Evidence map›Paper›PMID 30940322›Full record

ArticleBMB reports2019

Insufficient radiofrequency ablation-induced autophagy contributes to the rapid progression of residual hepatocellular carcinoma through the HIF-1α/BNIP3 signaling pathway.

Wen-Lei Xu, Shao-Hong Wang, Wen-Bing Sun, Jun Gao, Xue-Mei Ding, Jian Kong, Li Xu, Shan Ke

Open access · goldAbstract readNews
PubMed Full text at PMC
In one paragraph

Article in BMB reports, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 29 papers.

0numbers the graph read from it
0cells of the map it votes in
29citing papers in PubMed
2.7field-weighted citation impact, top 10% 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

29 citing papers in PubMed, 42 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

8 authors at 2 institutions in 1 country.

Wen-Lei XuDepartment of Hepatobiliary Surgery, Beijing Chao-yang Hospital Affiliated to Capital Medical University, Beijing 100043, China.
Shao-Hong WangDepartment of Hepatobiliary Surgery, Beijing Chao-yang Hospital Affiliated to Capital Medical University, Beijing 100043, China.
Wen-Bing SunDepartment of Hepatobiliary Surgery, Beijing Chao-yang Hospital Affiliated to Capital Medical University, Beijing 100043, China.
Jun GaoDepartment of Hepatobiliary Surgery, Beijing Chao-yang Hospital Affiliated to Capital Medical University, Beijing 100043, China.
Xue-Mei DingDepartment of Hepatobiliary Surgery, Beijing Chao-yang Hospital Affiliated to Capital Medical University, Beijing 100043, China.
Jian KongDepartment of Hepatobiliary Surgery, Beijing Chao-yang Hospital Affiliated to Capital Medical University, Beijing 100043, China.
Li XuDepartment of Hepatobiliary Surgery, Beijing Chao-yang Hospital Affiliated to Capital Medical University, Beijing 100043, China.
Shan KeDepartment of Hepatobiliary Surgery, Beijing Chao-yang Hospital Affiliated to Capital Medical University, Beijing 100043, China.
Capital Medical University · CNBeijing Chao-Yang Hospital · CN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Currently speaking, it is noted that radiofrequency ablation (RFA) has been the most widely used treatment for hepatocellular carcinoma (HCC) occurring in patients. However, accumulating evidence has demonstrated that the incidence of insufficient RFA (IRFA) may result in the identified rapid progression of residual HCC in the patient, which can greatly hinder the effectiveness and patient reported benefits of utilizing this technique. Although many efforts have been proposed, the underlying mechanisms triggering the rapid progression of residual HCC after IRFA have not yet been fully clarified through current research literature reviews. It was shown in this study that cell proliferation, migration and invasion of residual HepG2 and SMMC7721 cells were significantly increased after the IRFA was simulated in vitro. In other words, it is noted that IRFA could do this by enhancing the image of autophagy of the residual HCC cell via the HIF-1α/BNIP3 pathway. Consequently, the down-regulation of BNIP3 may result in the inhibition of the residual HCC cell progression and autophagy after IRFA. Our present study results suggest that IRFA could promote residual HCC cell progression in vitro by enhancing autophagy via the HIF-1α/BNIP3 pathway. For this reason, it is noted that the targeting of the BNIP3 may be useful in preventing the rapid growth and metastasis of residual HCC after IRFA. [BMB Reports 2019; 52(4): 277-282].

Indexed as

AutophagyCarcinoma, HepatocellularCell Line, TumorDisease ProgressionHep G2 CellsHumansHypoxia-Inducible Factor 1, alpha SubunitLiver NeoplasmsMembrane ProteinsProto-Oncogene ProteinsRadiofrequency AblationSignal TransductionBNIP3 protein, humanHIF1A protein, humanHypoxia-Inducible Factor 1, alpha SubunitMembrane ProteinsProto-Oncogene Proteins

Identifiers

PMID30940322
PMCPMC6507849
OpenAlexW2943786348

What OpenQuestion holds

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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.