Evidence map›Paper›PMID 30464609›Full record

ArticleCancer management and research2018

NKAP functions as an oncogene and its expression is induced by CoCl

Jiangtao Liu, Honghui Wang, Yanhai Yin, Qing Li, Mei Zhang

Open access · goldAbstract read
In one paragraph

Article in Cancer management and research, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 5 papers.

0numbers the graph read from it
0cells of the map it votes in
5citing papers in PubMed
0.6field-weighted citation impact, top 34% 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

5 citing papers in PubMed, 12 citations in OpenAlex.

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  5. Cancers · 2019
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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

5 authors at 2 institutions in 1 country.

Jiangtao LiuDepartment of Internal Medical Oncology, Binzhou Central Hospital, Binzhou 251700, Shandong, People's Republic China.
Honghui WangDepartment of Breast and Thyroid Surgery, Binzhou Central Hospital, Binzhou 251700, Shandong, People's Republic of China.
Yanhai YinDepartment of Internal Medical Oncology, Binzhou Central Hospital, Binzhou 251700, Shandong, People's Republic China.
Qing LiDepartment of Breast and Thyroid Surgery, Shandong Provincial Qianfoshan Hospital, Shandong University, Jinan 250000, Shandong, People's Republic of China, 13356678009@163.com; meizhang2017@163.com.
Mei ZhangDepartment of Breast and Thyroid Surgery, Shandong Provincial Qianfoshan Hospital, Shandong University, Jinan 250000, Shandong, People's Republic of China, 13356678009@163.com; meizhang2017@163.com.
Binzhou People's Hospital · CNShandong University · CN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

purposeNKAP plays an important role in transcriptional repression, T-cell development, maturation and function acquisition, maintenance and survival of hematopoietic stem cells, and RNA splicing. In this study, we tried to explore the physiological role of NKAP in breast cancer.

methodsWe investigated NKAP expression in breast cancer patients and normal controls and its correlation with survival in breast cancer patients by searching on GEPIA. We knocked down the expression of NKAP in MCF-7 cells by RNAi technique and studied its effect on cell proliferation, migration, invasion, and apoptosis. And we revealed the effect of NKAP on MCF-7 cells under hypoxic conditions in vitro.

resultsNKAP was differentially expressed in breast cancer and normal tissues and is a potential prognostic indicator of breast cancer. Subsequently, NKAP knockdown significantly inhibited the proliferation and clonality of MCF-7 cells and induced its apoptosis through caspase 3-dependent pathway. In addition, knockdown of NKAP could strongly inhibit the migration and invasion of MCF-7 cells. In MCF-7 cells, NKAP affected the AKT/mTOR signaling pathway and markedly reduced the phosphorylation of AKT and mTOR, as well as the downstream protein. What's interesting is CoCl

conclusionNKAP functioned as an oncogene, and its expression was induced by hypoxia in breast cancer via AKT/mTOR signaling pathway.

Indexed as

AKT/mTOR signaling pathwaybreast cancerhypoxiaNKAP

Identifiers

PMID30464609
PMCPMC6214303
OpenAlexW2898301733

What OpenQuestion holds

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LicenceCC BY-NC
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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.