Evidence map›Paper›PMID 27367023›Full record

ArticleOncotarget2016

Extracellular translationally controlled tumor protein promotes colorectal cancer invasion and metastasis through Cdc42/JNK/ MMP9 signaling.

Bin Xiao, Daxiang Chen, Shuhong Luo, Wenbo Hao, Fangyan Jing, Tiancai Liu, Suihai Wang, Yan Geng, Linhai Li, Weiwen Xu and 6 more

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 35 papers.

0numbers the graph read from it
0cells of the map it votes in
35citing papers in PubMed
5.1field-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

35 citing papers in PubMed, 49 citations in OpenAlex.

  1. Review
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  8. High Plasma Levels of Fortilin in Patients with Coronary Artery Disease.International journal of molecular sciences · 2022
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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 5 institutions in 2 countries.

Bin XiaoState Key Laboratory of Organ Failure Research, Institute of Antibody Engineering, School of Biotechnology, Southern Medical University, Guangzhou, 510515, Guangdong, China.
Daxiang ChenState Key Laboratory of Organ Failure Research, Institute of Antibody Engineering, School of Biotechnology, Southern Medical University, Guangzhou, 510515, Guangdong, China.
Shuhong LuoState Key Laboratory of Organ Failure Research, Institute of Antibody Engineering, School of Biotechnology, Southern Medical University, Guangzhou, 510515, Guangdong, China.
Wenbo HaoState Key Laboratory of Organ Failure Research, Institute of Antibody Engineering, School of Biotechnology, Southern Medical University, Guangzhou, 510515, Guangdong, China.
Fangyan JingDepartment of Anorectal Surgery, Nanfang Hospital, Southern Medical University, Guangzhou, Guangdong Province, 510515, China.
Tiancai LiuState Key Laboratory of Organ Failure Research, Institute of Antibody Engineering, School of Biotechnology, Southern Medical University, Guangzhou, 510515, Guangdong, China.
Suihai WangState Key Laboratory of Organ Failure Research, Institute of Antibody Engineering, School of Biotechnology, Southern Medical University, Guangzhou, 510515, Guangdong, China.
Yan GengDepartment of Intensive Care Unit, 303 Hospital of People's Liberation Army, Nanning 530021, China.
Linhai LiDepartment of Laboratory Medicine, Guangzhou General Hospital of Guangzhou Military Command of PLA, Guangzhou, Guangdong 510010, China.
Weiwen XuState Key Laboratory of Organ Failure Research, Institute of Antibody Engineering, School of Biotechnology, Southern Medical University, Guangzhou, 510515, Guangdong, China.
Yajie ZhangDivision of Clinical Immunology Laboratory, Nanfang Hospital, Southern Medical University, Guangzhou, Guangdong Province, 510515, China.
Xiaoqing LiaoState Key Laboratory of Organ Failure Research, Institute of Antibody Engineering, School of Biotechnology, Southern Medical University, Guangzhou, 510515, Guangdong, China.
Daming ZuoDepartment of Immunology, School of Basic Medicine, Southern Medical University, Guangzhou, 510515, China.
Yingsong WuState Key Laboratory of Organ Failure Research, Institute of Antibody Engineering, School of Biotechnology, Southern Medical University, Guangzhou, 510515, Guangdong, China.
Ming LiState Key Laboratory of Organ Failure Research, Institute of Antibody Engineering, School of Biotechnology, Southern Medical University, Guangzhou, 510515, Guangdong, China.
Qiang MaState Key Laboratory of Organ Failure Research, Institute of Antibody Engineering, School of Biotechnology, Southern Medical University, Guangzhou, 510515, Guangdong, China.
Southern Medical University · CNNanfang Hospital · CN303 Hospital of People's Liberation Army · CNGeneral Hospital of Guangzhou Military Command · CNRayBiotech (China) · CN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

The translationally controlled tumor protein (TCTP) can be secreted independently of the endoplasmic reticulum/Golgi pathway and has extrinsic activities when it is characterized as the histamine releasing factor (HRF). Despite its important role in allergies and inflammation, little is known about how extracellular TCTP affects cancer progression. In this study, we found that TCTP was overexpressed in the interstitial tissue of colorectal cancer (CRC) and its expression correlated with poor survival, high pathological grades and metastatic TNM stage in CRC patients. TCTP expression was greater in metastatic liver tissue than in primary tumors and was increased in highly invasive CRC cells. We demonstrated that the expression of TCTP was regulated by HIF-1α and its release was increased in response to low serum and hypoxic stress. Recombinant human TCTP (rhTCTP) promoted the migration and invasiveness of CRC cells in vitro and contributed to distant liver metastasis in vivo. Furthermore, rhTCTP activated Cdc42, phosphorylated JNK (p-JNK), increasing the translocation of p-JNK from the cytoplasm to the nucleus, as well as the secretion of MMP9. In addition, the expression of TCTP positively correlated with that of Cdc42 and p-JNK in clinical CRC samples. The silencing of Cdc42, JNK and MMP9 significantly inhibited the Matrigel invasion of rhTCTP-enhanced CRC cells. Collectively, these results identify a new role for extracellular TCTP as a promoter of CRC progression and liver metastases via Cdc42/JNK/MMP9 activation.

Indexed as

AgedAnimalsBiomarkers, Tumorcdc42 GTP-Binding ProteinCell Line, TumorCell MovementColorectal NeoplasmsDisease ProgressionFemaleGene SilencingHumansHypoxiaInflammationLiverMaleMAP Kinase Kinase 4Biomarkers, Tumorcdc42 GTP-Binding ProteinMAP Kinase Kinase 4Matrix Metalloproteinase 9MMP9 protein, humanRecombinant ProteinsTPT1 protein, humanTpt1 protein, mouseTumor Protein, Translationally-Controlled 1Cdc42extracellular TCTPmetastasisp-JNK

Identifiers

PMID27367023
PMCPMC5226568
OpenAlexW2464248307

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.