LncRNA <i>SNHG1</i> enhances cell proliferation, migration, and invasion in cervical cancer

Liu, Yang; Yang, Yanling; Li, Lei; Liu, Yuan; Geng, Peng; Li, Guilin; Song, Hongjuan

doi:10.1139/bcb-2017-0188

Cited by 128 publications

(104 citation statements)

References 24 publications

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“…For example, the expression of lnc-MEG3 gradually decreased whereas the expression of lnc-HOTAIR gradually increased in invasive pituitary adenomas, indicating that lnc-MEG3 and lnc-HOTAIR are potential diagnostic markers of invasive non-functioning pituitary adenoma [21]. Recently, Liu et al reported that up-regulation of lnc-SNHG1 enhances cell proliferation, migration, and invasion in cervical cancer [22]. Further, Sun et al reported that lnc-SNHG1 promotes tumorigenesis and cancer progression by regulating transcription of both proximal and distal genes in multiple types of cancer [23].…”

Section: Discussionmentioning

confidence: 99%

Lnc-SNHG1 Activates the TGFBR2/SMAD3 and RAB11A/Wnt/β-Catenin Pathway by Sponging MiR-302/372/373/520 in Invasive Pituitary Tumors

Wang¹,

Wang²,

Gao³

et al. 2018

Cell Physiol Biochem

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Background/Aims: Long noncoding RNAs (lncRNAs) are critical regulators in various diseases including human cancer and could function as competing endogenous RNAs (ceRNAs) to regulate microRNAs (miRNAs). Methods: Quantitative real-time PCR (qRT-PCR) was used to analyze the expression of lnc-SNHG1 and miR-302/372/373/520 in pituitary tumor tissues and cell lines. Cell proliferation was investigated using MTT and cell count assays. The mechanisms by which lnc-SNHG1 affects pituitary tumor progression were investigated using Western blot assays, transwell migration assays, immunohistochemistry, immunofluorescence, luciferase reporter assays, tumor xenografts, and flow cytometry Results: We found that lnc-SNHG1 was overexpressed in invasive pituitary tumor tissues and cell lines. Ectopic expression of lnc-SNHG1 promoted cell proliferation, migration, and invasion, as well as the epithelial-mesenchymal transition (EMT), by affecting the cell cycle and cell apoptosis in vitro and tumor growth in vivo. Further study indicated that overexpression of lnc-SNHG1 markedly inhibited the expression of miR-302/372/373/520 (miRNA-pool) which is down-regulated in invasive pituitary tumor cells. Moreover, overexpression of lnc-SNHG1 significantly promoted the expression of TGFBR2 and RAB11A, the direct targets of miR-302/372/373/520. Finally, lnc-SNHG1 activates the TGFBR2/SMAD3 and RAB11A/Wnt/β-catenin pathways in pituitary tumor cells via sponging miR-302/372/373/520. Conclusions: Our data suggest that lnc-SNHG1 promotes the progression of pituitary tumors and is a potential therapeutic target for invasive pituitary tumor.

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Section: Discussionmentioning

confidence: 99%

Lnc-SNHG1 Activates the TGFBR2/SMAD3 and RAB11A/Wnt/β-Catenin Pathway by Sponging MiR-302/372/373/520 in Invasive Pituitary Tumors

Wang¹,

Wang²,

Gao³

et al. 2018

Cell Physiol Biochem

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“…Studies from Zhang et al, suggested that lncRNA, myosin heavy chain associated RNA transcripts (MHRT) is a protective factor for cardiomyocytes and the plasma concentration of MHRT may serve as a biomarker for myocardial infarction diagnosis in acute myocardial infarction [13]. The lncRNA, small nucleolar RNA host gene 1 (SNHG1) is a newly-identified lncRNA and has been found to modulate cancer progression in various types of cancers via different molecular mechanisms, and in vitro studies revealed that SNGH1 increased cell viability and inhibited cell apoptosis in the cancer cells [14][15][16][17]. However, whether SNHG1 involves in the cellular behaviors of cardiomyocytes is unknown.…”

Section: Introductionmentioning

confidence: 99%

The Long Non-Coding RNA SNHG1 Attenuates Cell Apoptosis by Regulating miR-195 and BCL2-Like Protein 2 in Human Cardiomyocytes

Zhang

Meng

Mei

et al. 2018

Cell Physiol Biochem

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Background/Aims: Long non-coding RNAs (lncRNAs) are theorized to play key roles in the development of heart diseases. However, the role of lncRNAs in cardiomyocyte apoptosis is largely unknown. The present study examined the role of lncRNA SNHG1 in the human cardiomyocytes (HCMs) apoptosis and explored the underlying molecular mechanisms. Methods: SNHG1, miR-195 and mRNA expression was detected by qRT-PCR; protein level was determined by western blot; cell viability was detected by MTT assay; cell apoptosis was evaluated by flow cytometry and caspase-3 activity assay; the interaction between SNHG1 and miR195 was examined by using luciferase reporter assay. Results: Hydrogen peroxide (H₂O₂) treatment significantly suppressed cell viability and increased cell apoptotic rate and caspase-3 activity in HCMs. Overexpression of SNHG1 attenuated the effects of H₂O₂ on HCMs viability and apoptosis; while SNHG1 exerted the opposite effects. SNHG1 was found to sponge miR-195 and suppress the expression of miR-195 in HCMs. Overexpression of miR-195 suppressed cell viability and induced apoptosis in HCMs, and miR-195 was found to negatively regulate the expression of BCL-2 like protein 2 (BCL2L2) via targeting its 3’ untranslated region. Overexpression of BCL2L2 partially reversed the effects of miR-195 overexpression on cell viability and cell apoptosis of HCMs. MiR-195 overexpression or BCL2L2 knockdown attenuated the effects of SNHG1 overexpression on cell viability, cell apoptosis and protein levels of cleaved caspase-3, cleaved caspase-9 and Bax in H₂O₂-treated HCMs. Conclusion: Our results suggest a novel SNHG1/miR-195/BCL2L2 axis in the regulation of cardiomyocyte apoptosis. Modulation of SNHG1 may represent a novel strategy to treat cardiomyocyte apoptosis-related heart diseases.

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“…Some related studies on SNHG1 in other cancers have been reported. Liu et al demonstrated that SNHG1 could promote cell growth, migration and invasion in cervical cancer [41]. These results indicate that SNHG1 may mainly act as a stimulator of invasion and migration for tumor cells, which needs more studies for further confirmation.…”

Section: Hepg2 Huh7mentioning

confidence: 96%

Long non-coding RNA SNHG1 promotes cell proliferation and invasion of hepatocellular carcinoma by acting as a molecular sponge to modulate miR-195

Zhang¹,

Song²

2020

aoms

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Introduction: Although long non-coding RNA SNHG1 (lncRNA SNHG1) action on cell proliferation and invasion of hepatocellular carcinoma (HCC) cells has been reported, the effects of lncRNA SNHG1 on migration of HCC cells and the mechanisms are still unclear. The present study aimed to investigate the influence of lncRNA SNHG1 on metastasis in HCC cells and the possible mechanisms underlying this phenotype. Material and methods: Expression of lncRNA SNHG1 and miR-195 was determined using qRT-PCR in both HCC cell lines Huh7 and HepG2. Si-RNA was used to silence SNHG1 and miR-195 inhibitor was used to inhibit expression of miR-195. Luciferase reporter assay was conducted to confirm whether miR-195 was the direct binding target of SNHG1. Results: lncRNA SNHG1 was significantly up-regulated and miR-195 was significantly down-regulated in HCC cell lines. When transfected with si-SN-HG1, migration and invasion of HCC cells, as well as expression of astrocyte elevated gene 1 (AEG-1) protein, were significantly inhibited compared with the control cells. Results of dual luciferase reporter assay showed that lncRNA SNHG1 acted as an endogenous sponge of miR-195. On the other hand, the expression of miR-195 in tumor tissue was much lower than that of miR-195 in the corresponding normal tissue. Furthermore, the correlation analysis showed a strong negative relationship between lncRNA SNHG1 and miR-195 expression in HCC tissues. Conclusions: SNHG1 may promote cell invasion and migration in HCC cells by sponging miR-195. These results can provide deeper understanding of SNHG1 in hepatocellular cancer and give new potential targets for treatment of HCC.

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LncRNA SNHG1 enhances cell proliferation, migration, and invasion in cervical cancer

Abstract: LncRNA SNHG1 promotes the development of cervical cancer cells.

Cited by 128 publications

References 24 publications

Lnc-SNHG1 Activates the TGFBR2/SMAD3 and RAB11A/Wnt/β-Catenin Pathway by Sponging MiR-302/372/373/520 in Invasive Pituitary Tumors

Lnc-SNHG1 Activates the TGFBR2/SMAD3 and RAB11A/Wnt/β-Catenin Pathway by Sponging MiR-302/372/373/520 in Invasive Pituitary Tumors

The Long Non-Coding RNA SNHG1 Attenuates Cell Apoptosis by Regulating miR-195 and BCL2-Like Protein 2 in Human Cardiomyocytes

Long non-coding RNA SNHG1 promotes cell proliferation and invasion of hepatocellular carcinoma by acting as a molecular sponge to modulate miR-195

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