Evidence map›Paper›PMID 33787085›Full record

ArticleCancer medicine2021

Elevated TAB182 enhances the radioresistance of esophageal squamous cell carcinoma through G2-M checkpoint modulation.

Yuandong Cao, Aidi Gao, Xiaoqing Li, Han Min, Chao He, Xinchen Sun, Wei-Qun Ding, Jundong Zhou

Open access · goldAbstract read
In one paragraph

Article in Cancer medicine, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 14 papers.

0numbers the graph read from it
0cells of the map it votes in
14citing papers in PubMed
1.1field-weighted citation impact, top 23% 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

14 citing papers in PubMed, 17 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

8 authors at 3 institutions in 2 countries.

Yuandong CaoDepartment of Radiation Oncology, The First Affiliated Hospital of Nanjing Medical University, Nanjing, Jiangsu, P.R. China.
Aidi GaoSuzhou Cancer Center Core Laboratory, The Affiliated Suzhou Hospital of Nanjing Medical University, Suzhou, Jiangsu, P.R. China.
Xiaoqing LiSuzhou Cancer Center Core Laboratory, The Affiliated Suzhou Hospital of Nanjing Medical University, Suzhou, Jiangsu, P.R. China.
Han MinSuzhou Cancer Center Core Laboratory, The Affiliated Suzhou Hospital of Nanjing Medical University, Suzhou, Jiangsu, P.R. China.
Chao HeSuzhou Cancer Center Core Laboratory, The Affiliated Suzhou Hospital of Nanjing Medical University, Suzhou, Jiangsu, P.R. China.ORCID 0000-0002-9023-1595
Xinchen SunDepartment of Radiation Oncology, The First Affiliated Hospital of Nanjing Medical University, Nanjing, Jiangsu, P.R. China.
Wei-Qun DingDepartment of Pathology, University of Oklahoma Health Science Center, Oklahoma City, OK, USA.
Jundong ZhouSuzhou Cancer Center Core Laboratory, The Affiliated Suzhou Hospital of Nanjing Medical University, Suzhou, Jiangsu, P.R. China.
Suzhou Municipal Hospital · CNJiangsu Province Hospital · CNUniversity of Oklahoma Health Sciences Center · US

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

backgroundRadiotherapy is one of the main strategies for the treatment of esophageal squamous cell carcinoma (ESCC). However, treatment failure often occurs due to the emergence of radioresistance. In this study, we report a key regulator of radiation sensitivity, termed TAB182 that may become an ideal biomarker and therapeutic target to overcome radioresistance. MATERIALS AND

methodsBy applying qRT-PCR and immunohistochemical staining, the expression of TAB182 was detected in patient tissues. We next assessed the influence of TAB182 downregulation to radiosensitivity using clonogenic survival assay and γ-H2A.X foci analysis in TE-1, TE-10, and radioresistant TE-1R cell lines after ionizing radiation. To unveil the mechanism underlying, TAB182 interacting proteins were identified by mass spectrometry following co-immunoprecipitation. Furthermore, flow cytometry and western blot assay were applied to validate the identified proteins.

resultsOur results demonstrated that the expression of TAB182 is higher in cancer tissues than normal tissues and elevated expression of TAB182 correlates with poor outcomes of postoperative radiotherapy. Downregulation of TAB182 sensitized cancer cells to ionizing radiation, particularly in radioresistant TE-1R cells that spontaneously overexpress TAB182. Mechanically, TAB182 interacts with FHL2 to induce G2-M arrest through wiring the CHK2/CDC25C/CDC2 signaling pathway. Finally, overexpression of shRNA-resistant TAB182 restored the checkpoint and radioresistance.

conclusionTAB182 potentiates the radioresistance of ESCC cells by modulating the G2-M checkpoint through its interaction with FHL2. Thus, TAB182 may become an ideal biomarker and therapeutic target of ESCC radiotherapy.

Indexed as

G2 Phase Cell Cycle CheckpointsM Phase Cell Cycle CheckpointsBiomarkers, TumorCell Line, TumorDown-RegulationEsophageal NeoplasmsEsophageal Squamous Cell CarcinomaEsophagusHistonesHumansLIM-Homeodomain ProteinsMolecular Targeted TherapyMuscle ProteinsPostoperative PeriodPrognosisRadiation ToleranceBiomarkers, TumorFHL2 protein, humanH2AX protein, humanHistonesLIM-Homeodomain ProteinsMuscle ProteinsRNA, Small InterferingTelomeric Repeat Binding Protein 1TNKS1BP1 protein, humanTranscription Factorsesophageal squamous cell carcinomaFHL2G2-M cell cycle checkpointradioresistanceTAB182

Identifiers

PMID33787085
PMCPMC8085956
OpenAlexW3141222817

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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.