Events of alternative splicing in head and neck cancer via RNA sequencing – an update

Sharma, Vishwas; Nandan, Amrita; Singh, Harpreet; Agarwal, Suyash; Tripathi, Richa; Sinha, Dhirendra N; Mehrotra, Ravi

doi:10.1186/s12864-019-5794-y

Cited by 5 publications

(3 citation statements)

References 49 publications

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“…Therefore, a comprehensive understanding of the AS model is critical to the future treatment strategy for cancer. The emergence of RNA-Seq technology and the cancer genome database has become a new tool for studying AS events in pancreatic adenocarcinoma, helping to identify new therapeutic and molecular targets for pancreatic adenocarcinoma [34,35].…”

Section: Discussionmentioning

confidence: 99%

Signature of gene aberrant alternative splicing events in pancreatic adenocarcinoma prognosis

Yao

Tang

et al. 2021

J. Cancer

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Alternative splicing (AS), as an effective and universal mechanism of transcriptional regulation, is involved in the development and progression of cancer. Therefore, systematic analysis of alternative splicing in pancreatic adenocarcinoma (PAAD) is warranted. The corresponding clinical information of the RNA-Seq data and PAAD cohort was downloaded from the TCGA data portal. Then, a java application, SpliceSeq, was used to evaluate the RNA splicing pattern and calculate the splicing percentage index (PSI). Differentially expressed AS events (DEAS) were identified based on PSI values between PAAD cancer samples and normal samples of adjacent tissues. Kaplan-Meier and Cox regression analyses were used to assess the association between DEAS and patient clinical characteristics. Unsupervised cluster analysis used to reveal four clusters with different survival patterns. At the same time, GEO and TCGA combined with GTEx to verify the differential expression of AS gene and splicing factor. After rigorous filtering, a total of 45,313 AS events were identified, 1,546 of which were differentially expressed AS events. Nineteen DEAS were found to be associated with OS with a five-year overall survival rate of 0.946. And the subtype clusters results indicate that there are differences in the nature of individual AS that affect clinical outcomes. Results also identified 15 splicing factors associated with the prognosis of PAAD. And the splicing factors ESRP1 and RBM5 played an important role in the PAAD-associated AS events. The PAAD-associated AS events, splicing networks, and clusters identified in this study are valuable for deciphering the underlying mechanisms of AS in PAAD and may facilitate the establishment of therapeutic goals for further validation.

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Section: Discussionmentioning

confidence: 99%

Signature of gene aberrant alternative splicing events in pancreatic adenocarcinoma prognosis

Yao

Tang

et al. 2021

J. Cancer

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“…Previous studies have suggested that RPS9 dysregulation was involved in tumorigenesis, such as pancreatic cancer, head, and neck cancer (such as head and neck squamous cell carcinoma) and so on [13][14][15] . Moreover, evidence indicated suggested that RPS9 knockdown suppressed proliferation through P53 independent mechanisms in U2OS cells, impaired 18S rRNA production in glioma cells by P53 and accelerated cell death in cervical carcinoma HeLa cells [16] .…”

Section: Ivyspringmentioning

confidence: 99%

RPS9 promotes the progression of NSCLC via activation Stat3 and Erk signaling pathways

Kong¹,

Shuangshuang²,

Liang³

et al. 2022

J. Cancer

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Background: Non-small cell lung cancer (NSCLC) accounts for the largest pathological type of lung cancers, and it is characterized by high incidence and poor prognosis. However, the molecular mechanisms involved in development and progression of NSCLC are not well elucidated. In this study, we aimed to explore the role and regulatory mechanism of RPS9 in NSCLC. Materials and methods:The RPS9 expression in NSCLC tissues and cell lines was assessed by qRT-PCR and western blot. Knockdown of RPS9 induced by RNA interference (RNAi) method in PC9, A549 and H1299 cells. Overexpression of RPS9 induced by transient transfection in H292 cells. Cell proliferation, colony formation, metastasis and apoptosis abilities were determined by CCK-8 assay, colony formation assay, transwell assay and flow cytometry, respectively. The host signaling pathways affected by RPS9 were screened by antibody library and proved by western blot. Results: RPS9 was significantly upregulated in NSCLC tissues and cell lines. Overexpression of RPS9 predicted poor prognosis of NSCLC patients. Knockdown of RPS9 obviously repressed cell proliferation, metastasis, and induced apoptosis. Mechanistically, suppression of RPS9 inhibited the expression level of phosphorylation of Stat3 and Erk. Conclusion: Our study clarified that knockdown of RPS9 inhibits the progression of NSCLC via inactivation Stat3 and Erk signaling pathways.

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“…Prior literature suggests a role of alternative splicing in HNSCC. Multiple studies have attempted to systematically identify alternative splicing events associated with HNSCC prognosis. − For example, re-clustering TCGA HNSCC RNA-Seq data based on alternative splicing events resulted in four clusters that highly resemble the four molecular subtypes of HNSCC . Additionally, a previous phosphoproteomics and proteomics study comparing normal versus HNSCC cell lines identified RNA splicing as one of the most changed cellular processes in this cancer type .…”

Section: Introductionmentioning

confidence: 99%

IQGAP1 and RNA Splicing in the Context of Head and Neck via Phosphoproteomics

et al. 2022

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IQGAP1 (IQ motif-containing GTPase-activating protein 1) scaffolds several signaling pathways in mammalian cells that are implicated in carcinogenesis, including the RAS and PI3K pathways that involve multiple protein kinases. IQGAP1 has been shown to promote head and neck squamous cell carcinoma (HNSCC); however, the underlying mechanism(s) remains unclear. Here, we report a mass spectrometry-based analysis identifying differences in phosphorylation of cellular proteins in vivo and in vitro in the presence or absence of IQGAP1. By comparing the esophageal phosphoproteome profiles between Iqgap1 +/+ and Iqgap1 −/− mice, we identified RNA splicing as one of the most altered cellular processes. Serine/arginine-rich splicing factor 6 (SRSF6) was the protein with the most downregulated levels of phosphorylation in Iqgap1 −/− tissue. We confirmed that the absence of IQGAP1 reduced SRSF6 phosphorylation both in vivo and in vitro. We then expanded our analysis to human normal oral keratinocytes. Again, we found factors involved in RNA splicing to be highly altered in the phosphoproteome profile upon genetic disruption of IQGAP1. Both the Clinical Proteomic Tumor Analysis Consortium (CPTAC) and the Cancer Genome Atlas (TCGA) data sets indicate that phosphorylation of splicing-related proteins is important in HNSCC prognosis. The Biological General Repository for Interaction Datasets (BioGRID) repository also suggested multiple interactions between IQGAP1 and splicingrelated proteins. Based on these collective observations, we propose that IQGAP1 regulates the phosphorylation of splicing proteins, which potentially affects their splicing activities and, therefore, contributes to HNSCC. Raw data are available from the MassIVE database with identifier MSV000087770.

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Events of alternative splicing in head and neck cancer via RNA sequencing – an update

Cited by 5 publications

References 49 publications

Signature of gene aberrant alternative splicing events in pancreatic adenocarcinoma prognosis

Signature of gene aberrant alternative splicing events in pancreatic adenocarcinoma prognosis

RPS9 promotes the progression of NSCLC via activation Stat3 and Erk signaling pathways

IQGAP1 and RNA Splicing in the Context of Head and Neck via Phosphoproteomics

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