Evidence map›Paper›PMID 26675547›Full record

ArticleOncotarget2016

IL-6 promotes growth and epithelial-mesenchymal transition of CD133+ cells of non-small cell lung cancer.

Soo Ok Lee, Xiaodong Yang, Shanzhou Duan, Ying Tsai, Laura R Strojny, Peter Keng, Yuhchyau Chen

Open access · diamondAbstract 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 55 papers.

0numbers the graph read from it
0cells of the map it votes in
55citing papers in PubMed
4.7field-weighted citation impact, top 4% 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

55 citing papers in PubMed, 75 citations in OpenAlex.

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  19. Radiation oncology (London, England) · 2020
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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 1 institution in 1 country.

Soo Ok LeeDepartment of Radiation Oncology, University of Rochester School of Medicine and Dentistry, Rochester, NY 14642, USA.
Xiaodong YangDepartment of Radiation Oncology, University of Rochester School of Medicine and Dentistry, Rochester, NY 14642, USA.
Shanzhou DuanDepartment of Radiation Oncology, University of Rochester School of Medicine and Dentistry, Rochester, NY 14642, USA.
Ying TsaiDepartment of Radiation Oncology, University of Rochester School of Medicine and Dentistry, Rochester, NY 14642, USA.
Laura R StrojnyDepartment of Radiation Oncology, University of Rochester School of Medicine and Dentistry, Rochester, NY 14642, USA.
Peter KengDepartment of Radiation Oncology, University of Rochester School of Medicine and Dentistry, Rochester, NY 14642, USA.
Yuhchyau ChenDepartment of Radiation Oncology, University of Rochester School of Medicine and Dentistry, Rochester, NY 14642, USA.
University of Rochester · US

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

We examined IL-6 effects on growth, epithelial-mesenchymal transition (EMT) process, and metastatic ability of CD133+ and CD133- cell subpopulations isolated from three non-small cell lung cancer (NSCLC) cell lines: A549, H157, and H1299. We developed IL-6 knocked-down and scramble (sc) control cells of A549 and H157 cell lines by lentiviral infection system, isolated CD133+ and CD133- sub-populations, and investigated the IL-6 role in self-renewal/growth of these cells. IL-6 showed either an inhibitory or lack of effect in modulating growth of CD133- cells depending on intracellular IL-6 levels, but there was higher self-renewal ability of IL-6 expressing CD133+ cells than IL-6 knocked down cells, confirming the promoter role of IL-6 in CD133+ cells growth. We then examined tumor growth of xenografts developed from CD133+ cells of A549IL-6si vs. A549sc cell lines. Consistently, there was retarded growth of tumors developed from A549IL-6si, CD133+ cells compared to tumors originating from A549sc, CD133+ cells. The effect of IL-6 in promoting CD133+ self-renewal was due to hedgehog (Hhg) and Erk signaling pathway activation and higher Bcl-2/Bcl-xL expression. We also investigated whether IL-6 regulates the EMT process of CD133- and CD133+ cells differently. Expression of the EMT/metastasis-associated molecules in IL-6 expressing cells was higher than in IL-6 knocked down cells. Together, we demonstrated dual roles of IL-6 in regulating growth of CD133- and CD133+ subpopulations of lung cancer cells and significant regulation of IL-6 on EMT/metastasis increase in CD133+ cells, not in CD133- cells.

Indexed as

AC133 AntigenAnimalsApoptosisBlotting, WesternCarcinoma, Non-Small-Cell LungCell ProliferationEpithelial-Mesenchymal TransitionFemaleHumansImmunoenzyme TechniquesInterleukin-6Lung NeoplasmsMiceMice, NudeNeoplastic Stem CellsReal-Time Polymerase Chain ReactionAC133 AntigenInterleukin-6PROM1 protein, humanRNA, Messengercancer stem cellsCD133+IL-6non-small cell lung cancerself-renewal

Identifiers

PMID26675547
PMCPMC4872738
OpenAlexW2205615606

What OpenQuestion holds

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LicenceCC BY
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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.