Evidence map›Paper›PMID 27298561›Full record

ArticleWorld journal of gastroenterology2016

miR-106b promotes cancer progression in hepatitis B virus-associated hepatocellular carcinoma.

Chia-Sheng Yen, Zhi-Ru Su, Yi-Ping Lee, I-Ting Liu, Chia-Jui Yen

Open access · hybridAbstract read
In one paragraph

Article in World journal of gastroenterology, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 36 papers.

0numbers the graph read from it
0cells of the map it votes in
36citing 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

36 citing papers in PubMed, 57 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

5 authors at 1 institution in 1 country.

Chia-Sheng YenChia-Sheng Yen, Institute of Clinical Medicine, National Cheng Kung University, Tainan 70101, Taiwan.
Zhi-Ru SuChia-Sheng Yen, Institute of Clinical Medicine, National Cheng Kung University, Tainan 70101, Taiwan.
Yi-Ping LeeChia-Sheng Yen, Institute of Clinical Medicine, National Cheng Kung University, Tainan 70101, Taiwan.
I-Ting LiuChia-Sheng Yen, Institute of Clinical Medicine, National Cheng Kung University, Tainan 70101, Taiwan.
Chia-Jui YenChia-Sheng Yen, Institute of Clinical Medicine, National Cheng Kung University, Tainan 70101, Taiwan.
National Cheng Kung University · TW

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

aimTo investigate the effect of miR-106b on tumor progression in hepatitis B virus (HBV)-associated hepatocellular carcinoma (HCC).

methodsA total of 120 patients who underwent liver resection for HCC at National Cheng Kung University Hospital were enrolled in the present study. MicroRNA (miRNA) array was first used to screen the miRNA expression profiles in HCC patients. The clinical records were retrospectively analyzed, and correlations with the miRNA expression profiles were evaluated. The mRNA expression levels of the miR-106b-25 cluster (miR-106b, miR-93 and miR-25), and MCM7 in tumor and non-tumor samples were quantitated using quantitative real-time reverse transcription-polymerase chain reaction (q-RT-PCR) analysis, and correlations in the levels of miR-106b, miR-93 and miR-25 expression were calculated. Kaplan-Meier overall and disease-free survival rates of HBV-associated HCC patients were analyzed using the log-rank test based on miR-106b expression. The comparison of the miR-106b expression levels in patients with different clinical outcomes was analyzed using Mann-Whitney U tests. Furthermore, a hepatitis B virus X protein (HBx) expression plasmid was transfected into Huh7 and Hep 3B cells. The expression levels of the miR-106b-25 cluster and MCM7 in HBx-expressing Huh7 and Hep 3B cells were detected using q-RT-PCR.

resultsmiRNA array screening showed that miR-106b and its cluster, miR-93 and miR-25 were up-regulated in HCC patients (P < 0.01). The value of miR-106b expression in HBV-associated HCC patients was significantly higher than that in HCV- (P < 0.05) or non-B/non-C- (P < 0.001) associated HCC patients. The expression of the miR-106b-25 cluster was significantly higher in tumor tissue (P < 0.001) and associated with the host gene, MCM7, in clinical specimens from HBV-associated HCC patients. Furthermore, the expression levels of miR-106b, miR-93 and miR-25 were positively correlated in HBV-associated HCC tissues (miR-106 vs miR-93, r = 0.75; miR-93 vs miR-25, r = 0.69; miR-106b vs miR-25, r = 0.33). The overall and disease-free survival curves showed that high-miR-106b expression was correlated with the poor prognosis of HBV-associated HCC. HCC differentiation was significantly correlated with miR-106b expression (P < 0.05). Lower miR-106b expression levels resulted in the well differentiation of HCC. Moreover, the expression of the miR106b-25 cluster and MCM7 was up-regulated in Huh7 and Hep 3B cells after transfection with the HBx expression plasmid.

conclusionThe data obtained in the present study suggests that HBx enhances miR-106b transcription to promote tumor progression in HBV-associated HCC.

Indexed as

AdultAgedAged, 80 and overCarcinoma, HepatocellularCell Line, TumorDisease-Free SurvivalFemaleGene Expression ProfilingGene Expression Regulation, NeoplasticHepatitis BHepatitis B virusHumansKaplan-Meier EstimateLiver NeoplasmsMaleMicroRNAshepatitis B virus X proteinMicroRNAsMIRN106 microRNA, humanTrans-ActivatorsViral Regulatory and Accessory ProteinsHepatitis B virusHepatitis B virus X proteinHepatocellular carcinomamiR-106bTumor progression

Identifiers

PMID27298561
PMCPMC4893465
OpenAlexW2415225663

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.