lncRNA HULC promotes the growth of hepatocellular carcinoma cells via stabilizing COX-2 protein

Xiong, Haojun; Li, Bo; He, Jintao; Zeng, Yijun; Zhang, Yan; He, Fengtian

doi:10.1016/j.bbrc.2017.06.103

Cited by 55 publications

(50 citation statements)

References 44 publications

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“…18 For instance, MALAT1 can induce HCC development via upregulating SRSF1 and activating mTOR. 20 Upregulation of UCA1 induces progression of HCC via regulating miR-216b and FGFR1/ERK. 20 Upregulation of UCA1 induces progression of HCC via regulating miR-216b and FGFR1/ERK.…”

Section: Discussionmentioning

confidence: 99%

LINC00346 promotes hepatocellular carcinoma progression via activating the JAK‐STAT3 signaling pathway

Yin

Zheng

Zhang

et al. 2019

J of Cellular Biochemistry

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Hepatocellular carcinoma (HCC) remains the most common malignant tumor worldwide. Long noncoding RNAs can modulate various tumorigenic processes. In addition, growing evidence has indicated tha the Janus kinase–signal transducer and activator of transcription (JAK‐STAT) pathway is activated in multiple cancers, including HCC. Recently, it was found that LINC00346 can participate in several cancers. Nevertheless, the biological roles of LINC00346 in HCC have been barely investigated. In this study, the function of LINC00346 was specifically concentrated upon. We observed that LINC00346 was obviously elevated in HCC cells (Bel7404, Huh‐6, HepG2, and QGY‐7703 cells). Then, Bel7404 and HepG2 cells were overexpressed with LINC00346. Overexpression of LINC00346 repressed HCC cell survival and cell proliferation. In addition, apoptosis of Bel7404 and HepG2 cells was triggered by LINC00346 upregulation. Bel7404 and HepG2 cell cycle was arrested in the G1 phase by LINC00346. Meanwhile, we conducted wound‐healing assay and Transwell invasion assays. As shown, we observed that the migratory and invasive capacities of Bel7404 and HepG2 cells were remarkably restrained by the increase of LINC00346. Moreover, we showed that LINC00346 overexpression activated the JAK‐STAT3 pathway, which is involved in many cancers. Afterward, in vivo experiments were utilized and we proved that LINC00346 was able to induce HCC tumor growth via activating the JAK‐STAT3 pathway. To conclude, we revealed the potential possibility of developing LINC00346 as an indicator for HCC.

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Section: Discussionmentioning

confidence: 99%

LINC00346 promotes hepatocellular carcinoma progression via activating the JAK‐STAT3 signaling pathway

Yin

Zheng

Zhang

et al. 2019

J of Cellular Biochemistry

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“…Various lncRNAs has been demonstrated to participate in the progression of HCC. For example, lncRNA HULC can promote the growth of HCC cells through stabilizing COX‐2 (Xiong et al, ). LncRNA CASC2 can regulate cell biological roles via regulating MAPK signalling pathway in HCC (Gan et al, ).…”

Section: Discussionmentioning

confidence: 99%

The long noncoding RNA NEAT1 contributes to hepatocellular carcinoma development by sponging miR‐485 and enhancing the expression of the STAT3

Zhang

Zhou

2018

Journal Cellular Physiology

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Accumulating evidence has supported the significance of lncRNAs in tumorigenesis. Recently, some studies indicate the oncogenic role of lncRNA Nuclear Enriched Abundant Transcript 1 (NEAT1) in hepatocellular carcinoma (HCC). In our present study, we focused on the biological mechanisms through which NEAT1 can regulate HCC development. We found that NEAT1 was greatly upregulated in human HCC cell lines including Huh7, Hep3B, HepG2, Bel-7404, and SK-Hep1 cells compared to the normal human liver cell line LO2. In addition, we observed that miR-485 was significantly downregulated in HCC cells. It was implied that miR-485 was increased by sh-NEAT1 and miR-485 can modulate NEAT1 expression negatively. Meanwhile, NEAT1inhibiton can repress HCC growth, migration, and invasion capacity in HepG2 and Hep3B cells. Through performing bioinformatic analysis, dual-luciferase reporter test, RNA-binding protein immunoprecipitation, and RNA pull-down assay, miR-485 was confirmed as a interacting target of NEAT1. Additionally, STAT3 was recognized as a direct target of miR-485 and miR-485 mimics can inhibit STAT3 expression. It was demonstrated that NEAT1 can increase STAT3 levels while miR-485 mimics can repress STAT3. Moreover, we found that sh-STAT3 was able to restrain HCC cell migration and invasion process. NEAT1 can act as a competing endogenous lncRNA (ceRNA) to regulated STAT3 by sponging miR-485 in HCC. Taken these together, NEAT1 can be used as an important biomarker in HCC diagnosis and treatment.

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“…Celecoxib COX-2. COX-2 also called PTGS2 that catalyzes arachidonic acid into prostaglandins and is up-regulated in HCC (Hao et al, 2017;Xiong et al, 2017;Zha et al, 2012) Luzindole A competitive antagonist of melatonin MT1/MT2 receptors Pescador et al (2011) LY294002 PI3K. PI3K/AKT signaling is a key pathway for the progression of HCC through modulating the malignant behaviour of the tumor, including cell proliferation, angiogenesis, invasiveness and metastasis (Carbajo-Pescador, Steinmetz et al, 2013;Chang, Wu, & Li, 2017; Inhibition of mTORC1, p70S6K, RP-S6 pathway Prieto-Domínguez et al (2017) Stattic STAT3.…”

Section: Inhibitor Name Factor's Inhibited With Description Refmentioning

confidence: 99%

Human hepatocellular carcinoma: Protection by melatonin

Mortezaee

2018

Journal Cellular Physiology

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Despite great scientific breakthroughs toward understanding the identity of human hepatocellular carcinoma (HCC) mechanistically, there are still no clinically efficient therapeutic methods for this cancer. Melatonin (N-acetyl-5-methoxytryptamine) is a multi-tasking hormone that has long been known for its anti-cancer activity against various human cancers including HCC, which is a focus of this review. PubMed database was searched for relevant articles with the keywords: hepatocellular carcinoma (HCC), melatonin, apoptosis, proliferation, invasion, angiogenesis, autophagy, oxidative stress, tumor immunity, and mitogen-activated protein kinase (MAPK) focusing on just human cell lines and English language articles. Melatonin inhibits apoptosis resistance and activates both extrinsic and intrinsic pathways of apoptosis in HCC. Melatonin induces ensoplasmic reticulum (ER)- and autophagy-mediated apoptosis in cancer cells. Melatonin works against cancer cell proliferation, motility, and invasiveness by modulating actions of a variety of transcription factors and related pathways. Melatonin also relieves an immunosuppressive state in HCC cancer cells through making a control over tumor-derived exosomes. Both pro-and anti-oxidative functions of melatonin are necessary for combating HCC. Combination of melatonin with chemotherapy could also provide cumulative effects on cancer cells. Melatonin exerts most of these roles by acting on the members of MAPK family.

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lncRNA HULC promotes the growth of hepatocellular carcinoma cells via stabilizing COX-2 protein

Cited by 55 publications

References 44 publications

LINC00346 promotes hepatocellular carcinoma progression via activating the JAK‐STAT3 signaling pathway

LINC00346 promotes hepatocellular carcinoma progression via activating the JAK‐STAT3 signaling pathway

The long noncoding RNA NEAT1 contributes to hepatocellular carcinoma development by sponging miR‐485 and enhancing the expression of the STAT3

Human hepatocellular carcinoma: Protection by melatonin

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