Evidence map›Paper›PMID 32901876›Full record

ArticleOncology reports2020

SRSF6 regulates alternative splicing of genes involved in DNA damage response and DNA repair in HeLa cells.

Xiao Yang, Peng Zhan, Shuqiang Feng, He Ji, Wenjie Tian, Mengdi Wang, Chao Cheng, Bin Song

Open access · hybridAbstract read
In one paragraph

Article in Oncology reports, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 21 papers.

0numbers the graph read from it
0cells of the map it votes in
21citing papers in PubMed
1.5field-weighted citation impact, top 18% of its field
1 · What the graph read from it

What it found

Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.

The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.

2 · The registry

The trial behind it

Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.

Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.

3 · Its place in the literature

Who cites it

21 citing papers in PubMed, 23 citations in OpenAlex.

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  19. Targeting Splicing Factor SRSF6 for Cancer Therapy.Frontiers in cell and developmental biology · 2021
    Review
  20. The rs74794265 SNP of theInternational journal of chronic obstructive pulmonary disease
    Article
4 · The record

Corrections and comments

PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.

5 · Who and what money

Authors and funding

8 authors at 1 institution in 1 country.

Xiao YangDepartment of Urology, The Second Hospital of Jilin University, Changchun, Jilin 130041, P.R. China.
Peng ZhanDepartment of Urology, The Second Hospital of Jilin University, Changchun, Jilin 130041, P.R. China.
Shuqiang FengDepartment of Urology, The Second Hospital of Jilin University, Changchun, Jilin 130041, P.R. China.
He JiDepartment of Neurosurgery, The Second Hospital of Jilin University, Changchun, Jilin 130041, P.R. China.
Wenjie TianDepartment of Urology, The Second Hospital of Jilin University, Changchun, Jilin 130041, P.R. China.
Mengdi WangABLife BioBigData Institute, Wuhan, Hubei 430075, P.R. China.
Chao ChengABLife BioBigData Institute, Wuhan, Hubei 430075, P.R. China.
Bin SongDepartment of Neurosurgery, The Second Hospital of Jilin University, Changchun, Jilin 130041, P.R. China.
Second Affiliated Hospital of Jilin University · CN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Alternative splicing (AS) occurs in nearly all human genes and abnormal AS has a close association with cancer. Serine and arginine‑rich splicing factor 6 (SRSF6), a canonical member of the serine/arginine‑rich protein family, has been characterized as an important regulator of AS. However, the role of SRSF6 in regulating AS in cancers has remained to be fully elucidated. In the present study, the median expression of SRSF6 in tumors was determined to be higher compared with that in matched normal tissues in 13 out of 16 cancer types from The Cancer Genome Atlas. To investigate the biological effects of SRSF6 overexpression, an SRSF6‑overexpression model of HeLa cells was constructed and it was revealed that SRSF6 overexpression resulted in significantly higher apoptosis and lower proliferation compared to control cells. Transcriptome analysis indicated that overexpression of SRSF6 in cancer cells induced large‑scale changes in transcriptional expression levels and AS. Two groups of cervical cancer tumor samples in which SRSF6 was differentially expressed were then selected to analyze potential SRSF6‑regulated AS. It was determined that the pattern of SRSF6‑regulated AS in clinical samples was similar to that in cancer cells and AS genes were enriched in DNA damage response (DDR) pathways, including DNA repair and double‑strand break repair via homologous recombination. Furthermore, AS events regulated by SRSF6 were validated using reverse transcription‑quantitative PCR. The present results highlighted that SRSF6 is able to trigger the activation of DDR pathways via regulation of AS to influence cancer progression. These results markedly expand the current understanding of the mechanisms underlying SRSF6‑mediated gene regulation and suggest the potential use of SRSF6 as a therapeutic target in cancer.

Indexed as

DNA DamageDNA RepairAlternative SplicingApoptosisCell ProliferationComputational BiologyDatabases, GeneticDNA Repair EnzymesFemaleHeLa CellsHumansNeoplasmsPhosphoproteinsSerine-Arginine Splicing FactorsDNA Repair EnzymesPhosphoproteinsSerine-Arginine Splicing FactorsSRSF6 protein, humanalternative splicingcancerDNA damage responseDNA repairSRSF6/SRP55

Identifiers

PMID32901876
PMCPMC7551351
OpenAlexW3082385364

What OpenQuestion holds

Textmetadata
LicenceCC BY-NC-ND
Read underepoch 390

Registered trials

None linked

Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.