Evidence map›Paper›PMID 27156963›Full record

ArticleScientific reports2016

Loss of the 14-3-3σ is essential for LASP1-mediated colorectal cancer progression via activating PI3K/AKT signaling pathway.

Ziyun Shao, Yanjun Cai, Lijun Xu, Xueqing Yao, Jiaolong Shi, Feifei Zhang, Yuhao Luo, Kehong Zheng, Jian Liu, Fengliu Deng and 6 more

Open access · goldAbstract read
In one paragraph

Article in Scientific reports, 2016. 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
1.7field-weighted citation impact, top 15% 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, 34 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

16 authors at 6 institutions in 1 country.

Ziyun ShaoDepartment of Pathology, Nanfang Hospital, Southern Medical University, Guangzhou, China.
Yanjun CaiDepartment of Gerontology, Guangzhou General Hospital of the Guangzhou Military Command of the People's Liberation Army (PLA), Guangzhou, China.
Lijun XuDepartment of Pathology, Nanfang Hospital, Southern Medical University, Guangzhou, China.
Xueqing YaoThe Department of General Surgery, Guangdong General Hospital, Guangdong Academy of Medical Science, Guangzhou, Guangdong, China.
Jiaolong ShiDepartment of Pathology, Nanfang Hospital, Southern Medical University, Guangzhou, China.
Feifei ZhangDepartment of Pathology, Nanfang Hospital, Southern Medical University, Guangzhou, China.
Yuhao LuoDepartment of Pathology, Nanfang Hospital, Southern Medical University, Guangzhou, China.
Kehong ZhengDepartment of General Surgery, Zhujiang Hospital, Southern Medical University, Guangzhou, China.
Jian LiuDepartment of Pathology, Nanfang Hospital, Southern Medical University, Guangzhou, China.
Fengliu DengDepartment of Pathology, Nanfang Hospital, Southern Medical University, Guangzhou, China.
Rui LiDepartment of Pathology, Nanfang Hospital, Southern Medical University, Guangzhou, China.
Lanzhi ZhangDepartment of Pathology, Nanfang Hospital, Southern Medical University, Guangzhou, China.
Hui WangDepartment of Medical Oncology, Affiliated Tumor Hospital of Guangzhou Medical University, Guangzhou, China.
Mingyi LiRadiotherapy Department, Affiliated Tumor Hospital of Guangzhou Medical University, Guangzhou, China.
Yanqing DingDepartment of Pathology, Nanfang Hospital, Southern Medical University, Guangzhou, China.
Liang ZhaoDepartment of Pathology, Nanfang Hospital, Southern Medical University, Guangzhou, China.
Nanfang Hospital · CNSouthern Medical University · CNGuangzhou Medical University Cancer Hospital · CNGeneral Hospital of Guangzhou Military Command · CNGuangdong General Hospital · CNZhujiang Hospital · CN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

LIM and SH3 protein 1 (LASP1) can promote colorectal cancer (CRC) progression and metastasis, but the direct evidence that elucidates the molecular mechanism remains unclear. Here, our proteomic data showed that LASP1 interacted with 14-3-3σ and decreased the expression of 14-3-3σ in CRC. Deletion of 14-3-3σ was required for LASP1-mediated CRC cell aggressiveness. In vitro gain- and loss-of-function assays showed that 14-3-3σ suppressed the ability of cell migration and decreased the phosphorylation of AKT in CRC cells. We further observed clearly co-localization between AKT and 14-3-3σ in CRC cells. Treatment of PI3K inhibitor LY294002 markedly prevented phosphorylation of AKT and subsequently counteract aggressive phenotype mediated by siRNA of 14-3-3σ. Clinically, 14-3-3σ is frequently down-regulated in CRC tissues. Down-regulation of 14-3-3σ is associated with tumor progression and poor prognosis of patients with CRC. Multivariate analysis confirmed low expression of 14-3-3σ as an independent prognostic factor for CRC. A combination of low 14-3-3σ and high LASP1 expression shows a worse trend with overall survival of CRC patients. Our research paves the path to future investigation of the LASP1-14-3-3σ axis as a target for novel anticancer therapies of advanced CRC.

Indexed as

Disease ProgressionSignal Transduction14-3-3 ProteinsAdaptor Proteins, Signal TransducingCell Line, TumorCell MovementColorectal NeoplasmsCytoskeletal ProteinsDown-RegulationElectrophoresis, Gel, Two-DimensionalHumansLIM Domain ProteinsModels, BiologicalNeoplasm InvasivenessPhosphatidylinositol 3-KinasesPhosphorylation14-3-3 ProteinsAdaptor Proteins, Signal TransducingCytoskeletal ProteinsLASP1 protein, humanLIM Domain ProteinsPhosphatidylinositol 3-KinasesProto-Oncogene Proteins c-akt

Identifiers

PMID27156963
PMCPMC4860602
OpenAlexW2346820475

What OpenQuestion holds

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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.