Evidence map›Paper›PMID 30202243›Full record

ArticleCancer cell international2018

SH2B1 promotes NSCLC cell proliferation through PI3K/Akt/mTOR signaling cascade.

Shaoqiang Wang, Yingying Zheng, Zhiwei He, Wolong Zhou, Yuanda Cheng, Chunfang Zhang

Open access · goldAbstract read
In one paragraph

Article in Cancer cell international, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 13 papers.

0numbers the graph read from it
0cells of the map it votes in
13citing papers in PubMed
1.2field-weighted citation impact, top 21% 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

13 citing papers in PubMed, 20 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

6 authors at 2 institutions in 1 country.

Shaoqiang Wang1Department of Thoracic Surgery, Affiliated Hospital of Jining Medical University, Jining Medical University, Jining, 272029 Shandong People's Republic of China.
Yingying Zheng2Department of Endocrinology, Affiliated Hospital of Jining Medical University, Jining Medical University, Jining, 272029 Shandong People's Republic of China.
Zhiwei He3Department of Thoracic Surgery, Xiangya Hospital, Central South University, No. 87, Xiangya Road, Changsha, 410008 Hunan People's Republic of China.
Wolong Zhou3Department of Thoracic Surgery, Xiangya Hospital, Central South University, No. 87, Xiangya Road, Changsha, 410008 Hunan People's Republic of China.
Yuanda Cheng3Department of Thoracic Surgery, Xiangya Hospital, Central South University, No. 87, Xiangya Road, Changsha, 410008 Hunan People's Republic of China.
Chunfang Zhang3Department of Thoracic Surgery, Xiangya Hospital, Central South University, No. 87, Xiangya Road, Changsha, 410008 Hunan People's Republic of China.ORCID 0000-0002-1339-4091
Central South University · CNAffiliated Hospital of Jining Medical University · CN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

backgroundNon-small cell lung cancer (NSCLC), the most prevalent type of human lung cancer, is characterized by many molecular abnormalities. SH2B1, a member of the SH2-domain containing family, have recently been shown to act as tumor activators in multiple cancers. The objective of this study was to investigate the role SH2B1 and the underlying molecular mechanism in NSCLC.

methodsCell functional analysis and cell line-derived xenograft model were performed to determine SH2B1 potential roles on NSCLC cell proliferation in vitro and in vivo. In vitro assays were performed to identify signal molecular mechanisms. Subsequently, 104 patients with NSCLC undergoing primary surgical resection were recruited to evaluated expression of SH2B1 and Akt/mTOR signaling markers by immunohistochemical staining to determine their clinicopathologic significance.

resultsModulation of SH2B1 expression levels had distinct effects on cell proliferation, cell cycle and apoptosis in the NSCLC cell lines A549 and H1299. At the molecular level, overexpression of SH2B1 resulted in the upregulation of the Akt/mTOR markers, p-Akt and p-mTOR, and downregulation of PTEN to promote NSCLC cell proliferation, while silencing SH2B1 had the opposite effect. In human NSCLC specimens, SH2B1 expression levels were positively associated with Akt/mTOR signaling pathway markers.

conclusionsThe SH2B1/Akt/mTOR/PTEN axis is required for regulating NSCLC cell proliferation and might prove to be a promising strategy for restraining tumor progression in NSCLC patients.

Indexed as

AKTNSCLCProliferationSH2B1

Identifiers

PMID30202243
PMCPMC6127928
OpenAlexW2891244375

What OpenQuestion holds

Textmetadata
LicenceCC BY
Read underepoch 390

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.