Rojalin Nayak, Trisha Chattopadhyay, Pooja Gupta and Bibekanand Mallick
{"title":"小非编码rna的整合分析预测了在胶质母细胞瘤中驱动肿瘤发生的piRNA/miRNA-CCND1/BRAF/HRH1/ATXN3调控回路","authors":"Rojalin Nayak, Trisha Chattopadhyay, Pooja Gupta and Bibekanand Mallick","doi":"10.1039/D2MO00245K","DOIUrl":null,"url":null,"abstract":"<p >The high-grade astrocytoma, glioblastoma multiforme (GBM), is the most common primary tumour of the brain, known for being aggressive and developing drug resistance. The non-coding RNAs (ncRNAs), such as microRNAs (miRNAs) and Piwi-interacting RNAs (piRNAs), have critical functions in tumorigenesis and cancer drug resistance. Hence, we profiled miRNAs, piRNAs, and genes in U-87 MG GBM cells by next-generation sequencing and performed target prediction, pathway enrichment, protein–protein interaction, co-expression studies, and qRT-PCR validations to predict their possible roles in the malignancy. The study identified 335 miRNAs, 665 piRNAs, and 4286 genes differentially expressed (DE) in GBM. Among them 128 DE genes (DEGs) were targeted by both miRNAs and piRNAs, while 1817 and 192 were targeted solely by miRNAs or piRNAs, respectively. Interestingly, all the DEG targets enriched in cancer processes were overexpressed in GBM. Among these, BRAF was solely targeted by two piRNAs and this was found to be co-expressed with 19 sole targets of 5 miRNAs, including CCND1, and both were found to regulate cell proliferation in cancer. We conjectured that upregulated HRH1 and ATXN3 were targeted by both piRNAs and miRNAs, and along with BRAF and CCND1 might induce cell proliferation in GBM through G-protein-coupled receptor or Akt signalling pathways due to downregulation of the respective targeting small RNAs. These targets were also linked to the progression and overall survival of GBM patients, suggesting that they could be used as biomarkers. Overall, this study has identified a few novel ncRNA targets, which might aid in a better understanding of GBM pathogenesis.</p>","PeriodicalId":19065,"journal":{"name":"Molecular omics","volume":" 3","pages":" 252-261"},"PeriodicalIF":3.0000,"publicationDate":"2023-01-09","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":"2","resultStr":"{\"title\":\"Integrative analysis of small non-coding RNAs predicts a piRNA/miRNA-CCND1/BRAF/HRH1/ATXN3 regulatory circuit that drives oncogenesis in glioblastoma†\",\"authors\":\"Rojalin Nayak, Trisha Chattopadhyay, Pooja Gupta and Bibekanand Mallick\",\"doi\":\"10.1039/D2MO00245K\",\"DOIUrl\":null,\"url\":null,\"abstract\":\"<p >The high-grade astrocytoma, glioblastoma multiforme (GBM), is the most common primary tumour of the brain, known for being aggressive and developing drug resistance. The non-coding RNAs (ncRNAs), such as microRNAs (miRNAs) and Piwi-interacting RNAs (piRNAs), have critical functions in tumorigenesis and cancer drug resistance. Hence, we profiled miRNAs, piRNAs, and genes in U-87 MG GBM cells by next-generation sequencing and performed target prediction, pathway enrichment, protein–protein interaction, co-expression studies, and qRT-PCR validations to predict their possible roles in the malignancy. The study identified 335 miRNAs, 665 piRNAs, and 4286 genes differentially expressed (DE) in GBM. Among them 128 DE genes (DEGs) were targeted by both miRNAs and piRNAs, while 1817 and 192 were targeted solely by miRNAs or piRNAs, respectively. Interestingly, all the DEG targets enriched in cancer processes were overexpressed in GBM. Among these, BRAF was solely targeted by two piRNAs and this was found to be co-expressed with 19 sole targets of 5 miRNAs, including CCND1, and both were found to regulate cell proliferation in cancer. We conjectured that upregulated HRH1 and ATXN3 were targeted by both piRNAs and miRNAs, and along with BRAF and CCND1 might induce cell proliferation in GBM through G-protein-coupled receptor or Akt signalling pathways due to downregulation of the respective targeting small RNAs. These targets were also linked to the progression and overall survival of GBM patients, suggesting that they could be used as biomarkers. 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Integrative analysis of small non-coding RNAs predicts a piRNA/miRNA-CCND1/BRAF/HRH1/ATXN3 regulatory circuit that drives oncogenesis in glioblastoma†
The high-grade astrocytoma, glioblastoma multiforme (GBM), is the most common primary tumour of the brain, known for being aggressive and developing drug resistance. The non-coding RNAs (ncRNAs), such as microRNAs (miRNAs) and Piwi-interacting RNAs (piRNAs), have critical functions in tumorigenesis and cancer drug resistance. Hence, we profiled miRNAs, piRNAs, and genes in U-87 MG GBM cells by next-generation sequencing and performed target prediction, pathway enrichment, protein–protein interaction, co-expression studies, and qRT-PCR validations to predict their possible roles in the malignancy. The study identified 335 miRNAs, 665 piRNAs, and 4286 genes differentially expressed (DE) in GBM. Among them 128 DE genes (DEGs) were targeted by both miRNAs and piRNAs, while 1817 and 192 were targeted solely by miRNAs or piRNAs, respectively. Interestingly, all the DEG targets enriched in cancer processes were overexpressed in GBM. Among these, BRAF was solely targeted by two piRNAs and this was found to be co-expressed with 19 sole targets of 5 miRNAs, including CCND1, and both were found to regulate cell proliferation in cancer. We conjectured that upregulated HRH1 and ATXN3 were targeted by both piRNAs and miRNAs, and along with BRAF and CCND1 might induce cell proliferation in GBM through G-protein-coupled receptor or Akt signalling pathways due to downregulation of the respective targeting small RNAs. These targets were also linked to the progression and overall survival of GBM patients, suggesting that they could be used as biomarkers. Overall, this study has identified a few novel ncRNA targets, which might aid in a better understanding of GBM pathogenesis.
Molecular omicsBiochemistry, Genetics and Molecular Biology-Biochemistry
CiteScore
5.40
自引率
3.40%
发文量
91
期刊介绍:
Molecular Omics publishes high-quality research from across the -omics sciences.
Topics include, but are not limited to:
-omics studies to gain mechanistic insight into biological processes – for example, determining the mode of action of a drug or the basis of a particular phenotype, such as drought tolerance
-omics studies for clinical applications with validation, such as finding biomarkers for diagnostics or potential new drug targets
-omics studies looking at the sub-cellular make-up of cells – for example, the subcellular localisation of certain proteins or post-translational modifications or new imaging techniques
-studies presenting new methods and tools to support omics studies, including new spectroscopic/chromatographic techniques, chip-based/array technologies and new classification/data analysis techniques. New methods should be proven and demonstrate an advance in the field.
Molecular Omics only accepts articles of high importance and interest that provide significant new insight into important chemical or biological problems. This could be fundamental research that significantly increases understanding or research that demonstrates clear functional benefits.
Papers reporting new results that could be routinely predicted, do not show a significant improvement over known research, or are of interest only to the specialist in the area are not suitable for publication in Molecular Omics.