Pan Junping, Hu Yingzhe, Yuan Chenlu, Wu Yafu, Zhu Xinhua
Department of Hepatobiliary Surgery, Affiliated Drum Tower Hospital, Medical School of Nanjing University, Nanjing, China.
Department of Hepatobiliary Surgery, Nanjing Drum Tower Hospital Clinical College of Traditional Chinese and Western Medicine, Nanjing University of Chinese Medicine, Nanjing, China.
Front Oncol. 2022 Sep 15;12:928022. doi: 10.3389/fonc.2022.928022. eCollection 2022.
OBJECTIVE: Hepatocellular carcinoma (HCC) is a malignant tumor. The occurrence of HCC is involved in the alteration of a variety of oncogenes or tumor suppressor genes, but the specific molecular mechanism remains unknown. This research proved the effects of long non-coding RNA NEAT1 (lncRNA NEAT1) on the viability, proliferation, migration, and invasion of hepatocellular carcinoma cells and explored the mechanism behind these effects. METHODS: NEAT1 in 97H and Huh7 cell lines was overexpressed or knocked down, respectively. The expression of FOXP3 and its target gene PKM2 was hinged on qRT-PCR and Western blot, respectively. RNA pulldown and RNA immunoprecipitation experiments were carried out to detect the interaction between NEAT1 and proteins. Finally, the effect of NEAT1 on the tumor volume of HCC was verified by animal experiments. RESULTS: A series of experiments have shown that NEAT1 knockdown can inhibit the viability, proliferation, migration, and invasion of HCC cells; NEAT1 can bind FOXP3 to promote PKM2 transcription; PKM2 knockdown can inhibit the viability, proliferation, migration, and invasion of HCC cells; and PKM2 knockdown reversed the function of NEAT1. CONCLUSION: lncRNA NEAT1 can promote the malignant behavior of HCC cells, while silencing of NEAT1 can inhibit that behavior of HCC cells. Mechanically, NEAT1 promotes the transcriptional activation of PKM2 by binding FOXP3, and PKM2 knockout reverses the function of NEAT1.
目的：肝细胞癌（HCC）是一种恶性肿瘤。HCC的发生涉及多种癌基因或肿瘤抑制基因的改变，但其具体分子机制仍不清楚。本研究证实了长链非编码RNA NEAT1（lncRNA NEAT1）对肝癌细胞活力、增殖、迁移和侵袭的影响，并探讨了其作用机制。 方法：分别在97H和Huh7细胞系中过表达或敲低NEAT1。FOXP3及其靶基因PKM2的表达分别通过qRT-PCR和蛋白质免疫印迹法检测。进行RNA下拉和RNA免疫沉淀实验以检测NEAT1与蛋白质之间的相互作用。最后，通过动物实验验证NEAT1对HCC肿瘤体积的影响。 结果：一系列实验表明，敲低NEAT1可抑制肝癌细胞的活力、增殖、迁移和侵袭；NEAT1可与FOXP3结合以促进PKM2转录；敲低PKM2可抑制肝癌细胞的活力、增殖、迁移和侵袭；敲低PKM2可逆转NEAT1的功能。 结论：lncRNA NEAT1可促进肝癌细胞的恶性行为，而沉默NEAT1可抑制肝癌细胞的这种行为。机制上，NEAT1通过结合FOXP3促进PKM2的转录激活，而敲除PKM2可逆转NEAT1的功能。
Am J Physiol Gastrointest Liver Physiol. 2017-8-1
Front Genet. 2025-3-5
Cancer Cell Int. 2024-7-5
Int J Clin Exp Pathol. 2019-3-1
J Cell Physiol. 2020-4
Commun Biol. 2019-4-30
J Cell Biochem. 2019-4-30
Zotero 插件
