Evidence map›Paper›PMID 27845896›Full record

ArticleOncotarget2016

Ribosomal protein L34 promotes the proliferation, invasion and metastasis of pancreatic cancer cells.

Feng Wei, Lijuan Ding, Zhentong Wei, Yandong Zhang, Yang Li, Luo Qinghua, Yuteng Ma, Liang Guo, Guoyue Lv, Yan Liu

Abstract read
In one paragraph

Article in Oncotarget, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 27 papers.

0numbers the graph read from it
0cells of the map it votes in
27citing papers in PubMed
–field-weighted citation impact
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

27 citing papers in PubMed.

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  15. Ribosome Biogenesis and Cancer: Overview on Ribosomal Proteins.International journal of molecular sciences · 2021
    Review
  16. Article
  17. Article
  18. Article
  19. Ubiquitin-Proteasome Axis, Especially Ubiquitin-Specific Protease-17 (Reproductive sciences (Thousand Oaks, Calif.) · 2019
    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

10 authors.

Feng WeiDepartment of Hepatobiliary & Pancreas Surgery, The First Hospital of Jilin University, Changchun, Jilin 130021, P.R. China.
Lijuan DingDepartment of Hepatobiliary & Pancreas Surgery, The First Hospital of Jilin University, Changchun, Jilin 130021, P.R. China.
Zhentong WeiOncologic Gynecology, The First Hospital of Jilin University, Changchun, Jilin 130021, P.R. China.
Yandong ZhangDepartment of Hepatobiliary & Pancreas Surgery, The First Hospital of Jilin University, Changchun, Jilin 130021, P.R. China.
Yang LiDepartment of Hepatobiliary & Pancreas Surgery, The First Hospital of Jilin University, Changchun, Jilin 130021, P.R. China.
Luo QinghuaGenetic Engineering Laboratory of PLA, The Eleventh Institute of Academy of Military Medical Sciences of PLA, Jilin 130122, P.R. China.
Yuteng MaDepartment of Hepatobiliary & Pancreas Surgery, The First Hospital of Jilin University, Changchun, Jilin 130021, P.R. China.
Liang GuoPathology, The First Hospital of Jilin University, Changchun, Jilin 130021, P.R. China.
Guoyue LvDepartment of Hepatobiliary & Pancreas Surgery, The First Hospital of Jilin University, Changchun, Jilin 130021, P.R. China.
Yan LiuGenetic Engineering Laboratory of PLA, The Eleventh Institute of Academy of Military Medical Sciences of PLA, Jilin 130122, P.R. China.

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Ribosomal proteins (RPs) are the main components of ribosomes and participate in the self-assembly of ribosomes and protein synthesis. Recent advance has shown that RPs play important roles in the tumorigenesis and drug resistance of various cancers. However, the expression status and function of RPL34 in pancreatic cancer (PC) remains unclear. In this study, we find that RPL34 is overexpressed in PC tissues and cell lines, which is correlated with decreased methylation of its promoter. Knockdown of RPL34 effectively suppresses the proliferation, colony formation, migration and drug-resistance of PC cells, which are accompanied by cell cycle arrest at the G2 phase and induction of apoptosis. In vivo assays demonstrate that RPL34 silencing inhibits PC tumor growth and metastasis. Moreover, gene expression profiling revealed that RPL34 silencing results in alteration of the MAPK and p53 signaling pathways. Clinically, our data indicate a positive association of RPL34 expression with tumor stage and metastasis in PCs. We revealed that RPL34 acts as a potential onco-protein in PC, and RPL34 may be a promising biomarker for prognosis prediction and a potential target for the treatment of PC.

Indexed as

CarcinogenesisGene Expression Regulation, NeoplasticAnimalsCell CycleCell Line, TumorCell MovementCell ProliferationDNA MethylationDrug Resistance, NeoplasmExtracellular Signal-Regulated MAP KinasesFemaleHumansMaleMiceMice, Inbred BALB CMice, NudeExtracellular Signal-Regulated MAP Kinasesribosomal protein L34Ribosomal ProteinsRNA, Small InterferingTumor Suppressor Protein p53ingenuity pathway analysisMAPKmetastasispancreatic cancerRPL34

Identifiers

PMID27845896
PMCPMC5356734

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Registered trials

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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.