Evidence map›Paper›PMID 30633341›Full record

ArticleJournal of cellular physiology2019

SRPK1 facilitates tumor cell growth via modulating the small nucleolar RNA expression in gastric cancer.

Yandong Li, Shijun Yu, Xiao Wang, Xiaojuan Ye, Bin He, Ming Quan, Yong Gao

Abstract read
In one paragraph

Article in Journal of cellular physiology, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 18 papers, 2 of them syntheses that pooled it.

0numbers the graph read from it
0cells of the map it votes in
18citing papers in PubMed, 2 pooled it
1.2field-weighted citation impact, top 22% 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

18 citing papers in PubMed, 2 syntheses or guidelines pooled it, 28 citations in OpenAlex.

  1. What is the Role of SNORA42 in Carcinogenesis? A Systematic Review.Asian Pacific journal of cancer prevention : APJCP · 2023
    Pooled it
  2. Pooled it
  3. Review
  4. Review
  5. Article
  6. Review
  7. Article
  8. SnoRNAs: The promising targets for anti-tumor therapy.Journal of pharmaceutical analysis · 2024
    Review
  9. SRPKs: a promising therapeutic target in cancer.Clinical and experimental medicine · 2023
    Review
  10. Review
  11. Article
  12. Article
  13. Article
  14. Review
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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

7 authors at 2 institutions in 2 countries.

Yandong LiDepartment of Oncology, Shanghai East Hospital, Tongji University School of Medicine, Shanghai, China.ORCID 0000-0001-8153-081X
Shijun YuDepartment of Oncology, Shanghai East Hospital, Tongji University School of Medicine, Shanghai, China.
Xiao WangDepartment of Oncology, Shanghai East Hospital, Tongji University School of Medicine, Shanghai, China.
Xiaojuan YeDepartment of Oncology, Shanghai East Hospital, Tongji University School of Medicine, Shanghai, China.
Bin HeResearch Center for Translational Medicine, Shanghai East Hospital, Tongji University School of Medicine, Shanghai, China.
Ming QuanDepartment of Oncology, Shanghai East Hospital, Tongji University School of Medicine, Shanghai, China.
Yong GaoDepartment of Oncology, Shanghai East Hospital, Tongji University School of Medicine, Shanghai, China.
Shanghai East Hospital · CNZero to Three · US

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Serine-arginine protein kinase 1 (SRPK1) is the main regulator in alternative splicing by phosphorylating splicing factors rich in serine/arginine repeats. Its overexpression has been found in multiple cancer types and contributes to cancer development. Here we report the role of SRPK1 and underlying mechanism in gastric cancer (GC) cell growth. We found that SRPK1 was frequently upregulated in GC samples compared with their adjacent corresponding normal tissues by immunohistochemistry and western blot analysis. Knockdown of SRPK1 in GC cells suppressed cell growth in cell viability assays, colony formation assays and nude mice xenograft model, whereas overexpression of SRPK1 promotes opposite phenotypes in these assays. By a complementary DNA microarray analysis, we found that SRPK1 knockdown had significant inhibitory effects on a majority of small nucleolar RNAs expression. Among them, snoRA42, snoRA74A, and snoRD10 were selected for further functional experiments. Cell growth curves on a plate and in soft agar indicated that the three snoRNAs play potential oncogenic function in GC. In addition, SRPK1 could co-immunoprecipitated with NCL, a nucleolar phosphoprotein involved in the synthesis and maturation of ribosomes. These results suggested that SRPK1 contributes to GC development by a new possible mechanism involving snoRNAs mediated signaling.

Indexed as

AnimalsCell ProliferationGene Expression Regulation, NeoplasticHeterograftsHumansMiceMice, NudeProtein Serine-Threonine KinasesRNA, Small NucleolarStomach NeoplasmsProtein Serine-Threonine KinasesRNA, Small NucleolarSRPK1 protein, humangastric cancersnoRNAsSRPK1tumor growth

Identifiers

PMID30633341
PMCPMC13483285
OpenAlexW2910948872

What OpenQuestion holds

Textmetadata
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.