Evidence map›Paper›PMID 26499944›Full record

ArticleTumour biology : the journal of the International Society for Oncodevelopmental Biology and Medicine2016

HMGB1 promotes HCC progression partly by downregulating p21 via ERK/c-Myc pathway and upregulating MMP-2.

Yanmei Chen, Chengzhao Lin, Yang Liu, Yan Jiang

Open access · hybridAbstract read
In one paragraph

Article in Tumour biology : the journal of the International Society for Oncodevelopmental Biology and Medicine, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 27 papers.

0numbers the graph read from it
0cells of the map it votes in
27citing papers in PubMed
3.0field-weighted citation impact, top 9% 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

27 citing papers in PubMed, 52 citations in OpenAlex.

  1. Article
  2. Emerging Roles of High-mobility Group Box-1 in Liver Disease.Journal of clinical and translational hepatology · 2024
    Review
  3. Article
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  12. The Journal of international medical research · 2021
    Article
  13. Frontiers in microbiology · 2021
    Article
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  15. Article
  16. Review
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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

4 authors at 1 institution in 1 country.

Yanmei ChenInstitutes of Biomedical Sciences, Shanghai Medical College, Fudan University, Yixueyuan Rd 138, Shanghai, 200032, China.
Chengzhao LinInstitutes of Biomedical Sciences, Shanghai Medical College, Fudan University, Yixueyuan Rd 138, Shanghai, 200032, China.
Yang LiuInstitutes of Biomedical Sciences, Shanghai Medical College, Fudan University, Yixueyuan Rd 138, Shanghai, 200032, China.
Yan JiangInstitutes of Biomedical Sciences, Shanghai Medical College, Fudan University, Yixueyuan Rd 138, Shanghai, 200032, China. jiangyan515@fudan.edu.cn.
Shanghai Medical College of Fudan University · CN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

High-mobility group box 1 (HMGB1) was found to be over-expressed in many kinds of human cancer, which binds with several receptors and activates RAGE-Ras-MAPK, Toll-like receptors, NF-κB, and Src family kinase signaling pathways and plays a crucial role in tumorigenesis and cancer progression. However, the function and mechanism of HMGB1 in hepatocellular carcinoma (HCC) remain unclear. The aim of this study was to investigate the effect of HMGB1 on HCC progression and explore new molecular mechanism. HMGB1 transient knockdown, stable knockdown, and re-expression were performed by transfection with specific siRNA, shRNA, or expression vector in HCCLM3 cells. Results showed that transient knockdown HMGB1 prevented cell proliferation, promoted apoptosis, induced S phase arrest, and inhibited migration and invasion in vitro, and stable knockdown HMGB1 inhibited xenograft growth in Balb/c athymic mice in vivo. Molecular mechanism investigation revealed that knockdown HMGB1 significantly reduced the activation of MAPKs, including ERK1/2, p38, SAPK/JNK, as well as MAPKKs (MEK1/2, SEK1) and its substrates (c-Jun, c-Myc); downregulated NF-κB/p65 expression and phosphorylation level; decreased MMP-2 expression and activity; and upregulated p21 expression. Interestingly, c-Myc was firstly found to be involved in the promoting function of HMGB1 on HCC progression, which provided a novel clue for the inhibitory effect of HMGB1 on p21 expression by a p53-independent pathway. Collectively, these findings indicated that HMGB1 promoted HCC progression partly by enhancing the ERK1/2 and NF-κB pathways, upregulating MMP-2, and downregulating p21 via an ERK/c-Myc pathway.

Indexed as

AnimalsCarcinogenesisCarcinoma, HepatocellularCell ProliferationCyclin-Dependent Kinase Inhibitor p21Disease ProgressionGene Expression Regulation, NeoplasticHMGB1 ProteinHumansLiver NeoplasmsMAP Kinase Signaling SystemMatrix Metalloproteinase 2MiceNeoplasm InvasivenessNF-kappa BProto-Oncogene Proteins c-mycCDKN1A protein, humanCyclin-Dependent Kinase Inhibitor p21HMGB1 ProteinMatrix Metalloproteinase 2MYC protein, humanNF-kappa BProto-Oncogene Proteins c-mycTumor Suppressor Protein p53c-MycHCCHMGB1MAPKsMMP-2p21

Identifiers

PMID26499944
PMCPMC4844642
OpenAlexW2145457154

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.