Evidence map›Paper›PMID 29451718›Full record

ArticleCancer science2018

KIAA0247 inhibits growth, migration, invasion of non-small-cell lung cancer through regulating the Notch pathway.

Yitong Xu, Hongjiu Ren, Jun Jiang, Qiongzi Wang, Muli Wudu, Qingfu Zhang, Hongbo Su, Chenglong Wang, Lihong Jiang, Xueshan Qiu

Open access · goldAbstract read
In one paragraph

Article in Cancer science, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 15 papers.

0numbers the graph read from it
0cells of the map it votes in
15citing 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

15 citing papers in PubMed, 23 citations in OpenAlex.

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  2. Deletion ofInternational journal of molecular sciences · 2022
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  13. Astrocyte Elevated Gene 1 (AEG-1) Acts as a Promoter Gene in Clear Cell Renal Cell Carcinoma Cell Growth and Metastasis.Medical science monitor : international medical journal of experimental and clinical research · 2018
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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.

Yitong XuDepartment of Pathology, College of Basic Medical Sciences and First Affiliated Hospital, China Medical University, Shenyang, China.
Hongjiu RenDepartment of Pathology, College of Basic Medical Sciences and First Affiliated Hospital, China Medical University, Shenyang, China.
Jun JiangDepartment of Pathology, College of Basic Medical Sciences and First Affiliated Hospital, China Medical University, Shenyang, China.
Qiongzi WangDepartment of Pathology, College of Basic Medical Sciences and First Affiliated Hospital, China Medical University, Shenyang, China.
Muli WuduDepartment of Pathology, College of Basic Medical Sciences and First Affiliated Hospital, China Medical University, Shenyang, China.
Qingfu ZhangDepartment of Pathology, College of Basic Medical Sciences and First Affiliated Hospital, China Medical University, Shenyang, China.
Hongbo SuDepartment of Pathology, College of Basic Medical Sciences and First Affiliated Hospital, China Medical University, Shenyang, China.
Chenglong WangDepartment of Pain Medicine, The First Affiliated Hospital, China Medical University, Shenyang, China.
Lihong JiangDepartment of Pathology, The General Hospital of Liaohe Oil Field, Panjin, China.
Xueshan QiuDepartment of Pathology, College of Basic Medical Sciences and First Affiliated Hospital, China Medical University, Shenyang, China.ORCID http://orcid.org/0000-0001-9481-8249
China Medical University · CNFirst Hospital of China Medical University · CNSecond Hospital of Liaohe Oilfield · CN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Lung cancer remains the leading cause of cancer-related death worldwide. Previous studies have shown that the novel KIAA0247 gene potentially targeted by the tumor suppressor p53 may inhibit the development of several cancers. However, the exact function of KIAA0247 in non-small-cell lung cancer (NSCLC) is unknown. The purpose of the present study was to clarify the role of KIAA0247 in NSCLC. KIAA0247 expression was evaluated in tumors and adjacent normal tissues of 197 NSCLC patients by immunohistochemistry and real-time PCR and analyzed for association with clinicopathological parameters. Results indicated that KIAA0247 levels positively correlated with cell differentiation (P < .001) and patient survival (P < .0001) and negatively correlated with lymph node metastasis (P < .001) and advanced p-TNM stage (P < .001). In cultured NSCLC cell lines, KIAA0247 overexpression inhibited cell migration, invasion, and proliferation and downregulated the expression of Jagged1, Notch1 intracellular domain (NICD), Snail, cyclin D1, RhoA, RhoC, and MMP9, while upregulating that of E-cadherin and p21. The Notch inhibitor DAPT reduced the biological effects of KIAA0247 knockdown, suggesting that KIAA0247 decreased the carcinogenic activity of NSCLC cells through downregulation of Notch signaling. Our results indicate that KIAA0247 inhibits NSCLC progression by reducing the metastatic potential of cancer cells through downregulation of the Notch pathway, which may underlie the association of KIAA0247 expression with favorable clinicopathological characteristics of NSCLC patients. These findings suggest that KIAA0247 is a candidate prognostic biomarker and potential therapeutic target in NSCLC.

Indexed as

A549 CellsCarcinogenesisCarcinoma, Non-Small-Cell LungCell Line, TumorCell MovementCell ProliferationComplement System ProteinsDown-RegulationFemaleHumansLung NeoplasmsLymphatic MetastasisMaleMembrane ProteinsMiddle AgedNeoplasm InvasivenessComplement System ProteinsMembrane ProteinsReceptor, Notch1SUSD6 protein, humancell migrationmetastasis-associated genemetastasis inhibitionp53-related generespiratory organ

Identifiers

PMID29451718
PMCPMC5891195
OpenAlexW2792048499

What OpenQuestion holds

Textmetadata
LicenceCC BY-NC
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.