SNHG5 Promotes Breast Cancer Proliferation by Sponging the miR-154-5p/PCNA Axis

Chi, Jiangrui; Yu, Zuwei; Liu, Bowen; Zhang, Di; Ge, Jie; Yu, Yue; Cao, Xuchen

doi:10.1016/j.omtn.2019.05.013

Cited by 67 publications

(45 citation statements)

References 44 publications

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“…And upregulation of lncRNA SNHG5 promoted cell proliferation, invasion, and migration in OSCC. Consistent with our results, SNHG5 was also upregulated in breast cancer and glioma (22,23). Functionally, SNHG5 was found to promote the survival of colorectal cancer cells (24).…”

Section: Discussionsupporting

confidence: 91%

lncRNA SNHG5 promotes cell proliferation, migration and invasion in oral squamous cell carcinoma by sponging miR‑655‑3p/FZD4 axis

Huo

Shao

et al. 2020

Oncol Lett

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Recently, previous studies have shown that long non-coding RNA (lncRNA) can act as a tumor promoter or inhibitor in the pathogenesis of oral squamous cell carcinoma (OSCC). However, the regulatory mechanism of lncRNA SNHG5 is unknown in OSCC. Therefore, the functional mechanism of lncRNA SNHG5 in OSCC was initially revealed in this study. Here, RT-qPCR and western blot analysis were used to assess mRNA and protein expression. The functional mechanism of SNHG5 was investigated by MTT, Transwell and luciferase reporter assays. The results showed that SNHG5 expression was upregulated in OSCC and promoted the viability, migration and invasion of OSCC cells. In addition, SNHG5 is the sponge of miR-655-3p in OSCC. And miR-655-3p was found to play an inhibitory effect in OSCC by interacting with SNHG5. Moreover, miR-655-3p directly targets FZD4 and negatively regulates its expression in OSCC. Functionally, FZD4 promoted the progression of OSCC by interacting with the SNHG5/miR-655-3p axis. In conclusion, lncRNA SNHG5 promotes cell proliferation, migration and invasion in OSCC by regulating miR-655-3p/FZD4 axis.

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Section: Discussionsupporting

confidence: 91%

lncRNA SNHG5 promotes cell proliferation, migration and invasion in oral squamous cell carcinoma by sponging miR‑655‑3p/FZD4 axis

Huo

Shao

et al. 2020

Oncol Lett

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“…In SNHG5, overexpression increases the ability of breast cancer cells to proliferate and go through cell cycle, by releasing PCNA (proliferating cell nuclear antigen) from the inhibition of miR-154-5p (83).…”

Section: Small Nucleolar Rna Host Gene 5 (Snhg5)mentioning

confidence: 99%

An Emerging Class of Long Non-coding RNA With Oncogenic Role Arises From the snoRNA Host Genes

et al. 2020

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The small nucleolar RNA host genes (SNHGs) are a group of long non-coding RNAs, which are reported in many studies as being overexpressed in various cancers. With very few exceptions, the SNHGs (SNHG1, SNHG3, SNHG5, SNHG6, SNHG7, SNHG12, SNHG15, SNHG16, SNHG20) are recognized as inducing increased proliferation, cell cycle progression, invasion, and metastasis of cancer cells, which makes this class of transcripts a viable biomarker for cancer development and aggressiveness. Through our literature research, we also found that silencing of SNHGs through small interfering RNAs or short hairpin RNAs is very effective in both in vitro and in vivo experiments by lowering the aggressiveness of solid cancers. The knockdown of SNHG as a new cancer therapeutic option should be investigated more in the future.

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“…into the nucleus through interacting with MTA [36]. On the other hand, SNHG5 was shown to have a cancer-promoting effect, as knockdown of SNHG5 inhibited the proliferation and apoptosis of breast cancer or colorectal cancer cell lines [35,37]. At the same time, SNHG5 was con rmed to play a pro-cancer role in hepatocellular carcinoma by upregulating GSK3β, activating the Wnt/β-catenin pathway and promoting EMT [38].…”

Section: Introductionmentioning

confidence: 99%

si-SNHG5-FOXF2 inhibits TGF-β1-induced fibrosis in human primary endometrial stromal cells by the Wnt/β-catenin signalling pathway

Liu

Chen

et al. 2020

Preprint

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Background: Intrauterine adhesions (IUAs) are manifestations of endometrial fibrosis characterized by inflammation and fibrinogen aggregation in the extracellular matrix (ECM). The available therapeutic interventions for IUA are insufficiently effective in the clinical setting for postoperative adhesion recurrence and infertility problems. In this study, we investigated whether si-SNHG5-FOXF2 can serve as a molecular mechanism for the inhibition of IUA fibrosis ex vivo.Methods: FOXF2, TGF-β1 and collagen expression levels were measured by microarray sequencing analysis in three normal endometrium groups and six IUA patients. We induced primary human endometrial stromal cells (HESCs) into myofibroblasts (MFs) to develop an IUA cell model with various concentrations of TGF-β1 at various times. Downstream target genes of FOXF2 were screened by chromatin immunoprecipitation combined with whole-genome high-throughput sequencing (ChIP-seq). We investigated ECM formation, cell proliferation and Wnt/β-catenin signalling pathway-related proteins in primary HESCs with FOXF2 downregulation by quantitative reverse transcription-polymerase chain reaction (qRT-PCR), western blotting (WB), immunohistochemistry (IHC), flow cytometry, ethylenediurea (EdU) and CCK8 assays. We identified lncRNA SNHG5 as the upstream regulatory gene of FOXF2 through RNA immunoprecipitation (RIP), RNA pulldown and fluorescence in situ hybridization (FISH). Finally, we examined FOXF2 expression, ECM formation, cell proliferation and Wnt/β-catenin signalling pathway-related proteins in primary HESCs upon FOXF2 downregulation.Results: FOXF2 was highly expressed in the endometrium of patients with IUA. Treatment of primary HESCs with 10 ng/ml TGF-β1 for 72 h was found to be most effective for developing an IUA cell model. FOXF2 regulated multiple downstream target genes, including collagen, vimentin (VIM) and cyclin D2/DK4, by ChIP-seq and ChIP-PCR. FOXF2 downregulation inhibited TGF-β1-mediated primary HESC fibrosis, including ECM formation, cell proliferation and Wnt/β-catenin signalling pathway-related protein expression. We identified lncRNA SNHG5 as an upstream gene that directly regulates FOXF2 by RIP-seq, qRT-PCR, WB, and FISH. SNHG5 downregulation suppressed FOXF2 expression in the IUA cell model, resulting in synergistic repression of the Wnt/β-catenin pathway, thereby altering TGF-β1-mediated ECM aggregation in endometrial stromal cells ex vivo. Conclusions: Regulation of the Wnt/β-catenin signalling pathway and ECM formation by si-SNHG5-FOXF2 effectively inhibited the profibrotic effect of TGF-β1 on primary HESCs. This finding can provide a molecular basis for antagonizing TGF-β1-mediated fibrosis in primary HESCs.

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SNHG5 Promotes Breast Cancer Proliferation by Sponging the miR-154-5p/PCNA Axis

Cited by 67 publications

References 44 publications

lncRNA SNHG5 promotes cell proliferation, migration and invasion in oral squamous cell carcinoma by sponging miR‑655‑3p/FZD4 axis

lncRNA SNHG5 promotes cell proliferation, migration and invasion in oral squamous cell carcinoma by sponging miR‑655‑3p/FZD4 axis

An Emerging Class of Long Non-coding RNA With Oncogenic Role Arises From the snoRNA Host Genes

si-SNHG5-FOXF2 inhibits TGF-β1-induced fibrosis in human primary endometrial stromal cells by the Wnt/β-catenin signalling pathway

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