Evidence map›Paper›PMID 30254375›Full record

ArticleCell death and differentiation2019

TC2N, a novel oncogene, accelerates tumor progression by suppressing p53 signaling pathway in lung cancer.

Xiang-Lin Hao, Fei Han, Ning Zhang, Hong-Qiang Chen, Xiao Jiang, Li Yin, Wen-Bin Liu, Dan-Dan Wang, Jian-Ping Chen, Zhi-Hong Cui and 3 more

Open access · hybridAbstract read
In one paragraph

Article in Cell death and differentiation, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 37 papers.

0numbers the graph read from it
0cells of the map it votes in
37citing papers in PubMed
2.5field-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

37 citing papers in PubMed, 76 citations in OpenAlex.

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  19. Construction and analysis of the ceRNA networkAnnals of translational medicine · 2021
    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

13 authors at 1 institution in 1 country.

Xiang-Lin HaoInstitute of Toxicology, College of Preventive Medicine, Third Military Medical University, Chongqing, 400038, China.ORCID 0000-0002-7583-8233
Fei HanInstitute of Toxicology, College of Preventive Medicine, Third Military Medical University, Chongqing, 400038, China.
Ning ZhangInstitute of Toxicology, College of Preventive Medicine, Third Military Medical University, Chongqing, 400038, China.
Hong-Qiang ChenInstitute of Toxicology, College of Preventive Medicine, Third Military Medical University, Chongqing, 400038, China.
Xiao JiangInstitute of Toxicology, College of Preventive Medicine, Third Military Medical University, Chongqing, 400038, China.
Li YinInstitute of Toxicology, College of Preventive Medicine, Third Military Medical University, Chongqing, 400038, China.
Wen-Bin LiuInstitute of Toxicology, College of Preventive Medicine, Third Military Medical University, Chongqing, 400038, China.
Dan-Dan WangInstitute of Toxicology, College of Preventive Medicine, Third Military Medical University, Chongqing, 400038, China.
Jian-Ping ChenInstitute of Toxicology, College of Preventive Medicine, Third Military Medical University, Chongqing, 400038, China.
Zhi-Hong CuiInstitute of Toxicology, College of Preventive Medicine, Third Military Medical University, Chongqing, 400038, China.
Lin AoInstitute of Toxicology, College of Preventive Medicine, Third Military Medical University, Chongqing, 400038, China.
Jia CaoInstitute of Toxicology, College of Preventive Medicine, Third Military Medical University, Chongqing, 400038, China. caojia1962@126.com.
Jin-Yi LiuInstitute of Toxicology, College of Preventive Medicine, Third Military Medical University, Chongqing, 400038, China. jinyiliutmmu@163.com.ORCID 0000-0003-1803-7752
Army Medical University · CN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

The protein containing the C2 domain has been well documented for its essential roles in endocytosis, cellular metabolism and cancer. Tac2-N (TC2N) is a tandem C2 domain-containing protein, but its function, including its role in tumorigenesis, remains unknown. Here, we first identified TC2N as a novel oncogene in lung cancer. TC2N was preferentially upregulated in lung cancer tissues compared with adjacent normal lung tissues. High TC2N expression was significantly associated with poor outcome of lung cancer patients. Knockdown of TC2N markedly induces cell apoptosis and cell cycle arrest with repressing proliferation in vitro, and suppresses tumorigenicity in vivo, whereas overexpression of TC2N has the opposite effects both in vitro and in vivo. Using a combination of TCGA database and bioinformatics, we demonstrate that TC2N is involved in regulation of the p53 signaling pathway. Mechanistically, TC2N attenuates p53 signaling pathway through inhibiting Cdk5-induced phosphorylation of p53 via inducing Cdk5 degradation or disrupting the interaction between Cdk5 and p53. Moreover, the blockade of p53 attenuates the function of TC2N knockdown in the regulation of cell proliferation and apoptosis. In addition, downregulated TC2N is involved in the apoptosis of lung cancer cells induced by doxorubicin, leading to p53 pathway activation. Overall, these findings uncover a role for the p53 inactivator TC2N in regulating the proliferation and apoptosis of lung cancer cells. Our present study provides novel insights into the mechanism of tumorigenesis in lung cancer.

Indexed as

Disease ProgressionSignal TransductionAntibiotics, AntineoplasticApoptosisCell Cycle CheckpointsCell LineCell ProliferationDoxorubicinHumansKaplan-Meier EstimateLung NeoplasmsOncogenesRNA-SeqTumor Suppressor Protein p53Antibiotics, AntineoplasticDoxorubicinTumor Suppressor Protein p53

Identifiers

PMID30254375
PMCPMC6748156
OpenAlexW2893463086

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.