SNHG7 accelerates cell migration and invasion through regulating miR-34a-Snail-EMT axis in gastric cancer

Zhang, Yangmei; Yuan, Yuan; Zhang, Youwei; Cheng, Long; Zhou, Xichang; Chen, Kai

doi:10.1080/15384101.2019.1699753

Cited by 58 publications

(38 citation statements)

References 34 publications

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“…It was found that the relative expression of SNHG7 was up-regulated in GC tissues and cells, and partially contributed to GC development and progression through regulating the expression of p15 and p16 [ 32 ]. SNHG7 was also shown to accelerate cell migration and invasion through regulating miR-34A-Snail-EMT axis in GC [ 33 ]. However, few investigations have addressed the m 6 A modification in this lncRNA yet.…”

Section: Discussionmentioning

confidence: 99%

Joint analysis of lncRNA m6A methylome and lncRNA/mRNA expression profiles in gastric cancer

Sun

et al. 2020

Cancer Cell Int

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Background N6-methyladenosine (m6A) modification might be closely associated with the genesis and development of gastric cancer (GC). Currently, the evidence established by high-throughput assay for GC-related m6A patterns based on long non-coding RNAs (lncRNAs) remains limited. Here, a joint analysis of lncRNA m6A methylome and lncRNA/mRNA expression profiles in GC was performed to explore the regulatory roles of m6A modification in lncRNAs. Methods Three subjects with primary GC were enrolled in our study and paired sample was randomly selected from GC tissue and adjacent normal tissue for each case. Methylated RNA Immunoprecipitation NextGeneration Sequencing (MeRIP-Seq) and Microarray Gene Expression Profiling was subsequently performed. Then co-expression analysis and gene enrichment analysis were successively conducted. Results After data analysis, we identified 191 differentially m6A-methylated lncRNAs, 240 differentially expressed lncRNAs and 229 differentially expressed mRNAs in GC. Furthermore, four differentially m6A-methylated and expressed lncRNAs (dme-lncRNAs) were discovered including RASAL2-AS1, LINC00910, SNHG7 and LINC01105. Their potential target genes were explored by co-expression analysis. And gene enrichment analysis suggested that they might influence the cellular processes and biological behaviors involved in mitosis and cell cycle. The potential impacts of these targets on GC cells were further validated by CCLE database and literature review. Conclusions Four novel dme-lncRNAs were identified in GC, which might exert regulatory roles on GC cell proliferation. The present study would provide clues for the lncRNA m6A methylation-based research on GC epigenetic etiology and pathogenesis.

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Section: Discussionmentioning

confidence: 99%

Joint analysis of lncRNA m6A methylome and lncRNA/mRNA expression profiles in gastric cancer

Sun

et al. 2020

Cancer Cell Int

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“…Moreover, we found that decreasing circDENND2A largely raised miR-34a level. miR-34a was found to suppress cancer development in colon cancer (Sun et al, 2018), gastric cancer (Zhang et al, 2020), osteosarcoma, pancreatic ductal adenocarcinoma, breast cancer, and prostate cancer. In NSCLC, miR-34a was found to inhibit tumor genesis via targeting SIRT6 (Ruan et al, 2018), hindering cell viability, inducing apoptosis, and blocking cell-cycle progress through epidermal growth factor receptor (EGFR) (Yin et al, 2013) and to modulate ionizing radiation-induced senescence via targeting c-MYC and regulating gefitinib-acquired resistance via targeting Axl.…”

Section: Discussionmentioning

confidence: 99%

CircDENND2A Promotes Non-small Cell Lung Cancer Progression via Regulating MiR-34a/CCNE1 Signaling

et al. 2020

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The mechanism regulating non-small cell lung cancers (NSCLCs) is unclear. In this study, we aimed to determine the roles of DENN domain containing 2A (circDENND2A) in the progression of NSCLC. Circular RNAs (circRNAs) are composited by "head to tail" splicing of coding or non-coding RNAs (ncRNAs), whose crucial roles in human cancers had been revealed. CircDENND2A, a new circRNA, was revealed to induce cell proliferation and migration. Our data indicated that circDENND2A was a probable oncogene in human cancers. However, the roles of circDENND2A in NSCLC remained unknown. Here, we demonstrated that circDENND2A was down-regulated in NSCLC samples. Loss-of-function assays showed circDENND2A knockdown suppressed cell growth via inducing cell cycle arrest and apoptosis and inhibited cell migration and invasion. Bioinformatics analysis and competing endogenous RNA (ceRNA) network analysis revealed that circDENND2A was involved in regulating cell cycle and tumor protein p53 (TP53) signaling via miR-34a/CCNE1 (cyclin E1). Further validation showed that circDENND2A could directly bind to miR-34a, promoting CCNE1 expression in NSCLC. In addition, rescue assays demonstrated that restoration of CCNE1 significantly impaired the suppressive effects of circDENND2A silencing in terms of NSCLC growth, migration, and invasion. We thought this study indicated that circDENND2A/miR-34a/CCNE1 may be a potential therapeutic target for NSCLC.

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“…In gastric cancer, miR-22 is also regulated by lncRNA H19 with effects on metastasis via the miR-22-3p/SNAIL axis [134]. Another example in gastric cancer is lncRNA SNHG7 (small nucleolar RNA host gene 7), which directly binds to miR-34a and suppresses the miR-34a-SNAIL-EMT axis, which regulates gastric cancer cell migration and invasion [135].…”

Section: Lncrna Circrnas and Their Relationship To Snail And Targetmentioning

confidence: 99%

“…This mechanism may be responsible for the regulation of tumor progression. miR-22 and miR-1-3p E-cadherin, vimentin, SLUG and SNAIL prostate cancer [132] miR-1 SLUG nasopharyngeal carcinoma [133] lncRNA H19 miR-22-3p SNAIL gastric cancer [134] lncRNA SNHG7 miR-34a SNAIL gastric cancer [135] lncRNA CAR10 miR-30 and miR-203 SNAIL and SLUG lung adenocarcinoma [137] lncRNA HCP5 miR-203 SNAIL lung adenocarcinoma [138] lncRNA UCA1 miR-203 SLUG hepatocellular carcinoma [139] lncRNA AB209371 miR199a-5p SNAIL hepatocellular carcinoma [140] lncRNA TINCR miR-125b SNAIL breast cancer [85] lncRNA SATB2-AS1 -SNAIL (epigenetic regulation involving SATB2) colorectal cancer [141] lncRNA NEAT1 -E-cadherin by association with G9a-DNMT1-SNAIL complex osteosarcoma cells [142] lncRNA SNHG15 -SNAIL (ubiquitination by interaction with zinc finger domain) colon cancer [143] lncRNA GAPLINC -SLUG (by binding to PSF/NONO) colorectal cancer [136] circ-ZNF652 miR-203 and miR-502-5p SNAIL hepatocellular carcinoma [96] circRNA_0084043 miR-153-3p SNAIL melanoma [144] circRNA PRMT5 miR-30c SNAIL urothelial carcinoma [145] circRNA-000284 miR-506 SLUG cervical cancer [146] hsa_circ_0008305 (circPTK2) miR-429 and miR-200b-3p SNAIL (indirectly by TIF1γ) non-small cell lung cancer [147] circPIP5K1A miR-600 SNAIL (indirectly by HIF-1α) non-small cell lung cancer [148] circ_0026344 miR-183 SNAIL (indirectly) colorectal cancer [149]…”

Section: Lncrna Circrnas and Their Relationship To Snail And Targetmentioning

confidence: 99%

Interplay among SNAIL Transcription Factor, MicroRNAs, Long Non-Coding RNAs, and Circular RNAs in the Regulation of Tumor Growth and Metastasis

Skrzypek

Majka

2020

Cancers

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SNAIL (SNAI1) is a zinc finger transcription factor that binds to E-box sequences and regulates the expression of genes. It usually acts as a gene repressor, but it may also activate the expression of genes. SNAIL plays a key role in the regulation of epithelial to mesenchymal transition, which is the main mechanism responsible for the progression and metastasis of epithelial tumors. Nevertheless, it also regulates different processes that are responsible for tumor growth, such as the activity of cancer stem cells, the control of cell metabolism, and the regulation of differentiation. Different proteins and microRNAs may regulate the SNAIL level, and SNAIL may be an important regulator of microRNA expression as well. The interplay among SNAIL, microRNAs, long non-coding RNAs, and circular RNAs is a key event in the regulation of tumor growth and metastasis. This review for the first time discusses different types of regulation between SNAIL and non-coding RNAs with a focus on feedback loops and the role of competitive RNA. Understanding these mechanisms may help develop novel therapeutic strategies against cancer based on microRNAs.

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SNHG7 accelerates cell migration and invasion through regulating miR-34a-Snail-EMT axis in gastric cancer

Cited by 58 publications

References 34 publications

Joint analysis of lncRNA m6A methylome and lncRNA/mRNA expression profiles in gastric cancer

Joint analysis of lncRNA m6A methylome and lncRNA/mRNA expression profiles in gastric cancer

CircDENND2A Promotes Non-small Cell Lung Cancer Progression via Regulating MiR-34a/CCNE1 Signaling

Interplay among SNAIL Transcription Factor, MicroRNAs, Long Non-Coding RNAs, and Circular RNAs in the Regulation of Tumor Growth and Metastasis

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