SRSF7 knockdown promotes apoptosis of colon and lung cancer cells

Fu, Yu; Wang, Yingze

doi:10.3892/ol.2018.8072

Cited by 28 publications

(32 citation statements)

References 30 publications

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“…Song et al also observed that the level of SRSF7 was upregulated in NSCLC tissues, meanwhile, the expression level of SRSF7 was negatively correlated with miR-374b-5p and positively correlated with MALAT1. Overexpression of SRSF7 could reverse the effects of MALAT1 knockdown on proliferation, apoptosis, and invasion in NSCLC cells [47]. In addition, SRSF1 was found to be upregulated in colon, kidney, lung, liver, pancreas and breast tumour [18,20,48,49].…”

Section: Abnormal Expression Of Srs and Cancermentioning

confidence: 92%

Serine/arginine-rich splicing factors: the bridge linking alternative splicing and cancer

Zheng¹,

Qiu

Wang

et al. 2020

Int. J. Biol. Sci.

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The serine/arginine-rich splicing factors (SRs) belong to the serine arginine-rich protein family, which plays an extremely important role in the splicing process of precursor RNA. The SRs recognize the splicing elements on precursor RNA, then recruit and assemble spliceosome to promote or inhibit the occurrence of splicing events. In tumors, aberrant expression of SRs causes abnormal splicing of RNA, contributing to proliferation, migration and apoptosis resistance of tumor cells. Here, we reviewed the vital role of SRs in various tumors and discussed the promise of analyzing mRNA alternative splicing events in tumor. Further, we highlight the challenges and discussed the perspectives for the identification of new potential targets for cancer therapy via SRs family members.

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Section: Abnormal Expression Of Srs and Cancermentioning

confidence: 92%

Serine/arginine-rich splicing factors: the bridge linking alternative splicing and cancer

Zheng¹,

Qiu

Wang

et al. 2020

Int. J. Biol. Sci.

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“…The SRSF6 is involved in the abnormal alternative splicing of the corticotropin-releasing hormone receptor type 1 (CRH-R1) causing indirect perturbation of oncogenic kinases, such as p38 MAPK, Akt and GSK3β, and accumulation of β-catenin in breast cancer (Lal et al, 2013). Knockdown experiments of SRSF7 in HCT116 colon and A549 lung cancer cell lines revealed the production of an exon 6-lacking isoform of the Fas receptor mRNA, that promotes cell survival (Fu and Wang, 2018).…”

Section: Oncogenic Functions Of Hnrnps and Srsfsmentioning

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.

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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.

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“…SRSF7 contains a motif with function of recognizing speci c RNAs at the N-terminus and a structure with function of facilitating spliceosome assembly, and based on this, SRSF7 participates in alternative splicing processes of multiple pre-mRNAs [23] . So far SRSF7 is known to express abnormally and play regulatory roles in multiple cancers including lung cancer, kidney cancer and colon cancer [7,23,24] . In this study, based on the TCGA database, we found for the rst time that SRSF7 was highly expressed in glioma tissues and cells, especially in high grade.…”

Section: Discussionmentioning

confidence: 99%

Biosynthetic circ-PLEKHA5 stabilized by SRSF7 promotes the vasculogenic mimicry of glioblastoma cells by encoding a novel protein 622aa

Su¹,

Liu

Teng

et al. 2020

Preprint

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Background: Increasing studies have been demonstrated that circRNAs play vital regulatory roles in the biological behaviors of glioblastoma cells, and increasing circRNAs are found to have the capacity of encoding small peptides, which are involved in the regulatory process.Methods: Western blot and qRT-PCR were conducted to confirm the expression of SRSF7 and circ-PLEKHA5 respectively. RNase R digestion assay and fluorescence in situ hybridization assays were conducted to evaluate the existence and cellular location of circ-PLEKHA5. RIP assay was used to access the relationship between SRSF7 and circ-PLEKHA5. Dual-luciferase assay and FLAG tag assays were performed to test the coding capability of circ-PLEKHA5. Immunofluorescence assay was conducted to evaluate the location of circ-PLEKHA5-622aa. CCK-8, vasculogenic mimicry (VM) formation and transwell assays were used to evaluate the roles of SRSF7, circ-PLEKHA5, circ-PLEKHA5-622aa on proliferation, VM formation, migration and invasion. Nude mice xenograft studys with PAS-CD34 staining were used to clarify the functional roles of SRSF7 and circ-PLEKHA5 on VM formation in vivo.Results: SRSF7 was up-regulated in glioma, and promoted the proliferation, migration, invasion, VM formation and the expression of VM-associated proteins of glioma cells by increasing the expression of circ-PLEKHA5. Circ-PLEKHA5 was mainly localized in cytoplasm and promoted the proliferation, migration, invasion, VM formation and the expression of VM-associated proteins of glioma cells by encoding a novel protein circ-PLEKHA5-622aa. The application of SRSF7 and circ-PLEKHA5 inhibitor significantly suppressed the tumor growth and VM formation in vivo.Conclusions: This study first demonstrated the coding ability of circ-PLEKHA5, and identified the regulatory roles of SRSF7/circ-PLEKHA5/circ-PLEKHA5-622aa pathway in VM formation of glioblastoma cells. Our findings might provide a novel strategy for glioma treatment.

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SRSF7 knockdown promotes apoptosis of colon and lung cancer cells

Cited by 28 publications

References 30 publications

Serine/arginine-rich splicing factors: the bridge linking alternative splicing and cancer

Serine/arginine-rich splicing factors: the bridge linking alternative splicing and cancer

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

Biosynthetic circ-PLEKHA5 stabilized by SRSF7 promotes the vasculogenic mimicry of glioblastoma cells by encoding a novel protein 622aa

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