1A-AS1 在胃 NENs 组织中表达下调（<0.01）。HNF1A-AS1 的过表达抑制了细胞的增殖、迁移和侵袭。转录因子 3 的敲低抑制了 HNF1A-AS1 的表达并促进了细胞的迁移和侵袭。肿瘤坏死因子-α被鉴定为 HNF1A-AS1 的下游靶标。转化生长因子-β 活性的抑制抑制了 HNF1A-AS1/肿瘤坏死因子-α介导的上皮间质转化。我们的数据表明，转录因子 3/HNF1A-AS1/肿瘤坏死因子-α轴通过转化生长因子-β 信号通路抑制胃肠胰神经内分泌肿瘤的发生和转移。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/ca43/8202880/65d5ca837558/aging-13-203024-g008.jpg
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https://cdn.ncbi.nlm.nih.gov/pmc/blobs/ca43/8202880/712a49d6a372/aging-13-203024-g007.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/ca43/8202880/65d5ca837558/aging-13-203024-g008.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/ca43/8202880/4a5e20ac5154/aging-13-203024-g001.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/ca43/8202880/7259c8f6455c/aging-13-203024-g002.jpg
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