Long non-coding RNA00364 represses hepatocellular carcinoma cell proliferation via modulating p-STAT3-IFIT2 signaling axis

Tang, Wei‐Guo; Hu, Bo; Sun, Haixiang; Sun, Qiqing; Sun, Chao; Fu, Pei-Yao; Yang, Zhixu; Zhang, Xin; Zhou, Chixing; Fan, Jia; Ren, Ning; Xu, Yang

doi:10.18632/oncotarget.22039

Cited by 30 publications

(21 citation statements)

References 35 publications

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“…Rather, IFIT2 induced apoptosis by regulating the balance between pro-and anti-apoptotic Bcl-2 family proteins, which altered the permeability of the mitochondrial membrane (Tait and Green, 2010;Stawowczyk et al, 2011). Several research studies have confirmed the ability of IFIT2 to promote the apoptotic death of cancer cells, including OSCC (Lai et al, 2013;Feng et al, 2014), colorectal cancer (Jia et al, 2017;Ohsugi et al, 2017), leukemia (Zhang et al, 2017), osteosarcoma (Wang et al, 2016), and hepatocellular carcinoma (Tang et al, 2017).…”

Section: Ifits In Apoptosismentioning

confidence: 99%

Emerging Functions of Human IFIT Proteins in Cancer

Pidugu

et al. 2019

Front. Mol. Biosci.

103

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Interferon-induced protein with tetratricopeptide repeats (IFIT) genes are prominent interferon-stimulated genes (ISGs). The human IFIT gene family consists of four genes named IFIT1, IFIT2, IFIT3, and IFIT5. The expression of IFIT genes is very low in most cell types, whereas their expression is greatly enhanced by interferon treatment, viral infection, and pathogen-associated molecular patterns (PAMPs). The proteins encoded by IFIT genes have multiple tetratricopeptide repeat (TPR) motifs. IFIT proteins do not have any known enzymatic roles. However, they execute a variety of cellular functions by mediating protein-protein interactions and forming multiprotein complexes with cellular and viral proteins through their multiple TPR motifs. The versatile tertiary structure of TPR motifs in IFIT proteins enables them to be involved in distinct biological functions, including host innate immunity, antiviral immune response, virus-induced translation initiation, replication, double-stranded RNA signaling, and PAMP recognition. The current understanding of the IFIT proteins and their role in cellular signaling mechanisms is limited to the antiviral immune response and innate immunity. However, recent studies on IFIT protein functions and their involvement in various molecular signaling mechanisms have implicated them in cancer progression and metastasis. In this article, we focused on critical molecular, biological and oncogenic functions of human IFIT proteins by reviewing their prognostic significance in health and cancer. Research suggests that IFIT proteins could be novel therapeutic targets for cancer therapy.

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Section: Ifits In Apoptosismentioning

confidence: 99%

Emerging Functions of Human IFIT Proteins in Cancer

Pidugu

et al. 2019

Front. Mol. Biosci.

103

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“…LncRNA XLOC_008466 can act as an oncogene in cervical cancer (F. Guo et al, ). LncRNA00364 can repress HCC cell proliferation through modulating phosphorylate‐signal transducer and activator of transcription 3‐interferon‐induced protein with tetratricopeptide repeats 2 (p‐STAT3‐IFIT2) signaling (Tang et al, ). Knockdown of linc‐integrin beta‐1 (ITGB1) can suppress the migration and invasion of HCC by regulating zinc finger E‐box‐binding homeobox 1 (ZEB1) (Q. Yu et al, ; W. W. Yu, Wang & Liao, ).…”

Section: Introductionmentioning

confidence: 99%

LncRNA DGCR5 represses the development of hepatocellular carcinoma by targeting the miR‐346/KLF14 axis

Wang

Liu

Shi

et al. 2018

Journal Cellular Physiology

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Long non-coding RNAs (lncRNAs) are a class of regulatory noncoding RNAs. Emerging evidence highlights the critical roles of lncRNAs in the progression of hepatocellular carcinoma (HCC). Although many lncRNAs have been identified in the development of HCC, the association between DiGeorge syndrome critical region gene 5 (DGCR5) and HCC remains unclear. In the current study, we focused on the biological role of DGCR5 in HCC. We observed that DGCR5 was decreased in HCC cells, including SMCC7721, Hep3B, HepG2, MHCC-97L, MHCC-97H, and SNU449 hepatocellular carcinoma cells, compared with the normal human liver cell line THLE-3 normal human liver cells. In addition, DGCR5 overexpression could repress HCC cell growth, migration, and invasion considerably. Increasing studies have indicated the interactions between lncRNAs and microRNAs. MicroRNAs are endogenous small noncoding RNAs and they can play important roles in tumorigenesis. MicroRNA 346 (miR-346) has been demonstrated in various human cancer types, including HCC. MiR-346 was found to be increased in HCC cells and DGCR5 can act as a sponge of miR-346 to modulate the progression of HCC. The binding correlation between DGCR5 and miR-346 was validated in our research. Subsequently, Krüppel-like factor 14 (KLF14) was predicted as a downstream target of miR-346 and miR-346 can induce the development of HCC by inhibiting KLF14. Finally, we proved that DGCR5 can rescue the inhibited levels of KLF14 repressed by miR-346 mimics in MHCC-97H and Hep3B cells. Taken together, it was indicated in our study that DGCR5 can restrain the progression of HCC through sponging miR-346 and modulating KLF14 in vitro.

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“…We have previously reported that decreased IFIT2 expression was found in gastric cancer tissues, and its expression level was signi cantly associated with tumor stage and postoperative prognoses of the patients [23]. Tang et al also found that lncRNA00364 could up-regulate IFIT2 via inhibiting STAT3 phosphorylation to repress hepatocellular carcinoma [24]. Ohsugi et al revealed that excessive Wnt/β-catenin signaling decreased IFIT2 expression to inhibit apoptosis in colorectal cancer [25].…”

Section: Discussionmentioning

confidence: 99%

Long Non-Coding RNA GRIK1-AS1 Inhibits the Proliferation and Invasion of Gastric Cancer Cells by Regulating the miR-375/IFIT2 axis

Zhou

Li²,

Chen³

et al. 2020

Preprint

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Backgroud Long non-coding RNAs (lncRNAs) played important roles in various biological processes and human diseases, including cancer. Methods In this study, RNAi technology, RNA-FISH, RNA-pull down assay and cellular function studies were used to demonstrate a regulatory relationship between lncRNA GRIK1-AS1 and miR-375/IFIT2 axis in gastric cancer. Results Our results show a decreased expression of GRIK1-AS1 in gastric cancer tissues compared to adjacent normal gastric tissues. Gastric cell lines also have reduced levels of GRIK1-AS1 compared to gastric epithelial cell line GES-1. Ectopic expression of GRIK1-AS1 in gastric cancer cell lines significantly inhibits cellular viability, migration and invasion. RNA-pull down and the luciferase activity assays show that GRIK1-AS1 mainly interacts specifically with miR-375. We further demonstrate a negatively regulatory relationship between lncRNA GRIK1-AS1 and miR-375. We discovered that IFIT2 was one of the direct key downstream target gene of miR-375, and established the important role of GRIK1-AS1/miR-375/IFIT2 axis in the progression of gastric cancer. Conclusions Our results revealed a novel mechanism of GRIK1-AS1 as sponge to miR-375that impact gastric cancer progression via modulating target mRNA IFIT2 translation, and as a result, open a new strategy to future GRIK1-AS1 based therapeutic development.

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Long non-coding RNA00364 represses hepatocellular carcinoma cell proliferation via modulating p-STAT3-IFIT2 signaling axis

Cited by 30 publications

References 35 publications

Emerging Functions of Human IFIT Proteins in Cancer

Emerging Functions of Human IFIT Proteins in Cancer

LncRNA DGCR5 represses the development of hepatocellular carcinoma by targeting the miR‐346/KLF14 axis

Long Non-Coding RNA GRIK1-AS1 Inhibits the Proliferation and Invasion of Gastric Cancer Cells by Regulating the miR-375/IFIT2 axis

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