Evidence map›Paper›PMID 26393879›Full record

ArticleOncotarget2015

HBx-related long non-coding RNA DBH-AS1 promotes cell proliferation and survival by activating MAPK signaling in hepatocellular carcinoma.

Jin-lan Huang, Ting-yu Ren, Shun-wang Cao, Shi-hao Zheng, Xiu-mei Hu, Yan-wei Hu, Li Lin, Jing Chen, Lei Zheng, Qian Wang

Open access · diamondAbstract read
In one paragraph

Article in Oncotarget, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 66 papers, 2 of them syntheses that pooled it.

0numbers the graph read from it
0cells of the map it votes in
66citing papers in PubMed, 2 pooled it
5.4field-weighted citation impact, top 3% 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

66 citing papers in PubMed, 2 syntheses or guidelines pooled it, 98 citations in OpenAlex.

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  4. Vitamin D Reprograms Non-Coding RNA Networks to Block Zika Virus in Human Macrophages.Pathophysiology : the official journal of the International Society for Pathophysiology · 2026
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6 more citing papers are in PubMed but not listed here.

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

10 authors at 3 institutions in 1 country.

Jin-lan HuangLaboratory Medicine Center, Nanfang Hospital, Southern Medical University, Guangzhou, Guangdong, China.
Ting-yu RenLaboratory Medicine Center, Nanfang Hospital, Southern Medical University, Guangzhou, Guangdong, China.
Shun-wang CaoLaboratory Medicine Center, Nanfang Hospital, Southern Medical University, Guangzhou, Guangdong, China.
Shi-hao ZhengDepartment of Neurosurgery, Fujian Provincial Hospital, Fuzhou, Fujian, China.
Xiu-mei HuLaboratory Medicine Center, Nanfang Hospital, Southern Medical University, Guangzhou, Guangdong, China.
Yan-wei HuLaboratory Medicine Center, Nanfang Hospital, Southern Medical University, Guangzhou, Guangdong, China.
Li LinLaboratory Medicine Center, Nanfang Hospital, Southern Medical University, Guangzhou, Guangdong, China.
Jing ChenLaboratory Medicine Center, Nanfang Hospital, Southern Medical University, Guangzhou, Guangdong, China.
Lei ZhengLaboratory Medicine Center, Nanfang Hospital, Southern Medical University, Guangzhou, Guangdong, China.
Qian WangLaboratory Medicine Center, Nanfang Hospital, Southern Medical University, Guangzhou, Guangdong, China.
Nanfang Hospital · CNSouthern Medical University · CNFujian Provincial Hospital · CN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Accumulating evidence supports an important role for the hepatitis B virus x protein (HBx) in the pathogenesis of hepatitis B virus (HBV)-induced hepatocellular carcinoma (HCC), but the underlying mechanisms are not entirely clear. Here, we identified a novel long noncoding RNA (lncRNA) DBH-AS1 involved in the HBx-mediated hepatocarcinogenesis. The levels of DBH-AS1 were positively correlated with hepatitis B surface antigen (HBsAg) and tumor size in HCC tissues. Functionally, transgenic expression of DBH-AS1 significantly enhanced cell proliferation and tumorigenesis, whereas short hairpin RNA knockdown of DBH-AS1 caused an inhibition of cell proliferation. Mechanistically, overexpression of DBH-AS1 induced cell cycle progression by accelerating G1/S and G2/M transition concomitantly with upregulation of CDK6, CCND1, CCNE1 and downregulation of p16, p21 and p27. We also found that enhanced DBH-AS1 expression inhibited serum starvation-induced apoptosis of HCC cells. In contrast, suppressed DBH-AS1 expression had opposite effects. Furthermore, DBH-AS1 was shown to activate MAPK pathway. We also provide evidence that DBH-AS1 could be significantly induced by HBx protein and markedly down-regulated by p53. Thus, we concluded that DBH-AS1 can be induced by HBx and inactivated by p53, and consequently promote cell proliferation and cell survival through activation of MAPK signaling in HCC. Our study suggests that DBH-AS1 acts as an oncogene for HCC.

Indexed as

MAP Kinase Signaling SystemAgedAnimalsApoptosisCarcinoma, HepatocellularCell CycleCell Line, TumorCell ProliferationCell SurvivalCell Transformation, NeoplasticDown-RegulationFemaleGene Expression Regulation, NeoplasticHepatitis B Surface AntigensHep G2 CellsHumansHepatitis B Surface Antigenshepatitis B virus X proteinlong non-coding RNA DBH-AS1, humanRNA, Long NoncodingTP53 protein, humanTrans-ActivatorsTumor Suppressor Protein p53Viral Regulatory and Accessory ProteinsDBH-AS1HBxHCClncRNAproliferation

Identifiers

PMID26393879
PMCPMC4741803
OpenAlexW2236101211

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.