Browse
Submit Data
Databases
API
Help

Dataset Information

0 Views

0 Connections

0 Citations

0 Reanalyses

0 Downloads

Omics score: 0

SNHG20 promotes the development of laryngeal squamous cell carcinoma via miR-342-3p/MTDH axis.

ABSTRACT: Long noncoding RNAs (lncRNAs) are important players in laryngeal squamous cell carcinoma (LSCC). However, the function of the long noncoding RNA small nucleolar RNA host gene 20 (SNHG20) in LSCC is hardly known. We therefore analyzed the role of this lncRNA in LSCC. Our data showed that SNHG20 was significantly overexpressed in LSCC cell lines and human LSCC tissue. SNHG20 significantly promoted cell proliferation, migration and invasion of LSCC cells. The actions of SNHG20 are likely mediated by miR-342-3p expression, which results in increased expression of MTDH. Finally, the results of in vivo models confirmed that SNHG20 promotes LSCC progression through modulating miR-342-3p and MTDH expression. Taken together, our study demonstrates that SNHG20/miR-342-3p/MTDH axis participates in LSCC progression.

SUBMITTER: Xie Z

PROVIDER: S-EPMC9399968 | biostudies-literature | 2022 Aug

REPOSITORIES: biostudies-literature

ACCESS DATA

Json Xml

Publications

SNHG20 promotes the development of laryngeal squamous cell carcinoma via miR-342-3p/MTDH axis.

Xie Zuozhong Z Xiang Hong H Li Jingkun J Zhang Xiaowei X Li Wei W Tan Guolin G

Heliyon 20220811 8

Long noncoding RNAs (lncRNAs) are important players in laryngeal squamous cell carcinoma (LSCC). However, the function of the long noncoding RNA small nucleolar RNA host gene 20 (SNHG20) in LSCC is hardly known. We therefore analyzed the role of this lncRNA in LSCC. Our data showed that SNHG20 was significantly overexpressed in LSCC cell lines and human LSCC tissue. SNHG20 significantly promoted cell proliferation, migration and invasion of LSCC cells. The actions of SNHG20 are likely mediated b ...[more]

PMID: 36033309

Similar Datasets

Long non-coding RNA SNHG20 promotes the tumorigenesis of oral squamous cell carcinoma via targeting miR-197/LIN28 axis.

Project description:Long non-coding RNA (lncRNA) has been verified to participate in the tumour regulation, including oral squamous cell carcinoma (OSCC). Nevertheless, the role of lncRNA SNHG20 on OSCC still remains elusive. Here, we investigate the physiopathologic functions of lncRNA SNHG20 in OSCC tumorigenesis and explore its potential mechanism. LncRNA SNHG20 was up-regulated in OSCC tissue compared with adjacent non-tumour tissue. Meanwhile, SNHG20 was overexpressed in cancer stem-like cells. In vitro and in vivo, loss-of-function experiments showed that lncRNA SNHG20 knockdown inhibited proliferative ability, mammosphere-forming ability, ALDH1 expression, stem factors (LIN28, Nanog, Oct4, SOX2) and tumour growth. Bioinformatics and luciferase reporter assay revealed that miR-197 targeted the 3'-untranslated regions of SNHG20 and LIN28 by complementary binding. Validation experiments confirmed the associated functions of SNHG20/miR-197/LIN28 axis on OSCC proliferation and stemness. In summary, our results reveal the important function of SNHG20/miR-197/LIN28 axis in the oncogenesis and stemness of OSCC, suggesting the vital role of SNHG20 in OSCC tumorigenesis.

| S-EPMC6307847 | biostudies-literature

NFIB-Mediated lncRNA PVT1 Aggravates Laryngeal Squamous Cell Carcinoma Progression via the miR-1301-3p/MBNL1 Axis.

Project description:Laryngeal squamous cell carcinoma (LSCC) is one of the most common malignant tumors of head and neck cancers. In the past decades, although the therapy strategies of LSCC have made considerable improvement, the terrible outcomes of LSCC still bring an enormous burden to the world health care system. Novel therapeutic targets for LSCC are urgently needed. lncRNAs exert important roles in various biological progressions, including LSCC. Here, we aimed to investigate the function of lncRNA PVT1 in LSCC progression and its underlying molecular mechanisms. By conducting multiple experiments, our results showed that lncRNA PVT1 was upregulated in LSCC cell lines and regulated LSCC cell proliferation, apoptosis, and its cell susceptibility to natural killer (NK) cells. Moreover, it was found that lncRNA PVT1 promotes MBNL1 expression to regulate LSCC cellular progression through sponging miR-1301-3p. Our study might provide novel targets for LSCC basic research or clinical management.

| S-EPMC8604577 | biostudies-literature

Circ_0006220 Contributes to NSCLC Progression through miR-342-3p/GOT2 Axis.

Project description:PurposeDysregulated circular RNAs (circRNAs) have shown crucial modulatory functions in tumorigenesis, containing non-small cell lung cancer (NSCLC). The purpose of this study was to explore the biological functions and regulatory theory of circ_0006220 in NSCLC.MethodsReverse transcription-quantitative polymerase chain reaction and Western blot assay were conducted to measure RNA and protein expression, respectively. A total of 73 cases of NSCLC tumor samples were collected for expression analysis, and A-549 and NCI-H1299 cell lines were used for functional experiments. Cell proliferation was assessed by cell counting kit-8 assay, colony formation assay, 5-ethynyl-2'-deoxyuridine assay, and flow cytometry. Cell apoptosis, motility, and angiogenesis ability were analyzed by flow cytometry, transwell assays, and capillary-like network formation assay. Dual-luciferase reporter assay and RNA immunoprecipitation assay were conducted to verify the target relationships.ResultsCirc_0006220 was highly expressed in NSCLC tissues and cell lines. Circ_0006220 silencing inhibited the proliferation, migration, invasion, and angiogenesis but induced the apoptosis of NSCLC cells. Circ_0006220 acted as a microRNA-342-3p (miR-342-3p) sponge, and circ_0006220 knockdown-induced changes on the phenotypes of NSCLC cells were largely overturned by the knockdown of miR-342-3p. miR-342-3p interacted with the 3' untranslated region of glutamic-oxaloacetic transaminase 2 (GOT2), and GOT2 overexpression largely diminished miR-342-3p overexpression-mediated influences in NSCLC cells. Circ_0006220 could up-regulate GOT2 expression by sponging miR-342-3p.ConclusionCirc_0006220 promoted the malignant behaviors of NSCLC cells through mediating the miR-342-3p/GOT2 regulation cascade.

| S-EPMC9939679 | biostudies-literature

A novel circular RNA circPPFIA1 promotes laryngeal squamous cell carcinoma progression through sponging miR-340-3p and regulating ELK1 expression.

Project description:Abnormal expression of circular RNA (circRNA) is closely related to the occurrence and development of many cancers. By screening the expression of circRNA, we identified a novel circRNA termed as has_circ_0023326 in laryngeal squamous cell carcinoma (LSCC). We verified the expression of circPPFIA1 and found that it was upregulated in LSCC tissues compared to the adjacent normal tissues. Functional studies were carried out to detect the effect of circPPFIA1 expression on the phenotype of LSCC cells. These results suggest that circPPFIA1 knockdown can suppress the proliferation, migration, and invasion of LSCC cells, while circPPFIA1 overexpression can promote these processes. Mechanistically, miR-340-3p was predicted to be the target miRNA sponged by circPPFIA1 as confirmed through the luciferase assay and rescue experiments. In addition, miR-340-3p was found to target ELK1 and inhibit its expression. Taken together, circPPFIA1 promotes the progression of LSCC via the miR-340-3p/ELK1 signaling axis, which may serve as a novel prognostic or therapeutic target for LSCC.

| S-EPMC8806628 | biostudies-literature

Antisense lncRNA PCNA-AS1 promotes esophageal squamous cell carcinoma progression through the miR-2467-3p/PCNA axis.

Project description:Multiple studies have indicated that long non-coding RNAs are aberrantly expressed in cancers and are pivotal in developing various tumors. No studies have investigated the expression and function of long non-coding antisense RNA PCNA-AS1 in esophageal squamous cell carcinoma (ESCC). In this study, the expression of PCNA-AS1 was identified by qRT-PCR. Cell function assays were used to explore the potential effect of PCNA-AS1 on ESCC progression. A prediction website was utilized to discover the relationships among PCNA-AS1, miR-2467-3p and proliferating cell nuclear antigen (PCNA). Dual luciferase reporter gene and RNA immunoprecipitation (RIP) assays were executed to verify the binding activity between PCNA-AS1, miR-2467-3p and PCNA. As a result, PCNA-AS1 was highly expressed in ESCC and was associated with patient prognosis. PCNA-AS1 overexpression strongly contributed to ESCC cell proliferation, invasion and migration. PCNA-AS1 and PCNA were positively correlated in ESCC. Bioinformatics analysis, RIP and luciferase reporter gene assays revealed that PCNA-AS1 could act as a competitive endogenous RNA to sponge miR-2467-3p, thus upregulating PCNA. In conclusion, the current outcome demonstrates that PCNA-AS1 may be a star molecule in the treatment of ESCC.

| S-EPMC9490863 | biostudies-literature

LncRNA TTN-AS1 promotes the progression of oral squamous cell carcinoma via miR-411-3p/NFAT5 axis.

Project description:Background:Oral squamous cell carcinoma (OSCC) is a common kind of squamous cell carcinoma of the head and neck, which is a threat to public health. Long noncoding RNAs (lncRNAs) are associated with the development of various diseases, including cancers. LncRNA titin antisense RNA 1 (TTN-AS1) is known as a crucial regulatory factor in several cancers. Nevertheless, the specific functions of TTN-AS1 in OSCC remains obscure. Methods:The expression of TTN-AS1 in OSCC samples or cells was analyzed through qRT-PCR. Colony formation assay, EdU assay, flow cytometry assay, TUNEL assay and wound healing assay were conducted to estimate the functions of TTN-AS1 in OSCC cells. RIP and luciferase reporter assays were utilized to detect the interaction between TTN-AS1 and miR-411-3p as well as between miR-411-3p and NFAT5. Results:TTN-AS1 expression was stronger in OSCC cells. Knockdown of TTN-AS1 effectively restrained cell proliferation and migration but had inductive role in apoptosis. Moreover, TTN-AS1 could function as the miR-411-3p sponge in OSCC and miR-411-3p exerted the inhibitory functions on OSCC cell growth. In addition, NFAT5 was proven as the target of miR-411-3p. Rescue assay indicated that overexpressing NFAT5 could reverse the inhibitory function of TTN-AS1 depletion on cell growth. Conclusion:lncRNA TTN-AS1 contributed to the progression of OSCC via miR-411-3p/NFAT5 axis.

| S-EPMC7453543 | biostudies-literature

Dual-strand tumor-suppressor microRNA-145 (miR-145-5p and miR-145-3p) coordinately targeted MTDH in lung squamous cell carcinoma.

Project description:Patients with lung adenocarcinoma may benefit from recently developed molecular targeted therapies. However, analogous advanced treatments are not available for patients with lung squamous cell carcinoma (lung SCC). The survival rate of patients with the advanced stage of lung SCC remains poor. Exploration of novel lung SCC oncogenic pathways might lead to new treatment protocols for the disease. Based on this concept, we have identified microRNA- (miRNA) mediated oncogenic pathways in lung SCC. It is well known that miR-145-5p (the guide strand) functions as a tumor suppressor in several types of cancer. However, the impact of miR-145-3p (the passenger strand) on cancer cells is still ambiguous. Expression levels of miR-145-5p and miR-145-3p were markedly reduced in cancer tissues, and ectopic expression of these miRNAs inhibited cancer cell aggressiveness, suggesting that both miR-145-3p as well as miR-145-5p acted as antitumor miRNAs. We identified seven putative target genes (MTDH, EPN3, TPD52, CYP27B1, LMAN1, STAT1 and TXNDC12) that were coordinately regulated by miR-145-5p and miR-145-3p in lung SCC. Among the seven genes, we found that metadherin (MTDH) was a direct target of these miRNAs. Kaplan-Meier survival curves showed that high expression of MTDH predicted reduced survival of lung SCC patients. We investigated pathways downstream from MTDH by using genome-wide gene expression analysis. Our data showed that several anti-apoptosis and pro-proliferation genes were involved in pathways downstream from MTDH in lung SCC. Taken together, both strands of miR-145, miR-145-5p and miR-145-3p are functional and play pivotal roles as antitumor miRNAs in lung SCC.

| S-EPMC5342147 | biostudies-literature

LncRNA PCAT6 promotes the occurrence of laryngeal squamous cell carcinoma via modulation of the miR-4731-5p/NOTCH3 axis.

Project description:Laryngeal squamous cell carcinoma (LSCC) is one of the most aggressive cancers that affect the head and neck region. Recent researches have confirmed that long non-coding RNAs (lncRNAs) present an emerging role in diversiform diseases including cancers. Prostate cancer-associated ncRNA transcript 6 (PCAT6) is an oncogene in lung cancer, cervical cancer, colon cancer and gastric cancer, but its role in LSCC is still unknown. In the current study, we attempted to figure out the role of PCAT6 in LSCC. RT-qPCR was to analyze PCAT6 expression in LSCC cells. Functional assays were to uncover the role of PCAT6 in LSCC. Mechanism assays were to explore the regulatory mechanism behind PCAT6 in LSCC. PCAT6 exhibited higher expression in LSCC cells and PCAT6 strengthened cell proliferation and inhibited cell apoptosis. Furthermore, lncRNA PCAT6 modulated notch receptor 3 expression and activated NOTCH signaling pathway via serving as a sponge for miR-4731-5p. Taken together, lncRNA PCAT6 was identified as an oncogene in LSCC, which revealed that PCAT6 might be used as potential therapeutic target for LSCC.

| S-EPMC11262867 | biostudies-literature

MIAT promotes myofibroblastic activities and transformation in oral submucous fibrosis through sponging the miR-342-3p/SOX6 axis.

Project description:Oral submucous fibrosis (OSF) is an oral potentially malignant disorder that is closely related to the habit of areca nut chewing. Long non-coding RNA (lncRNA) myocardial infarction-associated transcript (MIAT) has been identified as an essential regulator in the fibrosis progression. However, the role of MIAT in the development of OSF remains unknown. The transcriptomic profile showed that MIAT is significantly overexpressed in the OSF cohort, with a positive correlation to fibrotic markers. The silencing of MIAT expression in primary buccal mucosal fibroblasts (BMFs) markedly inhibited arecoline-induced myofibroblast transformation. Mechanistically, MIAT functioned as a miR-342-3p sponge and suppressed the inhibitory effect of miR-342-3p on SOX6 mRNA, thereby reinstating SOX6 expression. Subsequent RNA expression rescue experiments confirmed that MIAT enhanced resistance to apoptosis and facilitated myofibroblastic properties such as cell mobility and collagen gel contraction by regulating the miR-342-3p/SOX6 axis. Taken together, these results suggest that the abnormal upregulation of MIAT is important in contributing persistent activation of myofibroblasts in fibrotic tissue, which may result from prolonged exposure to the constituents of areca nut. Furthermore, our findings demonstrated that therapeutic avenues that target the MIAT/miR-342-3p/SOX6 axis may be a promising approach for OSF treatments.

| S-EPMC11501384 | biostudies-literature

miR-144-3p, a tumor suppressive microRNA targeting ETS-1 in laryngeal squamous cell carcinoma.

Project description:Regional lymph node metastasis and distant metastasis are critical in the prognosis of laryngeal squamous cell carcinoma (LSCC). This study investigated the roles of miR-144-3p and E26 transformation specific-1 (ETS-1) in the invasion and migration of LSCC cells. The effects of miR-144-3p and ETS-1 on FaDu and Hep2 cell growth, migration and invasion were determined. Suppression of ETS-1 by miR-144-3p was confirmed using luciferase assays; the effects of ETS-1 silencing were determined using a xenograft tumor model. The expression of ETS-1 was analyzed in 71 paraffin-embedded tissue biopsies and eight fresh frozen biopsies obtained from LSCC patients. miR-144-3p inhibited the growth, invasion and migration of FaDu and Hep2 cells in part through suppression of epithelial-mesenchymal transition as determined by increased E-cadherin and α-catenin and reduced fibronectin and vimentin expression. Additionally, ETS-1 is a molecular target of miR-144-3p, and silencing ETS-1 expression inhibited FaDu and Hep2 cell invasion and migration as well as reduced Hep2 xenograft tumor volume. In LSCC, the expression of ETS-1 is upregulated with disease progression, and higher ETS-1 expression, which was negatively associated with miR-144-3p levels, adversely corresponded with prognoses. Thus, upregulated ETS-1 levels may promote LSCC metastasis, resulting in poor patient prognosis.

| S-EPMC4905499 | biostudies-literature

OmicsDI is part of the ELIXIR infrastructure

OmicsDI is an Elixir interoperability service. Learn more ›

Tweets

OmicsDI Databases

PRIDE
PeptideAtlas
MassIVE
JPOST Repository
Physiome Model Repository

EGA
EVA
ENA
LINCS
PAXDB
Cell Collective

MetaboLights
Metabolomics Workbench
MetabolomeExpress
GNPS
BioModels
FAIRDOMHub

ArrayExpress
dbGaP
ExpressionAtlas
GEO
NODE

Information

Databases
Help
API
Contact us
Code on GitHub
Terms of use
Submit Data