Evidence map›Paper›PMID 30820716›Full record

ArticleJournal of cancer research and clinical oncology2019

Insufficient radiofrequency ablation promotes the metastasis of residual hepatocellular carcinoma cells via upregulating flotillin proteins.

Ning Zhang, Hui Li, Chengdong Qin, Dening Ma, Yiming Zhao, Weiping Zhu, Lu Wang

Open access · hybridAbstract read
In one paragraph

Article in Journal of cancer research and clinical oncology, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 38 papers.

0numbers the graph read from it
0cells of the map it votes in
38citing papers in PubMed
4.7field-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

38 citing papers in PubMed, 52 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

7 authors at 3 institutions in 1 country.

Ning ZhangDepartment of Hepatic Surgery, Fudan University Shanghai Cancer Center, 270 Dong-An Road, Shanghai, 200032, China.ORCID http://orcid.org/0000-0001-8758-5491
Hui LiDepartment of Abdominal Surgery, Linyi Tumor Hospital, 60 Ling-Yuan East Road, Linyi, 276000, China.
Chengdong QinDepartment of Breast Surgery, Zhejiang Cancer Hospital, 1 Ban-Shan East Road, Hangzhou, 310022, China.
Dening MaDepartment of Colorectal Surgery, Zhejiang Cancer Hospital, 1 Ban-Shan East Road, Hangzhou, 310022, China.
Yiming ZhaoDepartment of Hepatic Surgery, Fudan University Shanghai Cancer Center, 270 Dong-An Road, Shanghai, 200032, China.
Weiping ZhuDepartment of Hepatic Surgery, Fudan University Shanghai Cancer Center, 270 Dong-An Road, Shanghai, 200032, China.
Lu WangDepartment of Hepatic Surgery, Fudan University Shanghai Cancer Center, 270 Dong-An Road, Shanghai, 200032, China. cms024mm@163.com.ORCID http://orcid.org/0000-0002-1352-5848
Fudan University Shanghai Cancer Center · CNZhejiang Cancer Hospital · CNLinyi People's Hospital · CN

Funding

National Natural Science Foundation of China 81702371
6 · The paper itself

Abstract

purposeRadiofrequency ablation (RFA) therapy has proven to be effective and feasible for early-stage hepatocellular carcinoma (HCC); however, rapid progression of residual tumor cells after RFA has been confirmed, but the molecular mechanisms of this phenomenon are poorly understood. This study evaluated the effect of the lipid raft proteins known as flotillins on the invasive and metastatic potential of residual HCC.

methodsThe human HCC cell line HCCLM3 was used to establish insufficient RFA models in vivo and in vitro. Changes in cellular morphology, soft agar colony formation, motility, metastasis, and epithelial-mesenchymal transition (EMT) markers after insufficient RFA intervention in vitro and in vivo were detected by real-time PCR, western blotting, immunohistochemistry and transwell assays.

resultsThe results showed that flotillin-1 and flotillin-2 expression were upregulated in HCCLM3 cells following 45 °C heat treatment and in residual HCCLM3 xenografts cells after insufficient RFA. Knocking down flotillin-1 or flotillin-2 in HCCLM3 cells by shRNA significantly lowered insufficient RFA-induced tumor growth, EMT changes, and metastasis in vitro and in vivo. Furthermore, mechanism studies indicated that flotillins altered the EMT status and metastatic potential of heat-treated HCCLM3 cells by activating the Akt/Wnt/β-catenin signaling pathway.

conclusionsOur findings present new evidence that flotillins play a key role in the aggressive behaviors of residual cancer cells after insufficient RFA and provide new insights into the regulatory mechanism of Wnt/β-catenin signaling.

Indexed as

Animalsbeta CateninCarcinoma, HepatocellularCell Line, TumorCell MovementEpithelial-Mesenchymal TransitionHep G2 CellsHumansImmunohistochemistryLiver NeoplasmsMaleMembrane ProteinsMiceMice, Inbred BALB CMice, NudeNeoplasm Metastasisbeta CateninCTNNB1 protein, humanflotillinsMembrane ProteinsProto-Oncogene Proteins c-aktFlotillinHepatocellular cancerMetastasisRadiofrequency ablationβ-Catenin

Identifiers

PMID30820716
PMCPMC6435628
OpenAlexW2920464004

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.