Evidence map›Paper›PMID 27082011›Full record

ArticleInternational journal of oncology2016

Expression and function of CXCL12/CXCR4/CXCR7 in thyroid cancer.

Xiaoli Zhu, Qianming Bai, Yongming Lu, Yiqiong Lu, Linlin Zhu, Xiaoyan Zhou, Lijing Wu

Open access · hybridAbstract read
PubMed Full text at PMC Publisher
In one paragraph

Article in International journal of oncology, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 32 papers.

0numbers the graph read from it
0cells of the map it votes in
32citing papers in PubMed
4.3field-weighted citation impact, top 5% 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

32 citing papers in PubMed, 57 citations in OpenAlex.

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  20. CD163International journal of clinical and experimental pathology · 2018
    Article
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.

Xiaoli ZhuDepartment of Pathology, Fudan University Shanghai Cancer Center, Shanghai 200032, P.R. China.
Qianming BaiDepartment of Pathology, Fudan University Shanghai Cancer Center, Shanghai 200032, P.R. China.
Yongming LuDepartment of Pathology, Fudan University Shanghai Cancer Center, Shanghai 200032, P.R. China.
Yiqiong LuDepartment of Pathology, Fudan University Shanghai Cancer Center, Shanghai 200032, P.R. China.
Linlin ZhuDepartment of Pathology, Fudan University Shanghai Cancer Center, Shanghai 200032, P.R. China.
Xiaoyan ZhouDepartment of Pathology, Fudan University Shanghai Cancer Center, Shanghai 200032, P.R. China.
Lijing WuDepartment of Pathology, Fudan University Shanghai Cancer Center, Shanghai 200032, P.R. China.
Fudan University Shanghai Cancer Center · CN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

The contribution of CXCL12/CXCR4/CXCR7 axis to cancer progression has been increasingly recognized. However, its role in thyroid cancer development remains unclear. The present study aimed to examine the expression and function of CXCL12 and its receptors in thyroid cancer. The expression of CXCL12/CXCR4/CXCR7 in human tissue specimens of papillary, follicular, medullary, and anaplastic thyroid carcinoma, follicular adenoma, Hashimoto's thyroiditis and nodular goiter were examined by immunohistochemistry using a tissue microarray. CXCR4 and CXCR7 were over-expressed in human thyroid cancer cells K1 by transduction of recombinant lentivirus. The effect of overexpression of CXCR4 and CXCR7 on K1 cell proliferation and invasion and the molecular mechanism underlying the effect were investigated. CXCL12 was exclusively expressed in papillary thyroid carcinoma tissue but absent in other types of thyroid malignancies and benign lesions. CXCR7 was widely expressed in the endothelial cells of all types of malignancy but only occasionally detected in benign lesions. CXCR4 was expressed in 62.5% of papillary thyroid carcinoma tissue specimens and in 30-40% of other types of malignancy, and it was either absent or weakly expressed in benign lesions. CXCL12 stimulated the invasion and migration of K1 cells overexpressing CXCR4, but did not affect K1 cells overexpressing CXCR7. K1 cell proliferation was not affected by overexpression of CXCR4 or CXCR7. Overexpression of CXCR4 in K1 cells significantly increased AKT and ERK phosphorylation and markedly induced the expression and activity of matrix metalloproteinase-2 (MMP‑2). Thus, CXCL12 may be an effective diagnostic marker for papillary thyroid carcinoma, and CXCL12/CXCR4/CXCR7 axis may contribute to thyroid cancer development by regulating cancer cell migration and invasion via AKT and ERK signaling and MMP-2 activation.

Indexed as

Cell Line, TumorCell MovementCell ProliferationChemokine CXCL12Extracellular Signal-Regulated MAP KinasesHumansMatrix Metalloproteinase 2Neoplasm InvasivenessPhosphorylationProto-Oncogene Proteins c-aktReceptors, CXCRReceptors, CXCR4Thyroid NeoplasmsUp-RegulationACKR3 protein, humanChemokine CXCL12CXCL12 protein, humanCXCR4 protein, humanExtracellular Signal-Regulated MAP KinasesMatrix Metalloproteinase 2MMP2 protein, humanProto-Oncogene Proteins c-aktReceptors, CXCRReceptors, CXCR4

Identifiers

PMID27082011
PMCPMC4864059
OpenAlexW2342033711

What OpenQuestion holds

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LicenceCC BY-NC-ND
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Registered trials

None linked

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.