Evidence map›Paper›PMID 27593936›Full record

ArticleOncogene2017

TFAP2C promotes lung tumorigenesis and aggressiveness through miR-183- and miR-33a-mediated cell cycle regulation.

J Kang, W Kim, S Lee, D Kwon, J Chun, B Son, E Kim, J-M Lee, H Youn, B Youn

Abstract read
PubMed Publisher
In one paragraph

Article in Oncogene, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 42 papers.

0numbers the graph read from it
0cells of the map it votes in
42citing papers in PubMed
4.2field-weighted citation impact, top 5% 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

42 citing papers in PubMed, 75 citations in OpenAlex.

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  13. APE1 controls DICER1 expression in NSCLC through miR-33a and miR-130b.Cellular and molecular life sciences : CMLS · 2022
    Article
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  15. Gene expression profiling after LINC00472 overexpression in an NSCLC cell line1.Cancer biomarkers : section A of Disease markers · 2021
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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

10 authors at 3 institutions in 1 country.

J KangDepartment of Integrated Biological Science, Pusan National University, Busan, Republic of Korea.
W KimDepartment of Biological Sciences, Pusan National University, Busan, Republic of Korea.
S LeeDepartment of Integrated Biological Science, Pusan National University, Busan, Republic of Korea.
D KwonDepartment of Integrated Biological Science, Pusan National University, Busan, Republic of Korea.
J ChunDepartment of Integrated Biological Science, Pusan National University, Busan, Republic of Korea.
B SonDepartment of Integrated Biological Science, Pusan National University, Busan, Republic of Korea.
E KimDepartment of Integrated Biological Science, Pusan National University, Busan, Republic of Korea.
J-M LeeDepartment of Naval Architecture and Ocean Engineering, Pusan National University, Busan, Republic of Korea.
H YounDepartment of Integrative Bioscience and Biotechnology, Sejong University, Seoul, Republic of Korea.
B YounDepartment of Integrated Biological Science, Pusan National University, Busan, Republic of Korea.
Pusan National University · KRGlobal Core Research Center for Ships and Offshore Plants · KRSejong University · KR

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Non-small cell lung cancer (NSCLC) remains one of the leading causes of death worldwide, and thus new molecular targets need to be identified to improve treatment efficacy. Although epidermal growth factor receptor (EGFR)/KRAS mutation-driven lung tumorigenesis is well understood, the mechanism of EGFR/KRAS-independent signal activation remains elusive. Enhanced TFAP2C (transcription factor activating enhancer-binding protein 2C) expression is associated with poor prognosis in some types of cancer patients, but little is known of its relation with the pathogenesis of lung cancer. In the present study, we found that TFAP2C overexpression was associated with cell cycle activation and NSCLC cell tumorigenesis. Interestingly, TFAP2C blocked AKAP12-mediated cyclin D1 inhibition by inducing the overexpression of oncogenic microRNA (miRNA)-183 and simultaneously activated cyclin-dependent kinase 6-mediated cell cycle progression by downregulating tumor-suppressive miRNA-33a. In a mouse xenograft model, TFAP2C promoted lung tumorigenesis and disease aggressiveness via the miR-183 and miR-33a pathways. The study provides a mechanism of mitogenic and oncogenic signaling via two functionally opposed miRNAs and suggests that TFAP2C-induced cell cycle hyperactivation contributes to lung tumorigenesis.

Indexed as

Gene Expression Regulation, NeoplasticA Kinase Anchor ProteinsAnimalsCarcinogenesisCell CycleCell Cycle ProteinsCell Line, TumorCyclin-Dependent Kinase 6Disease Models, AnimalDisease ProgressionHeterograftsHumansLung NeoplasmsMiceMicroRNAsModels, BiologicalAKAP12 protein, humanA Kinase Anchor ProteinsCell Cycle ProteinsCyclin-Dependent Kinase 6MicroRNAsMIRN183 microRNA, humanMIRN33a microRNA, humanTFAP2C protein, humanTranscription Factor AP-2

Identifiers

PMID27593936
OpenAlexW2517609385

What OpenQuestion holds

Textmetadata
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.