LncRNA SNHG16 promotes epithelial- mesenchymal transition via down-regulation of DKK3 in gastric cancer

Zhou, Chunhuan; Zhao, Juanjuan; Liu, Juanjuan; Wei, Sixi; Xia, Ying; Xia, Wansong; Bi, Ying; Yan, Zhiqiang; Huang, Hai

doi:10.3233/cbm-190497

Cited by 37 publications

(26 citation statements)

References 27 publications

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“…[15][16][17] Notably, there is increasing evidence supporting a close relationship between lncRNA dysregulation and malignant characteristics in GC. 18,19 MicroRNAs (miRNAs, miRs) are classified as singlestranded noncoding short RNAs approximately 19-25 nucleotides in length. 20 MiRNAs serve as major posttranscriptional regulators of gene expression by directly interacting with the 3′ untranslated regions (3′-UTRs) of their target mRNAs, which can result in the subsequent degradation of a target mRNA or suppression of its translation.…”

Section: Introductionmentioning

confidence: 99%

<p>Long Noncoding RNA DLGAP1-AS1 Promotes the Aggressive Behavior of Gastric Cancer by Acting as a ceRNA for microRNA-628-5p and Raising Astrocyte Elevated Gene 1 Expression</p>

Deng¹,

Zhang²,

Lu³

et al. 2020

CMAR

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Purpose: The long noncoding RNA DLGAP1 antisense RNA 1 (DLGAP1-AS1) plays welldefined roles in the malignant progression of hepatocellular carcinoma. The purpose of this study was to determine whether DLGAP1-AS1 affects the aggressive behavior of gastric cancer (GC). Methods: DLGAP1-AS1 expression in GC tissue samples and cell lines was determined by reverse-transcription quantitative PCR. GC cell proliferation, apoptosis, migration, invasion, and tumor growth in vitro as well as in vivo were examined by the Cell Counting Kit-8 assay, flow-cytometric analysis, transwell migration and invasion assays, and xenograft model experiments, respectively. Results: DLGAP1-AS1 was overexpressed in GC tissue samples and cell lines. Among patients with GC, the increased level of DLGAP1-AS1 correlated with tumor size, TNM stage, lymph node metastasis, distant metastasis, and shorter overall survival. The knockdown of DLGAP1-AS1 suppressed GC cell proliferation, migration, and invasion in vitro, as well as promoted cell apoptosis and hindered tumor growth in vivo. Mechanistically, DLGAP1-AS1 functioned as a competing endogenous RNA for microRNA-628-5p (miR-628-5p) in GC cells, thereby increasing the expression of the miR-628-5p target astrocyte elevated gene 1 (AEG-1). Functionally, the recovery of the miR-628-5p/AEG-1 axis output attenuated the effects of DLGAP1-AS1 knockdown in GC cells. Conclusion: DLGAP1-AS1 is a pleiotropic oncogenic lncRNA in GC. DLGAP1-AS1 plays a pivotal part in the oncogenicity of GC in vitro and in vivo by regulating the miR-628-5p/ AEG-1 axis. DLGAP1-AS1, miR-628-5p, and AEG-1 form a regulatory pathway to facilitate GC progression, suggesting this pathway as an effective target for the treatment of GC.

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Section: Introductionmentioning

confidence: 99%

<p>Long Noncoding RNA DLGAP1-AS1 Promotes the Aggressive Behavior of Gastric Cancer by Acting as a ceRNA for microRNA-628-5p and Raising Astrocyte Elevated Gene 1 Expression</p>

Deng¹,

Zhang²,

Lu³

et al. 2020

CMAR

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“…International Publisher oral squamous cell carcinoma (OSCC) [7], osteosarcoma [8], non-small cell lung cancer (NSCLC) [9], bladder cancer [10], glioma [11], gastric cancer [12], pancreatic cancer [13], and so on [14]. Recently, Chen et al has reported that LncRNA SNHG16 promotes hepatocellular carcinoma proliferation, migration and invasion by regulating miR-186 expression [15].…”

Section: Ivyspringmentioning

confidence: 99%

Lnc-SNHG16/miR-128 axis modulates malignant phenotype through WNT/β-catenin pathway in cervical cancer cells

Guo²,

Liang

et al. 2020

J. Cancer

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Background: The lnc-SNHG16 serves as an oncogene and miR-128 acts as a tumor suppressor in various cancers. However, the functional role of lnc-SNHG16 and miR-128 in CC still remain unknown. This study aims to explore the expression level of lnc-SNHG16 and miR-128 and its biological roles in CC. Methods: lnc-SNHG16, miR-128, GSPT1 and WNT3A expression were analyzed using quantitative real-time PCR and bioinformatics in cervical cancer tissues and cells. Cell Counting Kit-8, EdU staining, colony formation assay, western blot, Transwell, immunofluorescence, immunohistochemical staining, luciferase reporter assay, electrophoretic mobility shift, tumor xenograft, and flow cytometry assays were employed to investigate the mechanisms underlying the effect of Lnc-SNHG16/miR-128 axis on cervical cancer. Results: lnc-SNHG16 was up-regulated in CC cell lines and tissues. lnc-SNHG16 knockdown inhibited proliferation, restrained the epithelial-mesenchymal transition (EMT) process by regulating cell apoptosis and cell cycle. The next study indicated that lnc-SNHG16 knockdown markedly increased miR-128 level which is down-regulated in CC. Moreover, miR-128 overexpression significantly inhibited proliferation, EMT process and tumor growth by directly targeting GSPT1 and WNT3A. Finally, lnc-SNHG16 activates but miR-128 inactivates the WNT/β-catenin pathways in CC cells. Conclusion: Our data suggest that lnc-SNHG16/miR-128 axis modulates malignant phenotype of CC cells through WNT/β-catenin pathway.

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“…In addition, there are some molecules reported to be mediated by SNHG16, including Stearoyl-CoA Acute Lymphoblastic Leukemia MOLT3 BALB/c nude mice promote [22] Cervical cancer HeLa BALB/c nude mice promote [29] Colorectal cancer LoVo BALB/c nude mice promote [30] Diffuse large B-cell lymphoma OCI-LY7 NOD/SCID mice promote [33] Esophageal squamous cell carcinoma kyse-70 BALB/c nude mice promote [35] Gastric cancer MGC-803 BALB/c nude mice promote [38] Hepatocellular carcinoma HuH7 athymic nude mice inhibit [44] HuH7 BALB/c nude mice promote [47] HepG2 BALB/c nude mice promote [48] HepG2 athymic nude mice promote [49] Hep-3B BALB/c nude mice promote [50] Neuroblastoma SK-N-SH BALB/c nude mice promote [51] Non small cell lung cancer A549 BALB/c nude mice promote [53,54] Oral squamous cell carcinoma TSCCA BALB/c nude mice promote [55] Pancreatic cancer AsPC-1 BALB/c nude mice promote [61] Retinoblastoma Y79 BALB/c nude mice promote [63] Desaturase (SCD) [31], p-AKT and matrix metallopeptidase 9 (MMP9) [60], Dickkopf-related protein 3 (DKK3) [39], and Wnt/β-catenin [36], but the underlying regulate mechanisms are not well uncovered. Furthermore, whether SNHG16 has other regulatory functions still needs further investigation.…”

Section: Snhg16 Regulates Various Genesmentioning

confidence: 99%

“…SNHG16 affects cancer metastasis predominantly by controlling epithelial-to-mesenchymal transition (EMT). Knockdown of SNHG16 inhibits EMT in bladder cancer [ 23 ], colon cancer [ 30 ], esophageal cancer [ 35 ], cervical cancer [ 28 ], oral squamous cell carcinoma [ 55 ], gastric cancer [ 39 ], and hepatocellular carcinoma [ 47 ], and regulates EMT-associated molecules (upregulates E-cadherin, and downregulates N-cadherin and vimentin).…”

Section: Functional Activities Of Snhg16 In Cancermentioning

confidence: 99%

“…In addition, there are some molecules reported to be mediated by SNHG16, including Stearoyl-CoA Desaturase (SCD) [ 31 ], p-AKT and matrix metallopeptidase 9 (MMP9) [ 60 ], Dickkopf-related protein 3 (DKK3) [ 39 ], and Wnt/β-catenin [ 36 ], but the underlying regulate mechanisms are not well uncovered. Furthermore, whether SNHG16 has other regulatory functions still needs further investigation.…”

Section: Mechanisms Of Snhg16 Action In Cancermentioning

confidence: 99%

See 1 more Smart Citation

LncRNA SNHG16 as a potential biomarker and therapeutic target in human cancers

Xiao

Ou³

et al. 2020

Biomark Res

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Long non-coding RNAs (lncRNAs) represent an important class of RNAs comprising more than 200 nucleotides, which are produced by RNA polymerase II. Although lacking an open reading framework and protein-encoding activity, lncRNAs can mediate endogenous gene expression by serving as chromatin remodeler, transcriptional or post-transcriptional modulator, and splicing regulator during gene modification. In recent years, increasing evidence shows the significance of lncRNAs in many malignancies, with vital roles in tumorigenesis and cancer progression. Moreover, lncRNAs were also considered potential diagnostic and prognostic markers in cancer. The lncRNA small nuclear RNA host gene 16 (SNHG16), found on chromosome 17q25.1, represents a novel tumor-associated lncRNA. SNHG16 was recently found to exhibit dysregulated expression in a variety of malignancies. There are growing evidence of SNHG16’s involvement in characteristics of cancer, including proliferation, apoptosis, together with its involvement in chemoresistance. In addition, SNHG16 has been described as a promising diagnostic and prognostic biomarker in cancer patients. The current review briefly summarizes recently reported findings about SNHG16 and discuss its expression, roles, mechanisms, and diagnostic and prognostic values in human cancers.

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LncRNA SNHG16 promotes epithelial- mesenchymal transition via down-regulation of DKK3 in gastric cancer

Cited by 37 publications

References 27 publications

<p>Long Noncoding RNA DLGAP1-AS1 Promotes the Aggressive Behavior of Gastric Cancer by Acting as a ceRNA for microRNA-628-5p and Raising Astrocyte Elevated Gene 1 Expression</p>

<p>Long Noncoding RNA DLGAP1-AS1 Promotes the Aggressive Behavior of Gastric Cancer by Acting as a ceRNA for microRNA-628-5p and Raising Astrocyte Elevated Gene 1 Expression</p>

Lnc-SNHG16/miR-128 axis modulates malignant phenotype through WNT/β-catenin pathway in cervical cancer cells

LncRNA SNHG16 as a potential biomarker and therapeutic target in human cancers

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