Evidence map›Paper›PMID 32519472›Full record

ArticleCancer medicine2020

Downregulation of KIAA1199 by miR-486-5p suppresses tumorigenesis in lung cancer.

Anqi Wang, Jianjie Zhu, Juan Li, Wenwen Du, Yang Zhang, Tingting Cai, Ting Liu, Yulong Fu, Yuanyuan Zeng, Zeyi Liu and 1 more

Abstract read
In one paragraph

Article in Cancer medicine, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 16 papers.

0numbers the graph read from it
0cells of the map it votes in
16citing papers in PubMed
–field-weighted citation impact
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

16 citing papers in PubMed.

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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

11 authors.

Anqi WangDepartment of Respiratory Medicine, the First Affiliated Hospital of Soochow University, Suzhou, China.
Jianjie ZhuDepartment of Respiratory Medicine, the First Affiliated Hospital of Soochow University, Suzhou, China.
Juan LiDepartment of Respiratory Medicine, the First Affiliated Hospital of Soochow University, Suzhou, China.
Wenwen DuDepartment of Respiratory Medicine, the First Affiliated Hospital of Soochow University, Suzhou, China.
Yang ZhangDepartment of Respiratory Medicine, the First Affiliated Hospital of Soochow University, Suzhou, China.
Tingting CaiDepartment of Respiratory Medicine, the First Affiliated Hospital of Soochow University, Suzhou, China.
Ting LiuDepartment of Respiratory Medicine, the First Affiliated Hospital of Soochow University, Suzhou, China.
Yulong FuDepartment of Respiratory Medicine, the First Affiliated Hospital of Soochow University, Suzhou, China.
Yuanyuan ZengDepartment of Respiratory Medicine, the First Affiliated Hospital of Soochow University, Suzhou, China.
Zeyi LiuDepartment of Respiratory Medicine, the First Affiliated Hospital of Soochow University, Suzhou, China.ORCID 0000-0003-2528-6909
Jian-An HuangDepartment of Respiratory Medicine, the First Affiliated Hospital of Soochow University, Suzhou, China.

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Lung cancer is the primary cause of death among cancer patients in China, among which nonsmall cell lung cancer (NSCLC) makes up the great majority. Hence, it is imperative to identify the biomarkers and mechanisms involved in NSCLC oncogenesis. Our present research found that KIAA1199 expression was significantly increased in NSCLC and closely related to cell proliferation, motility, and poor prognosis. We demonstrated that knockdown of KIAA1199 reduced NSCLC cell growth and motility in vitro whereas overexpression of KIAA1199 had the opposite effect. Inhibition of KIAA1199 significantly suppressed tumor growth in mouse NSCLC xenograft models. Mechanistically, as an epidermal growth factor receptor (EGFR)-binding protein, KIAA1199 promotes EGFR signaling and regulates EGFR-dependent Src, Erk, and Akt phosphorylation, as well as downstream kinases in the EGF-mediated EMT pathway. We demonstrated that KIAA1199 can function as a direct binding target for miR-486-5p and that miR-486-5p overexpression can attenuate proliferation and migration of NSCLC cells via regulating the EGFR signaling pathways. To conclude, our results defined KIAA1199 as an oncogenic protein that promotes cancer cell proliferation and migration by regulating EGF-mediated signaling pathways. This study provided new insight into NSCLC oncogenesis, which could lead to the development of innovative therapeutic plans for NSCLC.

Indexed as

AnimalsCarcinogenesisCell Line, TumorCell ProliferationDown-RegulationHumansHyaluronoglucosaminidaseLung NeoplasmsMiceMicroRNAsXenograft Model Antitumor AssaysCEMIP protein, humanHyaluronoglucosaminidaseMicroRNAsMIRN486 microRNA, humancell motilitycell proliferationKIAA1199microRNAmiR-486-5pNon-small cell lung cancer (NSCLC)

Identifiers

PMID32519472
PMCPMC7402811

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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.