Long non-coding RNA SNHG22 facilitates the malignant phenotypes in triple-negative breast cancer via sponging miR-324-3p and upregulating SUDS3

Fang, Xuan; Zhang, Jin; Li, Chunyan; Liu, Jinjin; Shi, Zhendong; Zhou, Peng

doi:10.1186/s12935-020-01321-9

Cited by 23 publications

(20 citation statements)

References 22 publications

(21 reference statements)

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“… 29 In line with our results, SNHG22 was measured to be highly expressed in triple-negative breast cancer tissues by a prior investigation. 20 These findings indirectly supported our results of SNHG22 overexpression in GC tissues. Moreover, our data suggested that SNHG22 silencing restrained cell proliferation, migration, invasion, and angiogenesis but facilitated cell apoptosis and cell cycle arrest in GC.…”

Section: Discussionsupporting

confidence: 87%

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<p>Long Noncoding RNA SNHG22 Induces Cell Migration, Invasion, and Angiogenesis of Gastric Cancer Cells via microRNA-361-3p/HMGA1/Wnt/β-Catenin Axis</p>

Cui¹,

Zhang²,

Chen³

et al. 2020

CMAR

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Background The correlation between long non-coding RNAs (lncRNAs) and gastric cancer (GC) has been indicated. As a newly found lncRNA, small nucleolar RNA host gene 22 (SNHG22) functions as an oncogene in ovarian carcinoma and breast cancer. However, its action has not been explored in GC. Herein, the purpose of the current research was to examine the influence of SNHG22 on GC development. Methods RT-qPCR was used to identify SNHG22 and microRNA-361-3p (miR-361-3p) in GC tissues and cells. Functional assays were implemented to measure changes on biological activities of GC cells under different transfections. Besides, after human umbilical vein endothelial cells (HUVECs) were co-cultured with supernatant of transfected GC cells, angiogenesis was assessed by tube formation assay in vitro. HMGA1 and β-catenin expression were determined. Finally, mechanistic assays, including RNA pull-down assay and dual-luciferase reporter assay, were employed to assess relationships among SNHG22, miR-361-3p, and HMGA1. Results SNHG22 and HMGA1 were highly expressed but miR-361-3p was poorly expressed in GC tissues. Mechanistically, SNHG22 bound to miR-361-3p, and miR-361-3p targeted HMGA1 to disrupt the Wnt/β-catenin pathway. Following SNHG22 or HMGA1 silencing or miR-361-3p upregulation, we observed a decline of proliferation, migration, and invasion of GC cells and HUVEC angiogenesis but acceleration of GC cell apoptosis and cell cycle arrest. Conclusion Collectively, SNHG22 silencing possessed tumor-suppressing potentials in GC development via Wnt/β-catenin pathway by binding to miR-361-3p and downregulating HMGA1, highlighting a new promising road for GC treatment development.

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Section: Discussionsupporting

confidence: 87%

“…SNHG22 has shown cancer-promoting effects in numerous cancers. 11 , 20 , 21 However, little is acknowledged about whether SNHG22 orchestrated GC. Therefore, we tested whether SNHG22 mediated GC development.…”

Section: Resultsmentioning

confidence: 99%

<p>Long Noncoding RNA SNHG22 Induces Cell Migration, Invasion, and Angiogenesis of Gastric Cancer Cells via microRNA-361-3p/HMGA1/Wnt/β-Catenin Axis</p>

Cui¹,

Zhang²,

Chen³

et al. 2020

CMAR

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“…7 Next, Koduru et al 8 proposed that the level of SNHG22 could be served as a biomarker during the malignant transformation of hepatocellular carcinoma. Another, Fang et al 9 documented that SNHG22 regulated triple-negative breast cancer via the miR-324-3p/SUDS3 axis and provided a promising targeted therapy. Recently, SNHG22 acts as a ceRNA to regulate Gal-1 expression by competitively binding to miR-2467 in EOC.…”

Section: Discussionmentioning

confidence: 99%

SP1-Regulated Non-Coding RNA SNHG22 Promotes Ovarian Cancer Growth and Glycolysis

Guan¹,

Zheng²,

Wu³

et al. 2021

CMAR

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Objectives Long non-coding RNAs (lncRNAs) play a crucial part in cancer progression. However, in epithelial ovarian carcinoma (EOC), the role of SNHG22 needs to be further explained. Methods Quantitative real-time PCR was used to detect the expression of SNHG22. EOC cells were stably transfected with lentivirus approach and cell proliferation, glycolysis and cell apoptosis, as well as tumorigenesis in animal were performed to assess the effects of SNHG22 in EOC. Chromatin immunoprecipitation (ChIP) and luciferase reporter assay were conducted to confirm the relationship between SP1 and SNHG22. Results Higher expressed SNHG22 was associated with a poor prognosis in EOC tissues. SNHG22 facilitated glycolysis and proliferation. Mechanistically, LDHA deficiency and glycolysis inhibitor (2-DG, 3-BG) partly rescued proliferation. SP1 mediated SNHG22 expression at the transcriptional level and the SNHG22 promoter region (−900~ −600) was necessary for SP1 binding. Hypoxia and HIF-1α also upregulated SNHG22 expression. Conclusion SNHG22 is an independent prognostic biomarker for EOC. SNHG22 promotes EOC progression and is a prospective therapeutic target.

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“…MiRNAs can elicit biological functions by targeting and repressing their downstream messenger RNAs (mRNAs) 30 . Therefore, we sought to figure out the downstream targets of miR‐489‐3p.…”

Section: Resultsmentioning

confidence: 99%

Shikonin ameliorates injury and inflammatory response of LPS‐stimulated WI‐38 cells via modulating the miR‐489‐3p/MAP2K1 axis

Wang

Chen²,

Feng

et al. 2021

Environmental Toxicology

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Pneumonia is an inflammatory disease induced by infection with different pathogens. Currently, multiple preclinical studies have revealed that shikonin, a natural naphthoquinone, can mitigate lipopolysaccharide (LPS)‐induced inflammation, but its underlying mechanism in pneumonia remains unknown. This research was designed to explore the function and regulatory mechanism of shikonin in LPS‐induced cell injury and inflammation in WI‐38 cells. In‐vitro model of pneumonia was constructed by treating WI‐38 cells with LPS. Expression of miR‐489‐3p and MAP2K1 was tested by RT‐qPCR and (or) Western blot analysis. Cell viability was examined by 3‐(4,5)‐dimethylthiahiazo (−z‐y1)‐3,5‐di‐phenytetrazoliumromide assay. The productions of pro‐inflammatory cytokines were determined by enzyme‐linked immunosorbent assays. Cell apoptosis was detected by Western blot and flow cytometry analysis. In the current study, LPS induced WI‐38 cell damage by inhibiting cell viability and promoting cell apoptosis and inflammation. Shikonin ameliorated LPS‐induced cell injury and elevated miR‐489‐3p expression. LPS‐induced inflammatory injury was further mitigated by upregulation of miR‐489‐3p. In addition, MAP2K1, the target of miR‐489‐3p, was upregulated by LPS. Furthermore, upregulation of MAP2K1 reversed the influence of shikonin and miR‐489‐3p mimics on LPS‐induced cell injury and inflammation. This study revealed that shikonin protected WI‐38 cells against LPS‐induced cell injury and inflammatory response by regulating the miR‐489‐3p/MAP2K1 axis, thus affecting the progression of pneumonia.

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Long non-coding RNA SNHG22 facilitates the malignant phenotypes in triple-negative breast cancer via sponging miR-324-3p and upregulating SUDS3

Cited by 23 publications

References 22 publications

<p>Long Noncoding RNA SNHG22 Induces Cell Migration, Invasion, and Angiogenesis of Gastric Cancer Cells via microRNA-361-3p/HMGA1/Wnt/β-Catenin Axis</p>

<p>Long Noncoding RNA SNHG22 Induces Cell Migration, Invasion, and Angiogenesis of Gastric Cancer Cells via microRNA-361-3p/HMGA1/Wnt/β-Catenin Axis</p>

SP1-Regulated Non-Coding RNA SNHG22 Promotes Ovarian Cancer Growth and Glycolysis

Shikonin ameliorates injury and inflammatory response of LPS‐stimulated WI‐38 cells via modulating the miR‐489‐3p/MAP2K1 axis

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