Evidence map›Paper›PMID 25909168›Full record

ArticleOncotarget2015

Epigenetic silencing of BCL6B inactivates p53 signaling and causes human hepatocellular carcinoma cell resist to 5-FU.

Xin Li, Jie Yu, Malcolm V Brock, Qian Tao, James G Herman, Ping Liang, Mingzhou Guo

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 25 papers.

0numbers the graph read from it
0cells of the map it votes in
25citing papers in PubMed
2.6field-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

25 citing papers in PubMed, 34 citations in OpenAlex.

  1. Article
  2. Review
  3. Dynamic changes of DNA methylation induced by benzo(a)pyrene in cancer.Genes and environment : the official journal of the Japanese Environmental Mutagen Society · 2023
    Review
  4. Article
  5. IsolatedCancers · 2022
    Article
  6. Article
  7. Article
  8. Article
  9. Article
  10. Epigenetic heterogeneity in cancer.Biomarker research · 2019
    Review
  11. Article
  12. Article
  13. Article
  14. Article
  15. Article
  16. Article
  17. Article
  18. Article
  19. Article
  20. Article
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 2 countries.

Xin LiDepartment of Interventional Ultrasound, Chinese PLA General Hospital, Beijing, China.
Jie YuDepartment of Interventional Ultrasound, Chinese PLA General Hospital, Beijing, China.
Malcolm V BrockOncology Center, Johns Hopkins University, Baltimore, Maryland, USA.
Qian TaoDepartment of Clinical Oncology, The Chinese University of Hong Kong, Hong Kong, China.
James G HermanOncology Center, Johns Hopkins University, Baltimore, Maryland, USA.
Ping LiangDepartment of Interventional Ultrasound, Chinese PLA General Hospital, Beijing, China.
Mingzhou GuoDepartment of Gastroenterology & Hepatology, Chinese PLA General Hospital, Beijing, China.
Chinese PLA General Hospital · CNJohns Hopkins University · USChinese University of Hong Kong · CN

Funding

MIF in progression and treatment of ALDU01AA020821 · NIAAA · CLEVELAND CLINIC LERNER COM-CWRU · PI NAGY, LAURA E. · 2012 to 2016
$2.1M
Corticostriatal networks and NMDAR mediation of habitual and flexible actionK22AA020303 · NIAAA · UNIVERSITY OF NEW MEXICO HEALTH SCIS CTR · PI BRIGMAN, JONATHAN L · 2011 to 2013
$486k
NIAAA NIH HHS K22 AA020303NIAAA NIH HHS U01 AA020821
6 · The paper itself

Abstract

BCL6B is a potential tumor suppressor in human gastric cancer, but the regulation and mechanism of BCL6B in human hepatocellular carcinogenesis remain unclear. This study is to explore the epigenetic change and mechanism of BCL6B in human hepatocellular carcinoma (HCC). Nineteen hepatic cancer cell lines, 50 cases of adjacent tissue and 149 cases of HCC samples were employed. BCL6B is methylated in 100% (19/19) of human HCC cell lines, 40.0% (20/50) of adjacent tissue samples and 86.6% (129/149) of primary cancer samples. Methylation of BCL6B is associated with HBV positive (p < 0.05). But no association was found with age, sex, tumor size, differentiation, TNM stage, recurrence and survival. Loss of BCL6B expression was found in 19 of completely methylated HCC cell lines. BCL6B was re-expressed after 5-aza-2'-deoxycytidine treatment. Restoration of BCL6B expression suppressed cell proliferation, induced apoptosis and G1/S arrest in HCC cells. The expression of EGR1, a key component of p53 signaling, was increased after re-expression BCL6B in HCC cells. Re-expression of BCL6B activated p53 signaling and sensitized HCC cells to 5-fluorouracil. BCL6B is frequently methylated in human HCC and the expression of BCL6B is regulated by promoter region hypermethylation. BCL6B activates p53 signaling by increasing EGR1 expression in HCC.

Indexed as

Gene SilencingAgedAntimetabolites, AntineoplasticApoptosisAzacitidineCarcinoma, HepatocellularCell ProliferationDecitabineDNA MethylationDNA Modification MethylasesDrug Resistance, NeoplasmEarly Growth Response Protein 1Enzyme InhibitorsFemaleFluorouracilG1 Phase Cell Cycle CheckpointsAntimetabolites, AntineoplasticAzacitidineBCL6B protein, humanDecitabineDNA Modification MethylasesEarly Growth Response Protein 1EGR1 protein, humanEnzyme InhibitorsFluorouracilRepressor ProteinsTP53 protein, humanTumor Suppressor Protein p535-fluorouracilBCL6BDNA methylationhepatocellular carcinomap53 signaling

Identifiers

PMID25909168
PMCPMC4484475
OpenAlexW1938694911

What OpenQuestion holds

Textmetadata
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.