lncRNA prostate cancer-associated transcript 18 upregulates activating transcription factor 7 to prevent metastasis of triple-negative breast cancer via sponging miR-103a-3p

Zhang, Jinfeng; Liu, Donghua; Deng, Guoming; Wang, Qiuming; Li, Liang; Zhang, Jinxiang; Wu, Heming

doi:10.1080/21655979.2021.2003928

Cited by 6 publications

(4 citation statements)

References 48 publications

(42 reference statements)

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“…The expression of KDM5B enhances invasive TNBC by downregulating hsa-mir-448 ( Bamodu et al, 2016 ). Our identified three post-transcriptional regulators (hsa-mir-1-3p, hsa-mir-124-3p, and hsa-mir-34a-5p) are also supported by published articles that are associated with TNBC progression by using bioinformatics analysis and cellular experiments ( Volovat et al, 2020 ; Zhang et al, 2021a ; Zhang et al, 2021b ; Shadbad et al, 2021 ).…”

Section: Discussionsupporting

confidence: 77%

Gene expression profile analysis to discover molecular signatures for early diagnosis and therapies of triple-negative breast cancer

Alam

Sultana

Wang

et al. 2022

Front. Mol. Biosci.

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Triple-negative breast cancer (TNBC) is one of the most lethal subtypes of breast cancer (BC), and it accounts for approximately 10%–20% of all invasive BCs diagnosed worldwide. The survival rate of TNBC in stages III and IV is very low, and a large number of patients are diagnosed in these stages. Therefore, the purpose of this study was to identify TNBC-causing molecular signatures and anti-TNBC drug agents for early diagnosis and therapies. Five microarray datasets that contained 304 TNBC and 109 control samples were collected from the Gene Expression Omnibus (GEO) database, and RNA-Seq data with 116 tumor and 124 normal samples were collected from TCGA database to identify differentially expressed genes (DEGs) between TNBC and control samples. A total of 64 DEGs were identified, of which 29 were upregulated and 35 were downregulated, by using the statistical limma R-package. Among them, seven key genes (KGs) were commonly selected from microarray and RNA-Seq data based on the high degree of connectivity through PPI (protein–protein interaction) and module analysis. Out of these seven KGs, six KGs (TOP2A, BIRC5, AURKB, ACTB, ASPM, and BUB1B) were upregulated and one (EGFR) was downregulated. We also investigated their differential expression patterns with different subtypes and progression stages of BC by the independent datasets of RNA-seq profiles from UALCAN database, which indicated that they may be potential biomarkers for early diagnosis. Gene Ontology (GO) and the Kyoto Encyclopedia of Genes and Genomes (KEGG) pathway enrichment analyses with the proposed DEGs were performed using the online Enrichr database to investigate the pathogenetic processes of TNBC highlighting KGs. Then, we performed gene regulatory network analysis and identified three transcriptional (SOX2, E2F4, and KDM5B) and three post-transcriptional (hsa-mir-1-3p, hsa-mir-124-3p, and hsa-mir-34a-5p) regulators of KGs. Finally, we proposed five KG-guided repurposable drug molecules (imatinib, regorafenib, pazopanib, teniposide, and dexrazoxane) for TNBC through network pharmacology and molecular docking analyses. These drug molecules also showed significant binding performance with some cancer-related PTM-sites (phosphorylation, succinylation, and ubiquitination) of top-ranked four key proteins (EGFR, AURKB, BIRC5, and TOP2A). Therefore, the findings of this computational study may play a vital role in early diagnosis and therapies against TNBC by wet-lab validation.

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Section: Discussionsupporting

confidence: 77%

Gene expression profile analysis to discover molecular signatures for early diagnosis and therapies of triple-negative breast cancer

Alam

Sultana

Wang

et al. 2022

Front. Mol. Biosci.

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“…Consistent with this observation, Zhang et al. found that PCAT18 was expressed at low levels in TNBC and could play a protective element in metastatic TNBC ( 26 ). Moreover, several previous studies have indicated that PCAT18 could inhibit the proliferation, migration, and invasion of gastric cancer (GC) cells, which could provide a theoretical basis for GC therapy ( 27 – 29 ).…”

Section: Discussionmentioning

confidence: 63%

“…ARHGAP28-AS1, LINC01711, LRRC8C-DT, PCAT18, and SIAH2-AS1 were shown as protective lncRNAs in patients with BC, whereas TDRKH-AS1, SAMMSON, WDFY3-AS2, and LINC00393 were identified as risk factors. Consistent with this observation, Zhang et al found that PCAT18 was expressed at low levels in TNBC and could play a protective element in metastatic TNBC (26). Moreover, several previous studies have indicated that PCAT18 could inhibit the proliferation, migration, and invasion of gastric cancer (GC) cells, which could provide a theoretical basis for GC therapy (27-29).…”

Section: Discussionmentioning

confidence: 82%

Comprehensive analysis of cuproptosis-related long non-coding RNA signature and personalized therapeutic strategy of breast cancer patients

Guo

Qiu²,

Pan³

et al. 2022

Front. Oncol.

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BackgroundBreast cancer (BC) is considered to be one of the primary causes of cancer deaths in women. Cuproptosis was suggested to play an important role in tumor proliferation and tumor immune microenvironment. Therefore, an investigation was conducted to identify the relationship between cuproptosis-related long non-coding RNAs (lncRNAs) and BC prognosis.MethodBased on The Cancer Genome Atlas (TCGA), nine cuproptosis-related lncRNAs were identified by Pearson’s analysis and Cox regression analysis to create a cuproptosis-related lncRNA signature. Subsequently, patients with BC were divided into high-risk and low-risk groups. The Kaplan–Meier curves and a time-dependent receiver operating characteristic (ROC) analysis were employed to elucidate the predictive capability of the signature. After that, the Kyoto Encyclopedia of Genes and Genomes (KEGG) pathway analysis was conducted by Gene Set Enrichment Analysis (GSEA), and the lncRNA–mRNA co-expression network was established by Cytoscape software. Furthermore, the ESTIMATE score was calculated, and the immune cell type component analysis was conducted. Eventually, immunotherapy response analysis was applied to identify the predictive power of cuproptosis-related lncRNAs to tumor immunotherapy response, including immune checkpoint gene expression levels, tumor mutational burden (TMB), and microsatellite instability (MSI).ResultsPatients with BC in the low-risk groups showed better clinical outcomes. The KEGG pathways in the high-risk groups were mainly enriched in immune response and immune cell activation. Furthermore, the ESTIMATE scores were higher in the low-risk groups, and their immune cell infiltrations were dramatically different from those of the high-risk groups. The low-risk groups were shown to have higher infiltration levels of CD8+ T cells and TMB-high status, resulting in better response to immunotherapies.ConclusionThe findings of this study revealed that the nine-cuproptosis-related lncRNA risk score was an independent prognostic factor for BC. This signature was a potential predictor for BC immunotherapy response. What we found will provide novel insight into immunotherapeutic treatment strategies in BC.

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“…In conclusion, this study demonstrated that SNHG10 and miR-302b are downregulated in TNBC [ 34 , 35 ]. Overexpression of SNHG10 may serve as a potential target to treat TNBC by upregulating miR-302b through methylation, thereby increasing the sensitivity of TNBC cells to doxorubicin.…”

Section: Discussionmentioning

confidence: 98%

LncRNA SNHG10 suppresses the development of doxorubicin resistance by downregulating miR-302b in triple-negative breast cancer

et al. 2022

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Unlike other types of breast cancer, triple negative breast cancer (TNBC) does not respond to therapies targeting human epidermal growth factor receptor-2 (HER2) or hormone therapy, and the prognosis of patients with TNBC is usually poor. The role of long non-coding RNA (lncRNA) small nucleolar RNA host gene 10 (SNHG10) has been investigated in many types of cancer, but its role in TNBC is unknown. This study aimed to explore the role of SNHG10 in TNBC in the context of doxorubicin treatment, a common therapy for TNBC. Analysis of the TCGA dataset revealed the downregulation of SNHG10 in TNBC. The downregulation of SNHG10 of TNBC in TNBC was further confirmed by detecting its expression in 60 patients with TNBC by qPCR. The expression of SNHG10 was further downregulated after doxorubicin treatment. In TNBC, microRNA-302b (miR-302b) was downregulated and was positively correlated with SNHG10. In TNBC cells, overexpression of SNHG10 resulted in upregulation of miR-302b, and methylation-specific PCR analysis showed that SNHG10 negatively regulates the methylation of miR-302b. In addition, doxorubicin treatment resulted in the downregulation of SNHG10 in TNBC cells, and overexpression of SNHG10 and miR-302b promoted apoptosis of doxorubicin-treated TNBC cells. Furthermore, overexpression of both SNHG10 and miR-302b had a stronger effect on apoptosis than that of overexpression of SNHG10 alone. Our study showed that SNHG10 could inhibit the development of resistance to doxorubicin by upregulating miR-302b in TNBC through methylation. Our findings suggested that SNHG10 might serve as a molecular target for intervening in TBNC metastasis.

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lncRNA prostate cancer-associated transcript 18 upregulates activating transcription factor 7 to prevent metastasis of triple-negative breast cancer via sponging miR-103a-3p

Cited by 6 publications

References 48 publications

Gene expression profile analysis to discover molecular signatures for early diagnosis and therapies of triple-negative breast cancer

Gene expression profile analysis to discover molecular signatures for early diagnosis and therapies of triple-negative breast cancer

Comprehensive analysis of cuproptosis-related long non-coding RNA signature and personalized therapeutic strategy of breast cancer patients

LncRNA SNHG10 suppresses the development of doxorubicin resistance by downregulating miR-302b in triple-negative breast cancer

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