Evidence map›Paper›PMID 27344168›Full record

ArticleMolecular and cellular biochemistry2016

Valosin-containing protein (VCP) promotes the growth, invasion, and metastasis of colorectal cancer through activation of STAT3 signaling.

Qianfeng Fu, Yuling Jiang, Daxin Zhang, Xiuli Liu, Junfeng Guo, Jinlong Zhao

Open access · hybridAbstract read
In one paragraph

Article in Molecular and cellular biochemistry, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 22 papers.

0numbers the graph read from it
0cells of the map it votes in
22citing papers in PubMed
2.4field-weighted citation impact, top 11% 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

22 citing papers in PubMed, 38 citations in OpenAlex.

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  8. The mechanism of VCP-mediated metastasis of osteosarcoma based on cell autophagy and the EMT pathway.Clinical & translational oncology : official publication of the Federation of Spanish Oncology Societies and of the National Cancer Institute of Mexico · 2023
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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.

Qianfeng FuDepartment of Oncology, The First Affiliated Hospital of Harbin Medical University, No. 23 Youzheng Street, Harbin, 150001, Heilongjiang, China.
Yuling JiangDepartment of Clinical Laborotary, The First Affiliated Hospital of Harbin Medical University, No. 23 Youzheng Street, Harbin, 150001, Heilongjiang, China.
Daxin ZhangDepartment of Oncology, The First Affiliated Hospital of Harbin Medical University, No. 23 Youzheng Street, Harbin, 150001, Heilongjiang, China.
Xiuli LiuDepartment of Oncology, The First Affiliated Hospital of Harbin Medical University, No. 23 Youzheng Street, Harbin, 150001, Heilongjiang, China.
Junfeng GuoDepartment of Oncology, The First Affiliated Hospital of Harbin Medical University, No. 23 Youzheng Street, Harbin, 150001, Heilongjiang, China.
Jinlong ZhaoDepartment of Oncology, The First Affiliated Hospital of Harbin Medical University, No. 23 Youzheng Street, Harbin, 150001, Heilongjiang, China. fuqianfeng2016@yeah.net.
First Affiliated Hospital of Harbin Medical University · CNHarbin Medical University · CN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Valosin-containing protein (VCP) was previously shown to exhibit high expression in colorectal cancer (CRC) tissues as compared with that in normal tissues; however, the role of VCP in human CRC cells has remained to be elucidated. Two colorectal cancer cell lines HCT116 and RKO were used in the experiment. We introduced lentiviral constructs expressing VCP to infect RKO cells and lenti-shRNA targeting VCP into HCT116 cells, respectively. Cell proliferation, invasion, apoptosis, and cell cycle arrest were subsequently examined by MTT assay, transwell chamber assay, flow cytometry, and western blot analysis, respectively. Furthermore, a subcutaneous tumor mouse model and lung metastasis model was used to investigate the effects of VCP on the growth and metastasis of CRC cells in vivo. VCP knockdown was shown to inhibit cell proliferation, chemoresistance and invasion, and induce apoptosis in the HCT116 CRC cells, whereas VCP over-expression suppressed apoptosis and chemoresponse, promoted proliferation and invasion of the RKO CRC cells. In addition, in the subcutaneous tumor and lung metastasis mouse model, VCP knockdown in HCT116 cells suppressed carcinogenesis and metastasis in vivo. The findings of the present study indicated that VCP is very important for the proliferation and metastasis of CRC; therefore, targeting VCP and its downstream targets may represent novel therapies for the treatment of CRC.

Indexed as

Cell ProliferationSignal TransductionAdenosine TriphosphatasesAnimalsCell Cycle ProteinsCell Line, TumorColorectal NeoplasmsHeterograftsHumansMiceNeoplasm InvasivenessNeoplasm MetastasisNeoplasm ProteinsNeoplasm TransplantationSTAT3 Transcription FactorValosin Containing ProteinAdenosine TriphosphatasesCell Cycle ProteinsNeoplasm ProteinsSTAT3 protein, humanSTAT3 Transcription FactorValosin Containing ProteinVCP protein, humanVcp protein, mouseColorectal cancerMetastasisProliferationSTAT3Valosin-containing protein

Identifiers

PMID27344168
PMCPMC4927615
OpenAlexW2464814890

What OpenQuestion holds

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LicenceCC BY
Read underepoch 390

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.