Evidence map›Paper›PMID 36625246›Full record

ArticleJournal of cellular and molecular medicine2023

Ribosomal protein L22-like1 promotes prostate cancer progression by activating PI3K/Akt/mTOR signalling pathway.

Xiaoyu Yi, Chao Zhang, Baojie Liu, Guojun Gao, Yaqi Tang, Yongzheng Lu, Zhifang Pan, Guohui Wang, Weiguo Feng

Open access · goldAbstract read
In one paragraph

Article in Journal of cellular and molecular medicine, 2023. 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
3.4field-weighted citation impact, top 8% 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, 22 citations in OpenAlex.

  1. Experimental and therapeutic medicine · 2026
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  5. Development of ovine hepatic organoids: a powerfulFrontiers in veterinary science · 2026
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  12. Article
  13. Review
  14. Research Progress of Ribosomal Proteins in Reproductive Development.International journal of molecular sciences · 2024
    Review
  15. Review
  16. Article
  17. Review
  18. Article
  19. Article
  20. 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

9 authors at 2 institutions in 1 country.

Xiaoyu YiSchool of Life Science and Technology, Weifang Medical University, Weifang, China.
Chao ZhangDepartment of Urology Surgery, Shandong Cancer Hospital and Institute, Jinan, China.
Baojie LiuSchool of Life Science and Technology, Weifang Medical University, Weifang, China.
Guojun GaoDepartment of Urology Surgery, Affiliated Hospital of Weifang Medical University, Weifang, China.
Yaqi TangSchool of Life Science and Technology, Weifang Medical University, Weifang, China.
Yongzheng LuSchool of Life Science and Technology, Weifang Medical University, Weifang, China.
Zhifang PanSchool of Life Science and Technology, Weifang Medical University, Weifang, China.
Guohui WangSchool of Life Science and Technology, Weifang Medical University, Weifang, China.
Weiguo FengSchool of Life Science and Technology, Weifang Medical University, Weifang, China.ORCID 0000-0003-1366-9208
Weifang Medical University · CNShandong Tumor Hospital · CN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Prostate cancer (PCa) is one of the most common malignancies in men. Ribosomal protein L22-like1 (RPL22L1), a component of the ribosomal 60 S subunit, is associated with cancer progression, but the role and potential mechanism of RPL22L1 in PCa remain unclear. The aim of this study was to investigate the role of RPL22L1 in PCa progression and the mechanisms involved. Bioinformatics and immunohistochemistry analysis showed that the expression of RPL22L1 was significantly higher in PCa tissues than in normal prostate tissues. The cell function analysis revealed that RPL22L1 significantly promoted the proliferation, migration and invasion of PCa cells. The data of xenograft tumour assay suggested that the low expression of RPL22L1 inhibited the growth and invasion of PCa cells in vivo. Mechanistically, the results of Western blot proved that RPL22L1 activated PI3K/Akt/mTOR pathway in PCa cells. Additionally, LY294002, an inhibitor of PI3K/Akt pathway, was used to block this pathway. The results showed that LY294002 remarkably abrogated the oncogenic effect of RPL22L1 on PCa cell proliferation and invasion. Taken together, our study demonstrated that RPL22L1 is a key gene in PCa progression and promotes PCa cell proliferation and invasion via PI3K/Akt/mTOR pathway, thus potentially providing a new target for PCa therapy.

Indexed as

ProstateProstatic NeoplasmsCell Line, TumorCell MovementCell ProliferationHumansMalePhosphatidylinositol 3-KinasesProto-Oncogene Proteins c-aktRibosomal ProteinsTOR Serine-Threonine KinasesMTOR protein, humanPhosphatidylinositol 3-KinasesProto-Oncogene Proteins c-aktRibosomal ProteinsTOR Serine-Threonine KinasesinvasionPI3K/Akt/mTORproliferationprostate cancerRPL22L1

Identifiers

PMID36625246
PMCPMC9889667
OpenAlexW4315435063

What OpenQuestion 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 OpenQuestion graph.