LncRNA SNHG7 sponges miR-449a to promote pituitary adenomas progression

Yue, Xiongfei; Dong, Ce; Ye, Zhanying; Zhu, Lin; Zhang, Xiaoyang; Wang, Xiaoyan; Mo, Feng; Zheng, Lirong; Pan, Baogen

doi:10.1007/s11011-020-00611-5

Cited by 13 publications

(8 citation statements)

References 26 publications

Supporting

Mentioning

Contrasting

Order By: Relevance

“…LncRNA-SNHG7 was significantly downregulated in SCI rats and in vitro SCI models, thus supporting its potential role in the development of SCI. Previous studies demonstrated that lncRNA-SNHG7 directly binds to miR-449a to negatively regulate its expression [ 48 , 49 ]. The complex regulatory network of miRNAs can regulate the expression of multiple genes by a single miRNA, and the function of each miRNA varies among different cells and even among different cell states [ 18 ].…”

Section: Discussionmentioning

confidence: 99%

Long non-coding RNA-small nucleolar RNA host gene 7 regulates inflammatory responses following spinal cord injury by regulating the microRNA-449a/TNF-α-induced protein 3-interacting protein 2 axis

Xiao

et al. 2022

Bioengineered

View full text Add to dashboard Cite

The current study aimed to explore the anti-inflammatory effects of long non-coding RNA-small nucleolar RNA host gene 7 (lncRNA-SNHG7) and its mechanism in spinal cord injury (SCI) models. SCI models were established both in vivo and in vitro . Reverse transcription-quantitative PCR was performed to determine the expression levels of lncRNA-SNHG7 in SCI models. Bioinformatics analysis and dual-luciferase reporter assays were carried out to confirm the interaction between lncRNA-SNHG7 with microRNA (miR)-499a and TNF-α-induced protein 3-interacting protein 2 (TNIP2). In addition, cell viability, apoptosis, and the secretion of inflammatory cytokines were assessed by 3-(4,5-dimethyl-2-thiazolyl)-2,5-diphenyl-2-H-tetrazolium bromide (MTT) assay, flow cytometric analysis, and enzyme linked immunosorbent assay (ELISA), respectively. The results showed that lncRNA-SNHG7 was markedly downregulated in the SCI model group. LncRNA-SNHG7 directly bound to miR-499a, which in turn directly targeted TNIP2. In addition, TNIP2 was significantly decreased in SCI rats and lipopolysaccharide (LPS)-treated PC-12 cells. The in vitro results in PC-12 cells revealed that lncRNA-SNHG7 overexpression attenuated neuronal cell death and SCI-mediated inflammatory responses by regulating miR-449a expression. Furthermore, miR-499a knockdown inhibited LPS-induced PC-12 cell injury by targeting TNIP2. In conclusion, lncRNA-SNHG7 modulates the apoptosis and inflammation of PC-12 cells by regulating the miR-449a/TNIP2/NF-κB signaling pathway.

show abstract

Section: Discussionmentioning

confidence: 99%

Long non-coding RNA-small nucleolar RNA host gene 7 regulates inflammatory responses following spinal cord injury by regulating the microRNA-449a/TNF-α-induced protein 3-interacting protein 2 axis

Xiao

et al. 2022

Bioengineered

View full text Add to dashboard Cite

show abstract

“…D' Angelo et al (13) demonstrated that expression levels of ribosomal protein SA pseudogene 52 are significantly higher in pituitary tumor cells than in controls and accelerate pituitary tumor development via regulating high mobility group A. Clarin 1 antisense RNA 1 has also been confirmed to participate in the Wnt/β-actin signaling pathway, inhibit autophagy progress and suppress pathogenesis of pituitary tumors (14). There has been research on differential expression of lncRNAs in PA and the functional mechanisms involved in PA occurrence, development and prognosis (15,16). However, the expression levels, function and regulatory mechanisms of lncRNAs in PA need further investigation.…”

Section: Lncrna Meg3 Inhibits Pituitary Tumor Development By Participmentioning

confidence: 99%

lncRNA MEG3 inhibits pituitary tumor development by participating in cell proliferation, apoptosis and EMT processes

Wang

2021

Oncol Rep

View full text Add to dashboard Cite

Pituitary tumors do not pose a threat to life but can cause visual disturbances and serious clinical syndromes, such as infertility and metabolic syndrome. Therefore, screening of key genes involved in the occurrence and development of pituitary tumors can provide new targets for the treatment of pituitary tumors. The aim of the present study was to investigate the molecular mechanism of long non-coding (lnc.) RNA maternally expressed 3 (MEG3) in cell proliferation, apoptosis and epithelial-mesenchymal transition (EMT) processes of pituitary tumor. Tissue samples were obtained from 34 patients who underwent surgical treatment of pituitary tumors. Pituitary tumor cells (GH3 and MMQ) were transfected with pcDNA3.1(+)-MEG3, short hairpin (sh)MEG3, microRNA (miR)-23-3p inhibitor or their controls using Lipofectamine ® 2000. Reverse transcription-quantitative PCR and western blot analyses were used to detect the levels of MEG3, miR-23b-3p and FOXO4, as well as proliferation-, apoptosis-and EMT-associated genes and proteins. Cell Counting Kit-8 and flow cytometry assays were performed to detect proliferation and apoptosis, and Transwell assay was undertaken to assess invasion and migration. Luciferase reporter and RNA pulldown assays were performed to verify the binding between lncRNA MEG3, miR-23b-3p and FOXO4. Pearson's correlation analysis was used to analyze the correlation between expression levels of MEG3, miR-23b-3p and FOXO4. lncRNA MEG3 was expressed at lower levels in pituitary tumor tissues and cells. Overexpression of lncRNA MEG3 inhibited proliferation, invasion and migration and accelerated apoptosis of pituitary tumor cells. lncRNA MEG3 negatively regulated miR-23b-3p expression levels, while miR-23b-3p negatively regulated FOXO4 expression levels. Overexpression of lncRNA MEG3 inhibited the EMT process in pituitary tumor cells. miR-23-3p inhibitor rescued the effect of shMEG3 on proliferation, invasion, migration, apoptosis and the EMT process in pituitary tumor cells. lncRNA MEG3 inhibited pituitary tumor development by participating in cell proliferation, apoptosis and the EMT process, which may present a novel target for pituitary tumor treatment.

show abstract

“…For example, evidence shows that SNHGs, including SNHG1, SNHG3, SNHG5, SNHG7, and SNHG15, have an oncogenic role in cancer through the versatility of their interactions at the DNA-RNA-protein level. 25 These SNHGs could regulate methylase 26 or interact with transcription factors 27 in the nucleus, sponge miRNA, 28 directly bind to mRNA, 29 or bind to a protein 30 in the cytoplasm. In particular, for SHNG26, a member of SNHGs class, its function is unknown.…”

Section: Introductionmentioning

confidence: 99%

lncRNA SNHG26 promoted the growth, metastasis, and cisplatin resistance of tongue squamous cell carcinoma through PGK1/Akt/mTOR signal pathway

Jiang

Wang

et al. 2022

Molecular Therapy - Oncolytics

View full text Add to dashboard Cite

LncRNA SNHG7 sponges miR-449a to promote pituitary adenomas progression

Cited by 13 publications

References 26 publications

Long non-coding RNA-small nucleolar RNA host gene 7 regulates inflammatory responses following spinal cord injury by regulating the microRNA-449a/TNF-α-induced protein 3-interacting protein 2 axis

Long non-coding RNA-small nucleolar RNA host gene 7 regulates inflammatory responses following spinal cord injury by regulating the microRNA-449a/TNF-α-induced protein 3-interacting protein 2 axis

lncRNA MEG3 inhibits pituitary tumor development by participating in cell proliferation, apoptosis and EMT processes

lncRNA SNHG26 promoted the growth, metastasis, and cisplatin resistance of tongue squamous cell carcinoma through PGK1/Akt/mTOR signal pathway

Contact Info

Product

Resources

About