Evidence map›Paper›PMID 36260180›Full record

ArticleMolecular biology reports2022

HMGB1 induces radioresistance through PI3K/AKT/ATM pathway in esophageal squamous cell carcinoma.

Xueyuan Zhang, Naiyi Zou, Wenzhao Deng, Chunyang Song, Ke Yan, Wenbin Shen, Shuchai Zhu

Open access · hybridAbstract read
In one paragraph

Article in Molecular biology reports, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 13 papers.

0numbers the graph read from it
0cells of the map it votes in
13citing papers in PubMed
3.1field-weighted citation impact, top 8% 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

13 citing papers in PubMed, 14 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

7 authors at 1 institution in 1 country.

Xueyuan ZhangDepartment of Radiation Oncology, The Fourth Hospital of Hebei Medical University, 12 Jiankang Road, Shijiazhuang, Hebei, 050011, People's Republic of China.
Naiyi ZouDepartment of Radiation Oncology, The Fourth Hospital of Hebei Medical University, 12 Jiankang Road, Shijiazhuang, Hebei, 050011, People's Republic of China.
Wenzhao DengDepartment of Radiation Oncology, The Fourth Hospital of Hebei Medical University, 12 Jiankang Road, Shijiazhuang, Hebei, 050011, People's Republic of China.
Chunyang SongDepartment of Radiation Oncology, The Fourth Hospital of Hebei Medical University, 12 Jiankang Road, Shijiazhuang, Hebei, 050011, People's Republic of China.
Ke YanDepartment of Radiation Oncology, The Fourth Hospital of Hebei Medical University, 12 Jiankang Road, Shijiazhuang, Hebei, 050011, People's Republic of China.
Wenbin ShenDepartment of Radiation Oncology, The Fourth Hospital of Hebei Medical University, 12 Jiankang Road, Shijiazhuang, Hebei, 050011, People's Republic of China.
Shuchai ZhuDepartment of Radiation Oncology, The Fourth Hospital of Hebei Medical University, 12 Jiankang Road, Shijiazhuang, Hebei, 050011, People's Republic of China. sczhu1965@163.com.ORCID http://orcid.org/0000-0003-0787-3325
Hebei Medical University · CN

Funding

a grant from the Medical Research Institute of Hebei Province 20221365National Natural Science Foundation of China 81872456Natural Science Foundation of Hebei Province H2020206583
6 · The paper itself

Abstract

backgroundTo explore the effect of HMGB1 on the radio-sensitivity of esophageal cancer cells through regulating the PI3K/Akt/ATM pathway. METHODS AND

resultsWe observed the expression of HMGB1 and p-ATM in biopsies of esophageal cancer patients with immunohistochemical staining. Western blot and RT-qPCR were applied to detect the protein and RNA related to PI3K/Akt/ATM pathway, respectively. In addition, we inhibited the PI3K/Akt pathway with ly294002 and activated it with IGF1, then we explored the invasion, proliferation ability, and apoptosis of esophageal cancer cells in vitro by transwell, CCK8 assay, and flow cytometry respectively. In vivo, xenograft tumor model was established in nude mice to study the effect of HMGB1 on radioresistance via PI3K/AKT/ATM Signaling Pathway. The survival rate in patients with single positive/double negative expression of HMGB1 and p-ATM was significantly higher than in those with both positive expression of HMGB1 and p-ATM, the depletion of HMGB1 combined with ly294002 significantly inhibited cell proliferation and invasion ability, meanwhile, the addition of IGF1 reversed it. Meanwhile, depletion of HMGB1 and ly294002 promoted apoptosis and arrested the cancer cells in G0/G1 cell cycle with the decreased expression of Cyclin D1 and CDK4 and improved P16. We further validated these results in vivo, the application of HMGB1 silencing promoted apoptosis of xenograft tumors after radiation, especially combined with pathway inhibitor ly294002.

conclusionsEsophageal cancer patients with high expression of HMGB1 and p-ATM have a poor prognosis after chemo-radiotherapy. Down-regulation of HMGB1 may promote the radio-sensitivity of esophageal cancer cells through regulating PI3K/Akt/ATM pathway.

Indexed as

Esophageal NeoplasmsEsophageal Squamous Cell CarcinomaHMGB1 ProteinAnimalsApoptosisAtaxia Telangiectasia Mutated ProteinsCell Line, TumorCell ProliferationHumansMiceMice, NudePhosphatidylinositol 3-KinasesProto-Oncogene Proteins c-aktAtaxia Telangiectasia Mutated ProteinsATM protein, humanHMGB1 ProteinPhosphatidylinositol 3-KinasesProto-Oncogene Proteins c-aktApoptosisCell cycleESCCHMGB1Radioresistance

Identifiers

PMID36260180
PMCPMC9712304
OpenAlexW4306793158

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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.