Evidence map›Paper›PMID 30258050›Full record

ArticleCell death & disease2018

HMGB1 promotes ERK-mediated mitochondrial Drp1 phosphorylation for chemoresistance through RAGE in colorectal cancer.

Chih-Yang Huang, Shu-Fen Chiang, William Tzu-Liang Chen, Tao-Wei Ke, Tsung-Wei Chen, Ying-Shu You, Chen-Yu Lin, K S Clifford Chao, Chih-Yang Huang

Open access · goldAbstract read
In one paragraph

Article in Cell death & disease, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 110 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
110citing papers in PubMed, 1 pooled it
10.1field-weighted citation impact, top 1% 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

110 citing papers in PubMed, 1 synthesis or guideline pooled it, 156 citations in OpenAlex.

  1. Pooled it
  2. Article
  3. Article
  4. Berberine AlleviatesInternational journal of molecular sciences · 2026
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  6. Review
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  12. HMGB1: A Central Node in Cancer Therapy Resistance.International journal of molecular sciences · 2025
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  15. Review
  16. Article
  17. Article
  18. Article
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50 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

9 authors at 2 institutions in 1 country.

Chih-Yang HuangTranslation Research Core, China Medical University Hospital, China Medical University, 40402, Taichung, Taiwan.ORCID http://orcid.org/0000-0002-0266-3233
Shu-Fen ChiangCancer Center, China Medical University Hospital, China Medical University, 40402, Taichung, Taiwan.
William Tzu-Liang ChenDepartment of Colorectal Surgery, China Medical University Hospital, China Medical University, 40402, Taichung, Taiwan.
Tao-Wei KeDepartment of Colorectal Surgery, China Medical University Hospital, China Medical University, 40402, Taichung, Taiwan.
Tsung-Wei ChenDepartment of Pathology, China Medical University Hospital, China Medical University, 40402, Taichung, Taiwan.
Ying-Shu YouCancer Center, China Medical University Hospital, China Medical University, 40402, Taichung, Taiwan.
Chen-Yu LinCancer Center, China Medical University Hospital, China Medical University, 40402, Taichung, Taiwan.
K S Clifford ChaoCancer Center, China Medical University Hospital, China Medical University, 40402, Taichung, Taiwan.
Chih-Yang HuangGraduate Institute of Basic Medical Science, China Medical University, 40402, Taichung, Taiwan. cyhuang@mail.cmu.edu.tw.ORCID http://orcid.org/0000-0003-2347-0411
China Medical University · TWAsia University · TW

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Dysfunctional mitochondria have been shown to enhance cancer cell proliferation, reduce apoptosis, and increase chemoresistance. Chemoresistance develops in nearly all patients with colorectal cancer, leading to a decrease in the therapeutic efficacies of anticancer agents. However, the effect of dynamin-related protein 1 (Drp1)-mediated mitochondrial fission on chemoresistance in colorectal cancer is unclear. Here, we found that the release of high-mobility group box 1 protein (HMGB1) in conditioned medium from dying cells by chemotherapeutic drugs and resistant cells, which triggered Drp1 phosphorylation via its receptor for advanced glycation end product (RAGE). RAGE signals ERK1/2 activation to phosphorylate Drp1 at residue S616 triggerring autophagy for chemoresistance and regrowth in the surviving cancer cells. Abolishment of Drp1 phosphorylation by HMGB1 inhibitor and RAGE blocker significantly enhance sensitivity to the chemotherapeutic treatment by suppressing autophagy. Furthermore, patients with high phospho-Drp1

Indexed as

AnimalsAntigens, NeoplasmAntineoplastic AgentsApoptosisAutophagyCell Line, TumorColorectal NeoplasmsDisease-Free SurvivalDrug Resistance, NeoplasmDynaminsGTP PhosphohydrolasesHMGB1 ProteinHumansMAP Kinase Signaling SystemMiceMice, Inbred BALB CAntigens, NeoplasmAntineoplastic AgentsDNM1L protein, humanDynaminsGTP PhosphohydrolasesHMGB1 ProteinHMGB1 protein, humanMicrotubule-Associated ProteinsMitochondrial ProteinsMitogen-Activated Protein KinasesMOK protein, human

Identifiers

PMID30258050
PMCPMC6158296
OpenAlexW2894444025

What OpenQuestion holds

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LicenceCC BY
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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.