Metformin Suppresses Hypopharyngeal Cancer Growth by Epigenetically Silencing Long Non-coding RNA SNHG7 in FaDu Cells

Wu, Ping; Tang, Yurong; Fang, Xing; Xie, Chubo; Zeng, Junfeng; Wang, Wei; Zhao, Suping

doi:10.3389/fphar.2019.00143

Cited by 39 publications

(33 citation statements)

References 31 publications

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“…It has been reported that metformin can be used to treat diseases through the regulation of lncRNA expression. 43,44 Because metformin was found to attenuate TUG1 expression in a time-dependent manner in the present study, we further investigated its correlation with TUG1 expression. Figure 6 Anti-atherosclerosis (AS) effects of metformin and lncRNA TUG1 in vivo.…”

Section: Discussionmentioning

confidence: 95%

Metformin Activates the AMPK-mTOR Pathway by Modulating lncRNA TUG1 to Induce Autophagy and Inhibit Atherosclerosis

You¹,

Long²,

Song³

et al. 2020

DDDT

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Background: Metformin has been shown to inhibit the proliferation and migration of vascular wall cells. However, the mechanism through which metformin acts on atherosclerosis (AS) via the long non-coding RNA taurine up-regulated gene 1 (lncRNA TUG1) is still unknown. Thus, this research investigated the effect of metformin and lncRNA TUG1 on AS. Methods: First, qRT-PCR was used to detect the expression of lncRNA TUG1 in patients with coronary heart disease (CHD). Then, the correlation between metformin and TUG1 expression in vitro and their effects on proliferation, migration, and autophagy in vascular wall cells were examined. Furthermore, in vivo experiments were performed to verify the anti-AS effect of metformin and TUG1 to provide a new strategy for the prevention and treatment of AS. Results: qRT-PCR results suggested that lncRNA TUG1 expression was robustly upregulated in patients with CHD. In vitro experiments indicated that after metformin administration, the expression of lncRNA TUG1 decreased in a time-dependent manner. Metformin and TUG1 knockdown via small interfering RNA both inhibited proliferation and migration while promoted autophagy via the AMPK/mTOR pathway in vascular wall cells. In vivo experiments with a rat AS model further demonstrated that metformin and sh-TUG1 could inhibit the progression of AS. Conclusion: Taken together, our data demonstrate that metformin might function to prevent AS by activating the AMPK/mTOR pathway via lncRNA TUG1.

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Section: Discussionmentioning

confidence: 95%

Metformin Activates the AMPK-mTOR Pathway by Modulating lncRNA TUG1 to Induce Autophagy and Inhibit Atherosclerosis

You¹,

Long²,

Song³

et al. 2020

DDDT

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“…In the present study, the expression of SNHG9 was upregulated in GBM, thus it was assumed that SNHG9 may also be a potentially carcinogenic lncRNA. Moreover, it was found that the four lncRNAs were hypomethylated, and one lncRNA (SNHG7) has been reported to improve the survival of patients with hypopharyngeal cancer by inhibiting the hypomethylation of its promoter (56). Furthermore, two MlncBTs (SNHG16-HEATR1 and SNHG16-MUL1) were associated with a good prognosis.…”

Section: Discussionmentioning

confidence: 99%

Genome‑wide DNA methylation regulation analysis of long non‑coding RNAs in glioblastoma

Zhao

et al. 2020

Int J Mol Med

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Glioblastoma (GBM) is a malignant brain tumor associated with high mortality. Long non-coding RNAs (lncRNAs) are increasingly being recognized as its modulators. However, it remains mostly unexplored how lncRNAs are mediated by dNA methylation in GBM. The present study integrated multi-omics data to analyze the epigenetic dysregulation of lncRNAs in GBM. Widely aberrant methylation in the lncRNA promoters was observed, and the lncRNA promoters exhibited a more hypomethylated pattern in GBM. By combining transcriptional datasets, it was possible identify the lncRNAs whose transcriptional changes might be associated with the aberrant promoter methylation. Then, a methylation-mediated lncRNA regulatory network and functional enrichment analysis of aberrantly methylated lncRNAs showed that lncRNAs with different methylation patterns were involved in diverse GBM progression-related biological functions and pathways. Specifically, four lncRNAs whose increased expression may be regulated by the corresponding promoter hypomethylation were evaluated to have an excellent diagnostic effect and clinical prognostic value. Finally, through the construction of drug-target association networks, the present study identified potential therapeutic targets and small-molecule drugs for GBM treatment. The present study provides novel insights for understanding the regulation of lncRNAs by dNA methylation and developing cancer biomarkers in GBM.

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“…Moreover, BDNF expression was significantly increased in TC tissues and exhibited a positive correlation with SNHG7 expression. Recently, Wu et al ( 63 ) reported that the expression levels of SNHG7 were elevated in hypopharyngeal cancer (HPC) tissues and were repressed by metformin. Moreover, HPC patients with high SNHG7 expression exhibited a significant correlation with increased tumor size, lower differentiation, lymph node metastasis, distant metastasis, advanced TNM stage, lower overall survival time and resistance to taxol.…”

Section: Snhg7 Dysregulation In Human Cancersmentioning

confidence: 99%

The role of long noncoding RNA SNHG7 in human cancers (Review)

Zheng

et al. 2020

Mol Clin Oncol

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Long non-coding RNAs (lncRNAs) have been demonstrated to serve important roles in a variety of human tumor types. The lncRNA small nucleolar RNA host gene 7 (SNHG7) is associated with a variety of cancer types, such as esophageal cancer, breast cancer and gastric neoplasia. Based on previous studies that examined SNHG7 expression in tumors, it has become clear that SNHG7 modulates tumorigenesis and cancer progression by acting as a competing endogenous RNA. SNHG7 can sponge tumor-suppressive microRNAs and regulate downstream signaling pathways. In addition, overexpression of SNHG7 is associated with the clinical characteristics of patients with cancer by regulating cellular proliferation, invasion and metastasis and by inhibiting apoptosis via a variety of mechanisms of action. The function of SNHG7 in tumorigenesis and cancer progression indicates that it can potentially act as a novel therapeutic target or a diagnostic biomarker for cancer therapy or detection, respectively. Contents 1. Introduction 2. Characterization of SNHG7 3. SNHG7 dysregulation in human cancers 4. Conclusion and future perspectives

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Metformin Suppresses Hypopharyngeal Cancer Growth by Epigenetically Silencing Long Non-coding RNA SNHG7 in FaDu Cells

Cited by 39 publications

References 31 publications

<p>Metformin Activates the AMPK-mTOR Pathway by Modulating lncRNA <em>TUG1</em> to Induce Autophagy and Inhibit Atherosclerosis</p>

<p>Metformin Activates the AMPK-mTOR Pathway by Modulating lncRNA <em>TUG1</em> to Induce Autophagy and Inhibit Atherosclerosis</p>

Genome‑wide DNA methylation regulation analysis of long non‑coding RNAs in glioblastoma

The role of long noncoding RNA SNHG7 in human cancers (Review)

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