Serine/arginine-rich splicing factor 7 regulates p21-dependent growth arrest in colon cancer cells

Saijo, Saki; Kuwano, Yuki; Masuda, Kiyoshi; Nishikawa, Tatsuya; Rokutan, Kazuhito; Nishida, Kensei

doi:10.2152/jmi.63.219

Cited by 31 publications

(24 citation statements)

References 36 publications

Supporting

Mentioning

Contrasting

Order By: Relevance

“…It was observed that SRSF7 knockdown inhibited proliferation and promoted apoptosis of HCT116 and A549 cells. Similarly, Saijo et al ( 30 ) reported that SRSF7 knockdown induced G1 cell cycle arrest in HCT116 cells. These results indicate that SRSF7 exerts a crucial effect on the growth of colon and lung cancer cells.…”

Section: Discussionmentioning

confidence: 82%

SRSF7 knockdown promotes apoptosis of colon and lung cancer cells

Wang

2018

Oncol Lett

View full text Add to dashboard Cite

Serine/arginine-rich (SR) proteins are a family of important splicing factors, which are involved in multiple aspects of RNA processing, including splicing, mRNA nuclear export, mRNA stability and translation. Previous studies have identified a number of SR proteins that exhibit abnormal expression in various tumor types. In the present study, the expression and function of serine/arginine-rich splicing factor 7 (SRSF7) were investigated in colon and lung cancer. Using tissue immunohistochemistry, it was observed that SRSF7 was overexpressed in colon and lung cancer tissues. As the role of SRSF7 in cancer remains to be fully elucidated, the expression of SRSF7 was knocked down in the present study by transfecting SRSF7-specific small interfering RNAs (siRNAs) into the HCT116 colon cancer cell line and A549 lung cancer cell line, which exhibited elevated expression of SRSF7. MTS assays, western blot analysis, flow cytometry and spectrofluorometer analyses were performed to assess the effects of SRSF7 knockdown on the proliferation and apoptosis of cells. The results demonstrated that the expression of SRSF7 was efficiently knocked down by SRSF7 siRNA, and that SRSF7 knockdown inhibited proliferation and enhanced apoptosis of HCT116 and A549 cells. Further experiments involving BEAS-2B cells stably overexpressing SRSF7, and A549 cells with stable knockdown of SRSF7 revealed that SRSF7 regulated the splicing of the apoptosis regulator Fas. Collectively, these data indicated that SRSF7 is critical for the survival of colon and lung cancer cells, and may be a potential therapeutic target for the treatment of colon and lung cancer.

show abstract

Section: Discussionmentioning

confidence: 82%

SRSF7 knockdown promotes apoptosis of colon and lung cancer cells

Wang

2018

Oncol Lett

View full text Add to dashboard Cite

show abstract

“…Also known as splicing factor 9G8, is a member of serine/arginine-rich splicing factor family, which is important for regulation of pre-mRNA splicing, nuclear export, and translation (72). It has been reported recently that SRSF7 plays a major role in proliferation of cancer cells and apoptosis (73,74). Other serine/arginine-rich splicing factors, for example SRSF3, were shown to modulate their own alternative splicing, as well as that of other transcripts encoding SR proteins (75).…”

Section: Resultsmentioning

confidence: 99%

Integrative transcriptomic analysis suggests new autoregulatory splicing events coupled with nonsense-mediated mRNA decay

Pervouchine

Popov

Berry

et al. 2019

Nucleic Acids Research

View full text Add to dashboard Cite

Nonsense-mediated decay (NMD) is a eukaryotic mRNA surveillance system that selectively degrades transcripts with premature termination codons (PTC). Many RNA-binding proteins (RBP) regulate their expression levels by a negative feedback loop, in which RBP binds its own pre-mRNA and causes alternative splicing to introduce a PTC. We present a bioinformatic analysis integrating three data sources, eCLIP assays for a large RBP panel, shRNA inactivation of NMD pathway, and shRNA-depletion of RBPs followed by RNA-seq, to identify novel such autoregulatory feedback loops. We show that RBPs frequently bind their own pre-mRNAs, their exons respond prominently to NMD pathway disruption, and that the responding exons are enriched with nearby eCLIP peaks. We confirm previously proposed models of autoregulation in SRSF7 and U2AF1 genes and present two novel models, in which (i) SFPQ binds its mRNA and promotes switching to an alternative distal 3′-UTR that is targeted by NMD, and (ii) RPS3 binding activates a poison 5′-splice site in its pre-mRNA that leads to a frame shift and degradation by NMD. We also suggest specific splicing events that could be implicated in autoregulatory feedback loops in RBM39, HNRNPM, and U2AF2 genes. The results are available through a UCSC Genome Browser track hub.

show abstract

“…SRSF7 is a serine and arginine-rich splicing factor and is part of the spliceosome. Its expression has been connected to several types of cancer and it has been shown that its knockdown induced p21 expression and thus reduced cancer development (Saijo et al, 2016 ). Little is known about TRA2A protein.…”

Section: Discussionmentioning

confidence: 99%

In-Depth Bioinformatic Analyses of Nidovirales Including Human SARS-CoV-2, SARS-CoV, MERS-CoV Viruses Suggest Important Roles of Non-canonical Nucleic Acid Structures in Their Lifecycles

et al. 2020

View full text Add to dashboard Cite

Non-canonical nucleic acid structures play important roles in the regulation of molecular processes. Considering the importance of the ongoing coronavirus crisis, we decided to evaluate genomes of all coronaviruses sequenced to date (stated more broadly, the order Nidovirales) to determine if they contain non-canonical nucleic acid structures. We discovered much evidence of putative G-quadruplex sites and even much more of inverted repeats (IRs) loci, which in fact are ubiquitous along the whole genomic sequence and indicate a possible mechanism for genomic RNA packaging. The most notable enrichment of IRs was found inside 5 ′ UTR for IRs of size 12+ nucleotides, and the most notable enrichment of putative quadruplex sites (PQSs) was located before 3 ′ UTR, inside 5 ′ UTR, and before mRNA. This indicates crucial regulatory roles for both IRs and PQSs. Moreover, we found multiple G-quadruplex binding motifs in human proteins having potential for binding of SARS-CoV-2 RNA. Non-canonical nucleic acids structures in Nidovirales and in novel SARS-CoV-2 are therefore promising druggable structures that can be targeted and utilized in the future.

show abstract

Serine/arginine-rich splicing factor 7 regulates p21-dependent growth arrest in colon cancer cells

Cited by 31 publications

References 36 publications

SRSF7 knockdown promotes apoptosis of colon and lung cancer cells

SRSF7 knockdown promotes apoptosis of colon and lung cancer cells

Integrative transcriptomic analysis suggests new autoregulatory splicing events coupled with nonsense-mediated mRNA decay

In-Depth Bioinformatic Analyses of Nidovirales Including Human SARS-CoV-2, SARS-CoV, MERS-CoV Viruses Suggest Important Roles of Non-canonical Nucleic Acid Structures in Their Lifecycles

Contact Info

Product

Resources

About