Long non-coding RNA MIR205HG regulates KRT17 and tumor processes in cervical cancer via interaction with SRSF1

Dong, Mingli; Dong, Zhennan; Zhu, Xinyu; Zhang, Yunhe; Song, Lei

doi:10.1016/j.yexmp.2019.104322

Cited by 39 publications

(29 citation statements)

References 33 publications

Supporting

Mentioning

Contrasting

Order By: Relevance

“…In head and neck squamous cell carcinoma, where both MIR205HG and miR-205 are over-expressed, MIR205HG lncRNA was shown to enhance cancer cell proliferation and motility by sequestering miR-590-3p and preventing interaction with its target mRNAs, thus acting as "molecular sponge" 43 . Similar protumorigenic effects were reported for MIR205HG also in cervical cancer 59,60 and in lung squamous cell carcinoma 61,62 , though with different mechanisms of action (Table 2). This oncogenic role is remindful, though independent, to that of miR-205 in squamous cell carcinomas, where the miRNAs was shown to exert protumorigenic function through repression of tumor-suppressor genes 46 .…”

Section: Post-transcriptional Regulation Mir-205 Processing: Implicatsupporting

confidence: 79%

“…It is worth mentioning that, though processed from a common primary transcript, mature MIR205HG and miR-205 have been shown to act independently. In fact, recent studies on MIR205HG support its function as long noncoding RNA (lncRNA) in different cell contexts (Table 2) 43,54,[58][59][60][61][62] . LncRNAs are functional non-protein coding transcripts longer than 200 nucleotides 63 .…”

Section: Post-transcriptional Regulation Mir-205 Processing: Implicatmentioning

confidence: 99%

See 1 more Smart Citation

Unveiling the ups and downs of miR-205 in physiology and cancer: transcriptional and post-transcriptional mechanisms

Ferrari

Gandellini

2020

Cell Death Dis

View full text Add to dashboard Cite

miR-205 plays important roles in the physiology of epithelia by regulating a variety of pathways that govern differentiation and morphogenesis. Its aberrant expression is frequently found in human cancers, where it was reported to act either as tumor-suppressor or oncogene depending on the specific tumor context and target genes. miR-205 expression and function in different cell types or processes are the result of the complex balance among transcription, processing and stability of the microRNA. In this review, we summarize the principal mechanisms that regulate miR-205 expression at the transcriptional and post-transcriptional level, with particular focus on the transcriptional relationship with its host gene. Elucidating the mechanisms and factors regulating miR-205 expression in different biological contexts represents a fundamental step for a better understanding of the contribution of such pivotal microRNA to epithelial cell function in physiology and disease, and for the development of modulation strategies for future application in cancer therapy.

show abstract

Section: Post-transcriptional Regulation Mir-205 Processing: Implicatsupporting

confidence: 79%

Section: Post-transcriptional Regulation Mir-205 Processing: Implicatmentioning

confidence: 99%

Unveiling the ups and downs of miR-205 in physiology and cancer: transcriptional and post-transcriptional mechanisms

Ferrari

Gandellini

2020

Cell Death Dis

View full text Add to dashboard Cite

show abstract

“…Wu et al (2010) first demonstrated that SRSF1 was able to bind to CGGACAC motifs in the pri-miR-7-1, pri-miR-221 and pri-miR-222 stem loops thus enhancing Drosha cleavage and accumulation of miR-7, miR-221 and miR-222, promoting cervical cancer development (Pan et al, 2019). Moreover, Dong M. et al (2019) demonstrated that the lncRNA MIR205HG, which is overexpressed in cervical cancer, targets SRSF1 and up-regulates KRT17 causing cell proliferation and apoptosis inhibition in CaSKi, Hela, MS751 and SiHa cells. The silencing of SRSF3 in HeLa cells was shown to promote the production of ILF3 isoforms 1 and 2 as well as cell cycle progression to the S and G2/M phases and proliferation enhancement (Jia et al, 2019).…”

Section: Splicing Factors Deregulation In Cervical Cancermentioning

confidence: 99%

The Role of RNA Splicing Factors in Cancer: Regulation of Viral and Human Gene Expression in Human Papillomavirus-Related Cervical Cancer

Cerasuolo

Buonaguro

Tornesello

2020

Front. Cell Dev. Biol.

View full text Add to dashboard Cite

The spliceosomal complex components, together with the heterogeneous nuclear ribonucleoproteins (hnRNPs) and serine/arginine-rich (SR) proteins, regulate the process of constitutive and alternative splicing, the latter leading to the production of mRNA isoforms coding multiple proteins from a single pre-mRNA molecule. The expression of splicing factors is frequently deregulated in different cancer types causing the generation of oncogenic proteins involved in cancer hallmarks. Cervical cancer is caused by persistent infection with oncogenic human papillomaviruses (HPVs) and constitutive expression of viral oncogenes. The aberrant activity of hnRNPs and SR proteins in cervical neoplasia has been shown to trigger the production of oncoproteins through the processing of pre-mRNA transcripts either derived from human genes or HPV genomes. Indeed, hnRNP and SR splicing factors have been shown to regulate the production of viral oncoprotein isoforms necessary for the completion of viral life cycle and for cell transformation. Target-therapy strategies against hnRNPs and SR proteins, causing simultaneous reduction of oncogenic factors and inhibition of HPV replication, are under development. In this review, we describe the current knowledge of the functional link between RNA splicing factors and deregulated cellular as well as viral RNA maturation in cervical cancer and the opportunity of new therapeutic strategies.

show abstract

“…In addition, there are studies reporting splicing signatures associated with the prognosis of esophageal cancer ( Lin et al., 2018 ; Mao et al., 2019 ). Through the splicing mechanism, PRPF4, SRSF1, and HNRNPM regulate the cell proliferation, migration, and invasion in different cancers, including lung cancer ( Choi, 2012 ; Chang and Lin, 2019 ), breast cancer ( Anczuków et al., 2015 ; Sun et al., 2017 ; Park et al., 2019 ), cutaneous squamous cell carcinoma ( Zhang et al., 2018 ), hepatocellular carcinoma ( Tu et al., 2019 ), esophagus dysplasia ( Varghese et al., 2015 ; Fitzgerald et al., 2018 ), gastric cancer ( Wu et al., 2019 ), cervical cancer ( Dong et al., 2019 ), and Ewing's sarcoma ( Passacantilli et al., 2017 ).…”

Section: Discussionmentioning

confidence: 99%

“…(F) Protein levels of ORC2 in normal tissue (staining: not detected; intensity: low; quantity: <25%). et al, 2019), cervical cancer (Dong et al, 2019), and Ewing's sarcoma (Passacantilli et al, 2017).…”

mentioning

confidence: 99%

Integrated PPI- and WGCNA-Retrieval of Hub Gene Signatures Shared Between Barrett's Esophagus and Esophageal Adenocarcinoma

et al. 2020

View full text Add to dashboard Cite

Esophageal adenocarcinoma (EAC) is a deadly cancer with high mortality rate, especially in economically advanced countries, while Barrett's esophagus (BE) is reported to be a precursor that strongly increases the risk of EAC. Due to the complexity of these diseases, their molecular mechanisms have not been revealed clearly. This study aims to explore the gene signatures shared between BE and EAC based on integrated network analysis. We obtained EAC-and BE-associated microarray datasets GSE26886, GSE1420, GSE37200, and GSE37203 from the Gene Expression Omnibus and ArrayExpress using systematic meta-analysis. These data were accompanied by clinical data and RNAseq data from The Cancer Genome Atlas (TCGA). Weighted gene co-expression network analysis (WGCNA) and differentially expressed gene (DEG) analysis were conducted to explore the relationship between gene sets and clinical traits as well as to discover the key relationships behind the co-expression modules. A differentially expressed gene-based protein-protein interaction (PPI) complex was used to extract hub genes through Cytoscape plugins. As a result, 403 DEGs were excavated, comprising 236 upregulated and 167 downregulated genes, which are involved in the cell cycle and replication pathways. Forty key genes were identified using modules of MCODE, CytoHubba, and CytoNCA with different algorithms. A dark-gray module with 207 genes was identified which having a high correlation with phenotype (gender) in the WGCNA. Furthermore, five shared hub gene signatures (SHGS), namely, pre-mRNA processing factor 4 (PRPF4), serine and arginine-rich splicing factor 1 (SRSF1), heterogeneous nuclear ribonucleoprotein M (HNRNPM), DExH-Box Helicase 9 (DHX9), and origin recognition complex subunit 2 (ORC2), were identified between BE and EAC. SHGS enrichment denotes that RNA metabolism and splicosomes play a key role in

show abstract

Long non-coding RNA MIR205HG regulates KRT17 and tumor processes in cervical cancer via interaction with SRSF1

Cited by 39 publications

References 33 publications

Unveiling the ups and downs of miR-205 in physiology and cancer: transcriptional and post-transcriptional mechanisms

Unveiling the ups and downs of miR-205 in physiology and cancer: transcriptional and post-transcriptional mechanisms

The Role of RNA Splicing Factors in Cancer: Regulation of Viral and Human Gene Expression in Human Papillomavirus-Related Cervical Cancer

Integrated PPI- and WGCNA-Retrieval of Hub Gene Signatures Shared Between Barrett's Esophagus and Esophageal Adenocarcinoma

Contact Info

Product

Resources

About