Evidence map›Paper›PMID 28792981›Full record

ArticlePloS one2017

Hyperphosphorylation of RPS6KB1, rather than overexpression, predicts worse prognosis in non-small cell lung cancer patients.

Bojiang Chen, Lan Yang, Rui Zhang, Yuncui Gan, Wen Zhang, Dan Liu, Hong Chen, Huairong Tang

Open access · goldAbstract read
In one paragraph

Article in PloS one, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 22 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
22citing papers in PubMed, 1 pooled it
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

22 citing papers in PubMed, 1 synthesis or guideline pooled it, 41 citations in OpenAlex.

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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

8 authors at 3 institutions in 1 country.

Bojiang ChenDepartment of Respiratory and Critical Care Medicine, West China Hospital of Sichuan University, Chengdu, China.
Lan YangDepartment of Respiratory and Critical Care Medicine, West China Hospital of Sichuan University, Chengdu, China.
Rui ZhangDepartment of Respiratory and Critical Care Medicine, West China Hospital of Sichuan University, Chengdu, China.
Yuncui GanDepartment of Respiratory and Critical Care Medicine, West China Hospital of Sichuan University, Chengdu, China.
Wen ZhangDepartment of Respiratory and Critical Care Medicine, West China Hospital of Sichuan University, Chengdu, China.
Dan LiuDepartment of Respiratory and Critical Care Medicine, West China Hospital of Sichuan University, Chengdu, China.
Hong ChenDepartment of General Medicine, Sichuan Academy of Medical Sciences & Sichuan Provincial People's Hospital, Chengdu, China.
Huairong TangHealth Management Center, West China Hospital, Sichuan University Chengdu, Sichuan, China.
West China Hospital of Sichuan University · CNSichuan University · CNSichuan Academy of Medical Sciences & Sichuan Provincial People's Hospital · CN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

RPS6KB1 is the kinase of ribosomal protein S6 which is 70 kDa and is required for protein translation. Although the abnormal activation of RPS6KB1 has been found in types of diseases, its role and clinical significance in non-small cell lung cancer (NSCLC) has not been fully investigated. In this study, we identified that RPS6KB1 was over-phosphorylated (p-RPS6KB1) in NSCLC and it was an independent unfavorable prognostic marker for NSCLC patients. In spite of the frequent expression of total RPS6KB1 and p-RPS6KB1 in NSCLC specimens by immunohistochemical staining (IHC), only p-RPS6KB1 was associated with the clinicopathologic characteristics of NSCLC subjects. Kaplan-Meier survival analysis revealed that the increased expression of p-RPS6KB1 indicated a poorer 5-year overall survival (OS) for NSCLC patients, while the difference between the positive or negative RPS6KB1 group was not significant. Univariate and multivariate Cox regression analysis was then used to confirm the independent prognostic value of p-RPS6KB1. To illustrate the underlying mechanism of RPS6KB1 phosphorylation in NSCLC, LY2584702 was employed to inhibit the RPS6KB1 phosphorylation specifically both in lung adenocarcinoma cell line A549 and squamous cell carcinoma cell line SK-MES-1. As expected, RPS6KB1 dephosphorylation remarkably suppressed cells proliferation in CCK-8 test, and promoted more cells arresting in G0-G1 phase by cell cycle analysis. Moreover, apoptotic A549 cells with RPS6KB1 dephosphorylation increased dramatically, with an elevating trend in SK-MES-1, indicating a potential involvement of RPS6KB1 phosphorylation in inducing apoptosis. In conclusion, our data suggest that RPS6KB1 is over-activated as p-RPS6KB1 in NSCLC, rather than just the total protein overexpressing. The phosphorylation level of RPS6KB1 might be used as a novel prognostic marker for NSCLC patients.

Indexed as

AdenocarcinomaApoptosisBiomarkers, TumorCarcinoma, Squamous CellCell Line, TumorCell ProliferationHumansImmunohistochemistryLungLung NeoplasmsPhosphorylationPredictive Value of TestsPrognosisRibosomal Protein S6 Kinases, 70-kDaSurvival RateBiomarkers, Tumorribosomal protein S6 kinase, 70kD, polypeptide 1Ribosomal Protein S6 Kinases, 70-kDa

Identifiers

PMID28792981
PMCPMC5549961
OpenAlexW2744114848

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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.