Evidence map›Paper›PMID 30126368›Full record

ArticleBMC cell biology2018

Mutant TP53 G245C and R273H promote cellular malignancy in esophageal squamous cell carcinoma.

Nan Kang, Yu Wang, Shichao Guo, Yunwei Ou, Guangchao Wang, Jie Chen, Dan Li, Qimin Zhan

Open access · goldAbstract read
In one paragraph

Article in BMC cell biology, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 19 papers.

0numbers the graph read from it
0cells of the map it votes in
19citing papers in PubMed
1.5field-weighted citation impact, top 14% 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

19 citing papers in PubMed, 26 citations in OpenAlex.

  1. Genomic Enrichment and Functional Impact of TP53 and CYLD Alterations in Recurrent and Metastatic HPV-Associated Head and Neck Cancer.Clinical cancer research : an official journal of the American Association for Cancer Research · 2026
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  13. Molecular crosstalk between cancer and neurodegenerative diseases.Cellular and molecular life sciences : CMLS · 2020
    Review
  14. Identification of targeted therapy options for gastric adenocarcinoma by comprehensive analysis of genomic data.Gastric cancer : official journal of the International Gastric Cancer Association and the Japanese Gastric Cancer Association · 2020
    Article
  15. Article
  16. Non-disruptive mutation inAnnals of translational medicine · 2020
    Article
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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 2 institutions in 1 country.

Nan KangState Key Laboratory of Molecular Oncology, Chinese Academy of Medical Sciences and Peking Union Medical College, National Cancer Center/Cancer Hospital, Beijing, 100021, China.
Yu WangState Key Laboratory of Molecular Oncology, Chinese Academy of Medical Sciences and Peking Union Medical College, National Cancer Center/Cancer Hospital, Beijing, 100021, China.
Shichao GuoState Key Laboratory of Molecular Oncology, Chinese Academy of Medical Sciences and Peking Union Medical College, National Cancer Center/Cancer Hospital, Beijing, 100021, China.
Yunwei OuState Key Laboratory of Molecular Oncology, Chinese Academy of Medical Sciences and Peking Union Medical College, National Cancer Center/Cancer Hospital, Beijing, 100021, China.
Guangchao WangState Key Laboratory of Molecular Oncology, Chinese Academy of Medical Sciences and Peking Union Medical College, National Cancer Center/Cancer Hospital, Beijing, 100021, China.
Jie ChenLaboratory of Molecular Oncology, Peking University Cancer Hospital and Institute, Beijing, China.
Dan LiState Key Laboratory of Molecular Oncology, Chinese Academy of Medical Sciences and Peking Union Medical College, National Cancer Center/Cancer Hospital, Beijing, 100021, China. eileenld@gmail.com.
Qimin ZhanState Key Laboratory of Molecular Oncology, Chinese Academy of Medical Sciences and Peking Union Medical College, National Cancer Center/Cancer Hospital, Beijing, 100021, China. qiminzhan@vip.163.com.
Chinese Academy of Medical Sciences & Peking Union Medical College · CNPeking University · CN

Funding

Beijing Nova Program xx2018040CAMS Initiative for Innovative Medicine 2017-I2M-3-004National 973 Program 2015CB553904National Natural Science Foundation of China 81321091, 81230047national nature science 81672455National Sci-Tech Support Plan 2013BAI01B07
6 · The paper itself

Abstract

backgroundTP53 gene mutations occur in more than 50% of human cancers and the vast majority of these mutations in human cancers are missense mutations, which broadly occur in DNA binding domain (DBD) (Amino acids 102-292) and mainly reside in six "hotspot" residues. TP53 G245C and R273H point mutations are two of the most frequent mutations in tumors and have been verified in several different cancers. In the previous study of the whole genome sequencing (WGS), we found some mutations of TP53 DBD in esophageal squamous cell carcinoma (ESCC) clinical samples. We focused on two high-frequent mutations TP53 p.G245C and TP53 p.R273H and investigated their oncogenic roles in ESCC cell lines, p53-defective cell lines H1299 and HCT116 p53-/-.

resultsMTS and colony formation assays showed that mutant TP53 G245C and R273H increased cell vitality and proliferation. Flow cytometry results revealed inhibition of ultraviolet radiation (UV)- and ionizing radiation (IR)- induced apoptosis and disruption of TP53-mediated cell cycle arrest after UV, IR and Nocodazole treatment. Transwell assays indicated that mutant TP53 G245C and R273H enhanced cell migration and invasion abilities. Moreover, western blot revealed that they were able to suppress the expression of TP53 downstream genes in the process of apoptosis and cell cycle arrest induced by UV, which suggests that these two mutations can influence apoptosis and growth arrest might be due, at least in part, to down-regulate the expression of P21, GADD45α and PARP.

conclusionsThese results indicate that mutant TP53 G245C and R273H can lead to more aggressive phenotypes and enhance cancer cell malignancy, which further uncover TP53 function in carcinogenesis and might be useful in clinical diagnosis and therapy of TP53 mutant cancers.

Indexed as

ApoptosisCell Cycle CheckpointsCell Line, TumorCell MovementCell ProliferationCell Transformation, NeoplasticCyclin-Dependent Kinase Inhibitor p21DNA Mutational AnalysisEsophageal Squamous Cell CarcinomaGADD45 ProteinsHumansIntracellular Signaling Peptides and ProteinsMutationNeoplasm InvasivenessPoly(ADP-ribose) PolymerasesTumor Suppressor Protein p53Cyclin-Dependent Kinase Inhibitor p21GADD45 ProteinsIntracellular Signaling Peptides and ProteinsPoly(ADP-ribose) PolymerasesTP53 protein, humanTumor Suppressor Protein p53ApoptosisCell cycle arrestCell malignancyDownstream geneEsophageal squamous cell carcinomaInvasionMigrationTP53 mutation

Identifiers

PMID30126368
PMCPMC6102840
OpenAlexW2888658933

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.