Evidence map›Paper›PMID 25238232›Full record

ArticlePloS one2014

ROCK is involved in vasculogenic mimicry formation in hepatocellular carcinoma cell line.

Ji-Gang Zhang, Xiao-Yu Li, Yu-Zhu Wang, Qi-Di Zhang, Sheng-Ying Gu, Xin Wu, Guan-Hua Zhu, Qin Li, Gao-Lin Liu

Abstract read
PubMed Full text at PMC Publisher
In one paragraph

Article in PloS one, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 28 papers.

0numbers the graph read from it
0cells of the map it votes in
28citing papers in PubMed
–field-weighted citation impact
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

28 citing papers in PubMed.

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  17. [Nan fang yi ke da xue xue bao = Journal of Southern Medical University · 2018
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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

9 authors.

Ji-Gang ZhangDepartment of Pharmacy, Shanghai First People's Hospital, School of medicine, Shanghai Jiao Tong University, Shanghai, P.R. China.
Xiao-Yu LiDepartment of Pharmacy, Shanghai First People's Hospital, School of medicine, Shanghai Jiao Tong University, Shanghai, P.R. China.
Yu-Zhu WangDepartment of Pharmacy, Shanghai First People's Hospital, School of medicine, Shanghai Jiao Tong University, Shanghai, P.R. China.
Qi-Di ZhangDepartment of Gastroenterology, Shanghai First People's Hospital, School of medicine, Shanghai Jiao Tong University, Shanghai, P.R. China.
Sheng-Ying GuDepartment of Pharmacy, Shanghai First People's Hospital, School of medicine, Shanghai Jiao Tong University, Shanghai, P.R. China.
Xin WuDepartment of Pharmacy, Shanghai First People's Hospital, School of medicine, Shanghai Jiao Tong University, Shanghai, P.R. China.
Guan-Hua ZhuDepartment of Pharmacy, Shanghai First People's Hospital, School of medicine, Shanghai Jiao Tong University, Shanghai, P.R. China.
Qin LiDepartment of Pharmacy, Shanghai First People's Hospital, School of medicine, Shanghai Jiao Tong University, Shanghai, P.R. China.
Gao-Lin LiuDepartment of Pharmacy, Shanghai First People's Hospital, School of medicine, Shanghai Jiao Tong University, Shanghai, P.R. China.

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Ras homolog family member A (RhoA) and Rho-associated coiled coil-containing protein kinases 1 and 2 (ROCK1 and 2) are key regulators of focal adhesion, actomyosin contraction and cell motility. RhoA/ROCK signaling has emerged as an attractive target for the development of new cancer therapeutics. Whether RhoA/ROCK is involved in regulating the formation of tumor cell vasculogenic mimicry (VM) is largely unknown. To confirm this hypothesis, we performed in vitro experiments using hepatocellular carcinoma (HCC) cell lines. Firstly, we demonstrated that HCC cells with higher active RhoA/ROCK expression were prone to form VM channels, as compared with RhoA/ROCK low-expressing cells. Furthermore, Y27632 (a specific inhibitor of ROCK) rather than exoenzyme C3 (a specific inhibitor of RhoA) effectively inhibited the formation of tubular network structures in a dose-dependent manner. To elucidate the possible mechanism of ROCK on VM formation, real-time qPCR, western blot and immunofluorescence were used to detect changes of the key VM-related factors, including VE-cadherin, erythropoietin-producing hepatocellular carcinoma-A2 (EphA2), phosphoinositide 3-kinase (PI3K), matrix metalloproteinase (MMP)14, MMP2, MMP9 and laminin 5γ2-chain (LAMC2), and epithelial-mesenchymal-transition (EMT) markers: E-cadherin and Vimentin. The results showed that all the expression profiles were attenuated by blockage of ROCK. In addition, in vitro cell migration and invasion assays showed that Y27632 inhibited the migration and invasion capacity of HCC cell lines in a dose-dependent manner markedly. These data indicate that ROCK is an important mediator in the formation of tumor cell VM, and suggest that ROCK inhibition may prove useful in the treatment of VM in HCC.

Indexed as

AmidesApoptosisBiomarkers, TumorCarcinoma, HepatocellularCell Line, TumorCell MovementEpithelial-Mesenchymal TransitionHep G2 CellsHumansHuman Umbilical Vein Endothelial CellsLiver NeoplasmsNeoplasm InvasivenessNeovascularization, PathologicPyridinesrhoA GTP-Binding Proteinrho-Associated KinasesAmidesBiomarkers, TumorPyridinesrhoA GTP-Binding Proteinrho-Associated KinasesROCK1 protein, humanROCK2 protein, humanY 27632

Identifiers

PMID25238232
PMCPMC4169566

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.