Increased expression of long non-coding RNA SNHG16 correlates with tumor progression and poor prognosis in non-small cell lung cancer

Han, Wei; Du, Xuemei; Liu, Min; Wang, Jing; Sun, Lixin; Li, Yongchun

doi:10.1016/j.ijbiomac.2018.10.004

Cited by 62 publications

(68 citation statements)

References 29 publications

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“…Competitive endogenous RNA (ceRNA) theory indicated that lncRNA could sponge miRNA from target message RNA (mRNA) to form a lncRNA–miRNA–mRNA triple network . For instance, lncRNA SNHG16 was found increased in NSCLC and indicated poor outcome of cancer patients . In addition, SNHG16 was identified to promote NSCLC cell migration and invasion through targeting the expression of miR‐146a/MUC5AC axis .…”

Section: Introductionmentioning

confidence: 99%

“…For instance, lncRNA SNHG16 was found increased in NSCLC and indicated poor outcome of cancer patients . In addition, SNHG16 was identified to promote NSCLC cell migration and invasion through targeting the expression of miR‐146a/MUC5AC axis . Reduced expression of DiGeorge syndrome critical region gene 5 (DGCR5) in papillary thyroid carcinoma was identified and its overexpression decreased cancer cell growth and invasion .…”

Section: Introductionmentioning

confidence: 99%

“…5 For instance, lncRNA SNHG16 was found increased in NSCLC and indicated poor outcome of cancer patients. 6 In addition, SNHG16 was identified to promote NSCLC cell migration and invasion Abbreviations: DGCR5, DiGeorge syndrome critical region gene 5; EPHB6, EPH receptor B6; miR-211-5p, microRNA-211-5p; mt, mutant; NSCLC, non-small cell lung cancer; RT-qPCR, reverse transcription quantitative polymerase chain reaction; wt, wild-type.…”

Section: Introductionmentioning

confidence: 99%

“…through targeting the expression of miR-146a/MUC5AC axis. 6 Reduced expression of DiGeorge syndrome critical region gene 5 (DGCR5) in papillary thyroid carcinoma was identified and its overexpression decreased cancer cell growth and invasion. 7 Moreover, a recent study revealed that the upregulation of DGCR5 was indicator for better outcome of bladder cancer and interacted with AT-rich interaction domain 1A to regulate cancer cell progression.…”

Section: Introductionmentioning

confidence: 99%

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LncRNA DGCR5 regulates the non‐small cell lung cancer cell growth, migration, and invasion through regulating miR‐211‐5p/EPHB6 axis

Kang

Shi

et al. 2019

BioFactors

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Non‐small cell lung cancer (NSCLC) accounts for about 80% of lung cancers worldwide. In recent years, importance of noncoding RNAs including long noncoding RNA and microRNA in regulating tumor progression has been appreciated. Abnormally expression of DiGeorge syndrome critical region gene 5 (DGCR5) was found in multiple human cancers but its function in NSCLC is largely unknown. Reverse transcription quantitative polymerase chain reaction (RT‐qPCR) was conducted to explore DGCR5 expression level in NSCLC. Bioinformatic analyses were conducted to explore the targets of DGCR5. Cell counting kit‐8 assay, wound‐healing assay, and transwell invasion assay were performed to analyze functions of DGCR5. RT‐qPCR revealed that DGCR5 expression in NSCLC cells was significantly lower than in normal cell. DGCR5 overexpression suppresses NSCLC cell growth, migration, and invasion. Online algorithms found EPH receptor B6 (EPHB6) and DGCR5 contains same miR‐211‐5p binding region. The predicted connections were further validated by luciferase activity reporter assay. Recue experiments showed DGCR5 regulates NSCLC cell behaviors via targeting miR‐211‐5p/EPHB6. These findings collectively identified DGCR5/miR‐211‐5p/EPHB6 triple axis in NSCLC, which may novel understanding regarding the tumorigenesis of NSCLC.

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Section: Introductionmentioning

confidence: 99%

Section: Introductionmentioning

confidence: 99%

Section: Introductionmentioning

confidence: 99%

Section: Introductionmentioning

confidence: 99%

See 2 more Smart Citations

LncRNA DGCR5 regulates the non‐small cell lung cancer cell growth, migration, and invasion through regulating miR‐211‐5p/EPHB6 axis

Kang

Shi

et al. 2019

BioFactors

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“…Thus, lncRNAs may be promising candidates for developing effective therapeutics of NSCLC. Among these lncRNAs, lncRNA small nucleolar RNA host gene 16 (SNHG16) recently was discovered to be upregulated in NSCLC and was associated with cell carcinogenesis in NSCLC . However, the precise mechanisms underlying the tumorigenesis role of SNHG16 in NSCLC remain largely unclear.…”

Section: Introductionmentioning

confidence: 99%

LncRNA SNHG16 promotes non‐small cell lung cancer development through regulating EphA2 expression by sponging miR‐520a‐3p

Chen

Song

2020

Thoracic Cancer

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Background Recent evidence has found that lncRNA small nucleolar RNA host gene 16 (SNHG16) was associated with cell carcinogenesis in NSCLC. Here, we further investigated the precise functions and mechanisms of SNHG16 in NSCLC progression. Methods The expression of SNHG16, microRNA (miR)‐520a‐3p and EPH Receptor A2 (EphA2) was measured using quantitative real‐time polymerase chain reaction and western blot, respectively. Cell proliferation was determined using 3‐(4, 5)‐dimethylthiahiazo (−z‐y1)‐3, 5‐di‐phenytetrazoliumromide (MTT) assay. The migrated and invaded cells were measured by Transwell assay. Flow cytometry was used to detect apoptotic cells. The interaction between miR‐520a‐3p and SNHG16 or EphA2 was confirmed using a dual‐luciferase reporter assay. Results We found that SNHG16 was upregulated in NSCLC tissues and cell lines, knockdown of SNHG16 inhibited cell proliferation, migration, invasion and induced apoptosis in vitro as well as suppressed tumor growth in vivo. MiR‐520a‐3p directly bound to SNHG16 and miR‐520a‐3p, and SNHG16 acted as a ceRNA in regulating EphA2 through competitively binding to miR‐520a‐3p. Additionally, rescue assay exhibited the anticancer activity mediated by SNHG16 knockdown on NSCLC could be reversed by miR‐520a‐3p inhibition or EphA2 overexpression. Conclusion SNHG16 promoted NSCLC development by regulating the miR‐520a‐3p/EphA2 axis, suggesting novel insights for the pathogenesis of NSCLC and new potential therapeutic targets for the treatment of NSCLC. Key points Knockdown of SNHG16 inhibited NSCLC cell proliferation, migration, invasion and induced apoptosis in vitro as well as suppressed tumor growth in vivo. SNHG16 directly interacted with miR‐520a‐3p. EphA2 was a target of miR‐520a‐3p. SNHG16 could regulate the expression of EphA2 by binding to miR‐520a‐3p. SNHG16 promoted NSCLC development by regulating the miR‐520a‐3p/EphA2 axis.

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High eukaryotic initiation factor 5A2 expression predicts poor prognosis and may participate in the SNHG16/miR‐10b‐5p/EIF5A2 regulatory axis in head and neck squamous cell carcinoma

Wang

Jin

et al. 2022

Clinical Laboratory Analysis

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Background: This study attempted to investigate the significance of eukaryotic initiation factor 5A2 (EIF5A2) in the prognosis and regulatory network of head and neck squamous cell carcinoma (HNSCC).Methods: EIF5A2 expression, prognostic information, and methylation levels of HNSCC were collected from the Cancer Genome Atlas (TCGA) database. Quantitative real-time reverse transcription-polymerase chain reaction (qRT-PCR) and Western blot analyses were performed to determine EIF5A2 levels in HNSCC and normal tissue samples. R software was employed for expression analysis and prognosis assessment of EIF5A2 in HNSCC. A competing endogenous RNA (ceRNA) network was generated with the starBase database. Gene set enrichment analysis (GSEA) was used to determine the enriched physiological functions and network related to high expression of EIF5A2 in HNSCC. Immune infiltration-related outcomes were acquired from the CIBERSORT and Tumor Immune Estimation Resource (TIMER) database.Results: EIF5A2 overexpression was observed in HNSCC and linked to poor progression-free survival and overall survival time. Cox regression analyses showed that EIF5A2 level was a stand-alone indicator of HNSCC patients' prognosis. A ceRNA network analysis highlighted the SNHG16/miR-10b-5p/EIF5A2 axis in EIF5A2 regulation. The GSEA results indicated that EIF5A2 was involved in complex signaling pathways. The CIBERSORT and TIMER databases revealed significant associations between EIF5A2 expression and immune cell infiltration. Conclusion:EIF5A2 overexpression may be a risk factor for prognosis in HNSCC and may be regulated by the SNHG16/miR-10b-5p/EIF5A2 axis.

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Increased expression of long non-coding RNA SNHG16 correlates with tumor progression and poor prognosis in non-small cell lung cancer

Cited by 62 publications

References 29 publications

LncRNA DGCR5 regulates the non‐small cell lung cancer cell growth, migration, and invasion through regulating miR‐211‐5p/EPHB6 axis

LncRNA DGCR5 regulates the non‐small cell lung cancer cell growth, migration, and invasion through regulating miR‐211‐5p/EPHB6 axis

LncRNA SNHG16 promotes non‐small cell lung cancer development through regulating EphA2 expression by sponging miR‐520a‐3p

High eukaryotic initiation factor 5A2 expression predicts poor prognosis and may participate in the SNHG16/miR‐10b‐5p/EIF5A2 regulatory axis in head and neck squamous cell carcinoma

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