Evidence map›Paper›PMID 35879299›Full record

ReviewCell death & disease2022

Beyond controlling cell size: functional analyses of S6K in tumorigenesis.

Xueji Wu, Wei Xie, Wenxuan Xie, Wenyi Wei, Jianping Guo

Open access · goldAbstract readReview
In one paragraph

Review in Cell death & disease, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 43 papers.

0numbers the graph read from it
0cells of the map it votes in
43citing papers in PubMed
6.5field-weighted citation impact, top 2% 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

43 citing papers in PubMed, 80 citations in OpenAlex.

  1. Review
  2. Article
  3. Article
  4. An siRNA targetingMolecular therapy. Nucleic acids · 2026
    Article
  5. Article
  6. Article
  7. Article
  8. Long non-coding RNA (lncRNA)Translational cancer research · 2026
    Article
  9. Spirocyclic β-lactone secondary metabolites modulate spliceosome function.Proceedings of the National Academy of Sciences of the United States of America · 2026
    Article
  10. Review
  11. Article
  12. Review
  13. Article
  14. Review
  15. Article
  16. PI3 K/AKT/mTOR pathway and its role in breast cancer stem cells.Naunyn-Schmiedeberg's archives of pharmacology · 2025
    Review
  17. Article
  18. Review
  19. Article
  20. Review
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

5 authors at 2 institutions in 2 countries.

Xueji WuDepartment of Liver Surgery, Hepatobiliary Pancreatic Center, the First Affiliated Hospital, Sun Yat-sen University, Guangzhou, Guangdong, 5100080, China.ORCID 0000-0003-4947-7849
Wei XieInstitute of Precision Medicine, the First Affiliated Hospital, Sun Yat-sen University, Guangzhou, Guangdong, 5100080, China.ORCID 0000-0002-7636-1051
Wenxuan XieDepartment of Liver Surgery, Hepatobiliary Pancreatic Center, the First Affiliated Hospital, Sun Yat-sen University, Guangzhou, Guangdong, 5100080, China.
Wenyi WeiDepartment of Pathology, Beth Israel Deaconess Medical Center, Harvard Medical School, Boston, MA, 02115, USA. Wwei2@bidmc.harvard.edu.ORCID 0000-0003-0512-3811
Jianping GuoInstitute of Precision Medicine, the First Affiliated Hospital, Sun Yat-sen University, Guangzhou, Guangdong, 5100080, China. Guojp6@mail.sysu.edu.cn.ORCID 0000-0002-8158-0101
Sun Yat-sen University · CNBeth Israel Deaconess Medical Center · US

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

As a substrate and major effector of the mammalian target of rapamycin complex 1 (mTORC1), the biological functions of ribosomal protein S6 kinase (S6K) have been canonically assigned for cell size control by facilitating mRNA transcription, splicing, and protein synthesis. However, accumulating evidence implies that diverse stimuli and upstream regulators modulate S6K kinase activity, leading to the activation of a plethora of downstream substrates for distinct pathobiological functions. Beyond controlling cell size, S6K simultaneously plays crucial roles in directing cell apoptosis, metabolism, and feedback regulation of its upstream signals. Thus, we comprehensively summarize the emerging upstream regulators, downstream substrates, mouse models, clinical relevance, and candidate inhibitors for S6K and shed light on S6K as a potential therapeutic target for cancers.

Indexed as

Signal TransductionTOR Serine-Threonine KinasesAnimalsCarcinogenesisCell SizeMammalsMicePhosphorylationRibosomal Protein S6 KinasesRibosomal Protein S6 KinasesTOR Serine-Threonine Kinases

Identifiers

PMID35879299
PMCPMC9314331
OpenAlexW4287310036

What Socratic holds

Textmetadata
LicenceCC BY
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 Socratic graph.