LncRNA SNHG20 promotes migration and invasion of ovarian cancer via modulating the microRNA-148a/ROCK1 axis

Yang, Qi; Dong, Yujie

doi:10.1186/s13048-021-00889-8

Cited by 12 publications

(6 citation statements)

References 41 publications

Supporting

Mentioning

Contrasting

Order By: Relevance

“…ROCK1 regulates cellular processes such as actomyosin contractility, focal adhesion assembly, cytokinesis, and cell proliferation [6]. Accumulating evidence suggests that dysfunction of ROCK1 contributes to various cancers, including bladder [7], breast [8], ovarian [9], gastric [10], colon [11] and ovarian cancers [12]. Similarly, our study showed that ROCK1 is highly expressed in human LSCC tissues, and high expression of ROCK1 correlates with advanced stage and poor survival prognosis of LSCC patients.…”

Section: Introductionsupporting

confidence: 68%

Crosstalk between ROCK1 and PYROXD1 regulates CAFs activation and promotes laryngeal squamous cell carcinoma metastasis

Yang

Qiao

Zhang

et al. 2022

Preprint

View full text Add to dashboard Cite

We previously found the protein kinase ROCK1 actives CAFs to promote LSCC metastasis. Accumulating evidence indicates that the oxidoreductase PYROXD1 is an oncogene; however, the crosstalk between ROCK1 and PYROXD1 in LSCC metastasis is largely unknown. Here, we found that ROCK1 can target PYROXD1 and that knockdown of ROCK1 expression reduces the expression of PYROXD1, while knockdown of PYROXD1 expression cannot alter the expression of ROCK1; these results indicate that ROCK1 is upstream of PYROXD1. Furthermore, LSCC cells cocultured with PYROXD1-knockdown CAFs exhibit lower proliferation, migration, invasion and metastasis. Conversely, LSCC cells cocultured with PYROXD1-overexpressing CAFs show the opposite results. In conclusion, the crosstalk between ROCK1 and PYROXD1 regulates CAFs activation and promotes LSCC metastasis.

show abstract

Section: Introductionsupporting

confidence: 68%

Crosstalk between ROCK1 and PYROXD1 regulates CAFs activation and promotes laryngeal squamous cell carcinoma metastasis

Yang

Qiao

Zhang

et al. 2022

Preprint

View full text Add to dashboard Cite

show abstract

“…Moreover, a a multi-label fusion collaborative matrix factorization (MLFCMF) approach was proposed for predicting lncRNA-disease associations, especially, their method finally obtains an AUC value of 0.8612 [ 32 ]. In addition to the above bioinformatics studies, the role of most lncRNAs in OC cell lines has also been explored, such as MSC-AS1 [ 33 ], TONSL-AS1 [ 34 ], and SNHG20 [ 35 ], etc. However, lncRNAs participating in risk signature have not been well explored in OC, and this suggests that our study is an indicator for Vivo and Vitro assays in the future.…”

Section: Discussionmentioning

confidence: 99%

Integrated clinical characteristics and omics analysis identifies a ferroptosis and iron-metabolism-related lncRNA signature for predicting prognosis and therapeutic responses in ovarian cancer

et al. 2022

View full text Add to dashboard Cite

Background Ferroptosis and iron-metabolism are regulated by Long non-coding RNAs (lncRNAs) in ovarian cancer (OC). Therefore, a comprehensive analysis of ferroptosis and iron-metabolism related lncRNAs (FIRLs) in OC is crucial for proposing therapeutic strategies and survival prediction. Methods In multi-omics data from OC patients, FIRLs were identified by calculating Pearson correlation coefficients with ferroptosis and iron-metabolism related genes (FIRGs). Cox-Lasso regression analysis was performed on the FIRLs to screen further the lncRNAs participating in FIRLs signature. In addition, all patients were divided into two robust risk subtypes using the FIRLs signature. Receiver operator characteristic (ROC) curve, Kaplan–Meier analysis, decision curve analysis (DCA), Cox regression analysis and calibration curve were used to confirm the clinical benefits of FIRLs signature. Meanwhile, two nomograms were constructed to facilitate clinical application. Moreover, the potential biological functions of the signature were investigated by genes function annotation. Finally, immune microenvironment, chemotherapeutic sensitivity, and the response of PARP inhibitors were compared in different risk groups using diversiform bioinformatics algorithms. Results The raw data were randomized into a training set (n = 264) and a testing set (n = 110). According to Pearson coefficients between FIRGs and lncRNAs, 1075 FIRLs were screened for univariate Cox regression analysis, and then LASSO regression analysis was used to construct 8-FIRLs signature. It is worth mentioning that a variety of analytical methods indicated excellent predictive performance for overall survival (OS) of FIRLs signature (p < 0.05). The multivariate Cox regression analysis showed that FIRLs signature was an independent prognostic factor for OS (p < 0.05). Moreover, significant differences in the abundance of immune cells, immune-related pathways, and drug response were excavated in different risk subtypes (p < 0.05). Conclusion The FIRLs signature can independently predict overall survival and therapeutic effect in OC patients.

show abstract

“…LncNBAT1 represses the transcriptional activity of signal transducer and activator of transcription 1 (STAT1) to attenuate apolipoprotein B mRNA editing enzyme catalytic subunit 3 A (APOBEC3A) expression, which mediates chemoresistance in DLBCL cells [ 25 ]. The lncRNA SNHG20 has been demonstrated to play oncogenic roles in many cancers, including oral squamous cell carcinoma [ 26 ], ovarian cancer [ 27 ], colorectal cancer (CRC) [ 28 ], cervical cancer [ 29 ], lung cancer [ 10 ], glioma [ 11 ] and hepatocellular carcinoma [ 30 ]. However, its role in haematological diseases, especially DLBCL, has never been studied.…”

Section: Discussionmentioning

confidence: 99%

C-MYC-activated lncRNA SNHG20 accelerates the proliferation of diffuse large B cell lymphoma via USP14-mediated deubiquitination of β-catenin

Wang,

Fu,

Zhang

et al. 2024

Biol Direct

View full text Add to dashboard Cite

Background Long noncoding RNAs (lncRNAs) are implicated in the initiation and progression of diffuse large B-cell lymphoma (DLBCL). Small nucleolar RNA host gene 20 (SNHG20) has been recognized as a critical lncRNA in multiple human cancers. However, the role of SNHG20 and its underlying mechanism in DLBCL are still unclear. Methods The expression levels of SNHG20, c-MYC, β-catenin, and ubiquitin-specific peptidase 14 (USP14) were measured by reverse transcription-quantitative polymerase chain reaction (RT‒qPCR) and immunoblotting. Cell Counting Kit-8 (CCK-8), 5-Ethynyl-2′-deoxyuridine (EdU) incorporation, and flow cytometry assays were used to assess the proliferation and apoptosis of DLBCL cells. The transcriptional regulation of SNHG20 by c-MYC was confirmed by a luciferase reporter assay and RNA immunoprecipitation. The interaction between USP14 and β-catenin was demonstrated using coimmunoprecipitation. A subcutaneous xenograft model was constructed to determine the role of SNHG20 in vivo. Results In the present study, we found that SNHG20 expression was upregulated in DLBCL cell lines and tissues compared to their normal counterparts. SNHG20 knockdown prominently reduced the proliferation and induced the apoptosis of U2932 and OCI-LY3 cells. However, SNHG20 overexpression increased the proliferation and apoptosis resistance of DLBCL cells. Mechanistically, the expression of SNHG20 was positively regulated by c-MYC in DLBCL cells. C-MYC directly bound to the promoter of SNHG20 to activate its transcription. SNHG20 was expressed mainly in the cytosol in DLBCL cells. SNHG20 silencing did not impact USP14 expression but markedly decreased the level of β-catenin, the substrate of USP14, in DLBCL cells. USP14 overexpression increased the β-catenin level, and this increase was attenuated by SNHG20 knockdown. Treatment with the proteasome inhibitor MG132 abolished SNHG20 knockdown-induced β-catenin downregulation. Moreover, SNHG20 silencing reduced the half-life but increased the ubiquitination of β-catenin in DLBCL cells. SNHG20 knockdown weakened the interaction between both endogenous and exogenous USP14 and β-catenin. In turn, SNHG20 overexpression increased the c-MYC level, and this increase was attenuated by β-catenin knockdown. Importantly, β-catenin knockdown attenuated the SNHG20-mediated increase in DLBCL cell proliferation in vitro and tumour growth in vivo. Conclusions Taken together, our results suggested that c-MYC-activated SNHG20 accelerated the proliferation and increased the apoptosis resistance of DLBCL cells via USP14-mediated deubiquitination of β-catenin. The c-MYC/SNHG20 positive feedback loop may be a new target for anti-DLBCL treatment.

show abstract

LncRNA SNHG20 promotes migration and invasion of ovarian cancer via modulating the microRNA-148a/ROCK1 axis

Cited by 12 publications

References 41 publications

Crosstalk between ROCK1 and PYROXD1 regulates CAFs activation and promotes laryngeal squamous cell carcinoma metastasis

Crosstalk between ROCK1 and PYROXD1 regulates CAFs activation and promotes laryngeal squamous cell carcinoma metastasis

Integrated clinical characteristics and omics analysis identifies a ferroptosis and iron-metabolism-related lncRNA signature for predicting prognosis and therapeutic responses in ovarian cancer

C-MYC-activated lncRNA SNHG20 accelerates the proliferation of diffuse large B cell lymphoma via USP14-mediated deubiquitination of β-catenin

Contact Info

Product

Resources

About