Prognostic value of long non-coding RNAs in triple negative breast cancer

Zhang, Shuo; Ma, Fei-Xia; Xie, Xiaohong; Shen, Yong

doi:10.1097/md.0000000000021861

Cited by 14 publications

(19 citation statements)

References 45 publications

Supporting

Mentioning

Contrasting

Order By: Relevance

“…Nuclear enriched abundant transcript 1 (NEAT1) often reported as an oncogenic lncRNA, has been described to translocate from the nucleus to the cytoplasm to inflammasome assembly, thereby activating caspase 1 inducing inflammatory cytokine release [ 25 ]. LncRNA metastasis associated lung adenocarcinoma transcript 1 (MALAT1) has been described in several cancer types including breast [ 46 ], pancreatic [ 47 ], and lung adenocarcinoma [ 48 ], and has additionally been associated with inflammation responses and cytokine secretion, especially IL-6, promoting tissue damage [ 49 ]. Further research into the precise roles plays by different lncRNAs and how their expression affects the onset and severity of COVID-19 is needed to further clarify the precise roles played, which requires larger datasets and functional studies.…”

Section: Discussionmentioning

confidence: 99%

Identification of PBMC-based molecular signature associational with COVID-19 disease severity

Shaath¹,

Alajez²

2021

Heliyon

View full text Add to dashboard Cite

The longevity of COVID-19 as a global pandemic, and the devastating effects it has had on certain subsets of individuals thus far has highlighted the importance of identifying blood-based biomarkers associated with disease severity. We employed computational and transcriptome analyses of publicly available datasets from PBMCs from 126 patients with COVID-19 admitted to ICU (n=50), COVID-19 not admitted to ICU (n=50), non-COVID-19 admitted to ICU (n=16) and non-COVID-19 not admitted to ICU (n=10), and utilized the Gencode V33 assembly to analyze protein coding mRNA and long noncoding RNA (lncRNA) transcriptomes in the context of disease severity. Our data identified several aberrantly expressed mRNA and lncRNA based biomarkers associated with SARS-CoV-2 severity, which in turn significantly affected canonical, upstream, and disease functions in each group of patients. Immune, interferon, and antiviral responses were severely suppressed in COVID-19 admitted to ICU versus COVID-19 who were not admitted to ICU. Our data suggests a possible therapeutic approach for severe COVID-19 through administration of interferon therapy. Delving further into these biomarkers, roles and their implications on the onset and disease severity of COVID-19 could play a crucial role in patient stratification and identifying varied therapeutic options with diverse clinical implications.

show abstract

Section: Discussionmentioning

confidence: 99%

Identification of PBMC-based molecular signature associational with COVID-19 disease severity

Shaath¹,

Alajez²

2021

Heliyon

View full text Add to dashboard Cite

show abstract

“…SNHG12 exerts a carcinogenic effect in a variety of cancers [12][13][14][15][16][17][18][19][20][30][31][32]. In clear cell RCC, SNHG12, as a competitive endogenous RNA, competes with miR-30a-5p to bind downstream oncogenes RUNX2, IGF-1R and WNT2 to promote tumor cell invasiveness [33].…”

Section: Discussionmentioning

confidence: 99%

“…Some lncRNAs can encode small nucleolar RNA and are called small nucleolar RNA host genes (SNHGs). Of them, SNHG12 has been reported to be up-regulated in human endometrial cancer [12], bladder cancer [13], nasopharyngeal cancer [14], colorectal cancer [15], lung adenocarcinoma [16], breast cancer [17], liver cancer [18], and clear cell RCC [19], and plays an important role in proliferation and migration of cancer cells. The methylation of lncRNAs promoter can regulate expression of lncRNA, which is related to the occurrence of many diseases.…”

Section: Introductionmentioning

confidence: 99%

SNHG12 Regulated by KMT2B Participates in the Pathogenesis of Renal Cell Carcinoma via E2F1/CEP55

Feng

Wang

Xie

et al. 2022

Preprint

View full text Add to dashboard Cite

Objective: This study is to investigate the regulation of long non-coding RNA (lncRNA) SNHG12 promoter methylation modification by KMT2B and the mechanism of SNHG12 in the development of renal cell carcinoma (RCC) involving E2F1/CEP55 axis.Methods: TCGA and GEO databases were used to predict the involvement of SNHG12 in RCC. Knockdown of SNHG12/E2F1/CEP55 was performed. Next, SNHG12 expression and other mRNAs were analyzed by RT-qPCR. Subsequently, CCK-8 was used to detect cell proliferation. Wound healing test and Transwell assay was used to detect cell migration and invasion, respectively. The vascularization of HUVEC was explored by in vitro pseudotubule formation. CHIP was used to detect H3K4me3 in SNHG12 promoter region. The binding of E2F1 and CEP55 promoter region was analyzed with CHIP and dual luciferase reporter assay. RIP was used to detect the binding of SNHG12 and E2F1. Finally, the effect of SNHG12 on the tumor formation and angiogenesis of RCC was assessed in nude mouse xenograft model.Results: Bioinformatics analysis showed that SNHG12 was highly expressed in RCC tissues and cells, and it was related to the poor prognosis of RCC patients. SNHG12 knockdown significantly inhibited RCC cell proliferation, migration, and invasion and HUVEC angiogenesis. KMT2B up-regulated SNHG12 through modifying H3K4me3 in its promoter region. In addition, SNHG12 promoted CEP55 expression by recruiting the transcription factor E2F1. Knockdown of SNHG12 blocked E2F1 recruitment, thereby down-regulating the expression of CEP55, and inhibited tumor formation and angiogenesis of RCC cells in nude mice.Conclusion: KMT2B up-regulates SNHG12 via the modification of H3K4me3 in its promoter region. SNHG12 recruits E2F1 to promote the expression of CEP55, and ultimately promotes RCC cell proliferation, migration, and invasion and HUVEC angiogenesis.

show abstract

“…Some lncRNAs can encode small nucleolar RNA and are called small nucleolar RNA host genes (SNHGs). Of them, SNHG12 has been reported to be up-regulated in human endometrial cancer [ 12 ], bladder cancer [ 13 ], nasopharyngeal cancer [ 14 ], colorectal cancer [ 15 ], lung adenocarcinoma [ 16 ], breast cancer [ 17 ], liver cancer [ 18 ], and clear cell RCC [ 19 ], and plays an important role in the proliferation and migration of cancer cells. SNHG12 expression is upregulated in RCC tumor tissues while its knockdown markedly inhibits RCC cell viability and invasion, while increasing apoptosis [ 20 ].…”

Section: Introductionmentioning

confidence: 99%

KMT2B promotes the growth of renal cell carcinoma via upregulation of SNHG12 expression and promotion of CEP55 transcription

et al. 2022

View full text Add to dashboard Cite

Background This study aims to clarify the mechanistic action of long non-coding RNA (lncRNA) SNHG12 in the development of renal cell carcinoma (RCC), which may be associated with promoter methylation modification by KMT2B and the regulation of the E2F1/CEP55 axis. Methods TCGA and GEO databases were used to predict the involvement of SNHG12 in RCC. Knockdown of SNHG12/E2F1/CEP55 was performed. Next, SNHG12 expression and other mRNAs were quantified by RT-qPCR. Subsequently, CCK-8 was used to detect cell proliferation. Wound healing assay and Transwell assay were used to detect cell migration and invasion, respectively. The in vitro angiogenesis of human umbilical vein endothelial cells (HUVECs) was explored by matrigel-based capillary-like tube formation assay. ChIP assay was used to detect H3K4me3 in SNHG12 promoter region. The binding of E2F1 to CEP55 promoter region was analyzed with ChIP and dual luciferase reporter assays. RIP assay was used to detect the binding of SNHG12 to E2F1. Finally, the effect of SNHG12 on the tumor formation and angiogenesis of RCC was assessed in nude mouse xenograft model. Results SNHG12 was highly expressed in RCC tissues and cells, and it was related to the poor prognosis of RCC patients. SNHG12 knockdown significantly inhibited RCC cell proliferation, migration, and invasion and HUVEC angiogenesis. KMT2B up-regulated SNHG12 expression through modifying H3K4me3 in its promoter region. In addition, SNHG12 promoted CEP55 expression by recruiting the transcription factor E2F1. Knockdown of SNHG12 blocked E2F1 recruitment and down-regulated the expression of CEP55, thereby inhibiting tumor formation and angiogenesis in nude mice. Conclusion The evidence provided by our study highlighted the involvement of KMT2B in up-regulation of lncRNA as well as the transcription of CEP55, resulting in the promotion of angiogenesis and growth of RCC.

show abstract

Prognostic value of long non-coding RNAs in triple negative breast cancer

Cited by 14 publications

References 45 publications

Identification of PBMC-based molecular signature associational with COVID-19 disease severity

Identification of PBMC-based molecular signature associational with COVID-19 disease severity

SNHG12 Regulated by KMT2B Participates in the Pathogenesis of Renal Cell Carcinoma via E2F1/CEP55

KMT2B promotes the growth of renal cell carcinoma via upregulation of SNHG12 expression and promotion of CEP55 transcription

Contact Info

Product

Resources

About