Evidence map›Paper›PMID 34817735›Full record

ArticleMedical oncology (Northwood, London, England)2021

ELK1-induced up-regulation of KIF26B promotes cell cycle progression in breast cancer.

SuXia Wang, Hui Zhang, HaiTing Liu, XiangYu Guo, RanRan Ma, WenJie Zhu, P Gao

Abstract read
PubMed Publisher
In one paragraph

Article in Medical oncology (Northwood, London, England), 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 12 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
12citing papers in PubMed, 1 pooled it
1.5field-weighted citation impact, top 19% 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

12 citing papers in PubMed, 1 synthesis or guideline pooled it, 21 citations in OpenAlex.

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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

7 authors at 2 institutions in 1 country.

SuXia WangKey Laboratory for Experimental Teratology of Ministry of Education, Department of Pathology, School of Basic Medical Sciences, Cheeloo College of Medicine, Shandong University, Jinan Wen Hua Xi Road 44, Jinan, 250012, Shandong, China.
Hui ZhangKey Laboratory for Experimental Teratology of Ministry of Education, Department of Pathology, School of Basic Medical Sciences, Cheeloo College of Medicine, Shandong University, Jinan Wen Hua Xi Road 44, Jinan, 250012, Shandong, China.
HaiTing LiuKey Laboratory for Experimental Teratology of Ministry of Education, Department of Pathology, School of Basic Medical Sciences, Cheeloo College of Medicine, Shandong University, Jinan Wen Hua Xi Road 44, Jinan, 250012, Shandong, China.
XiangYu GuoKey Laboratory for Experimental Teratology of Ministry of Education, Department of Pathology, School of Basic Medical Sciences, Cheeloo College of Medicine, Shandong University, Jinan Wen Hua Xi Road 44, Jinan, 250012, Shandong, China.
RanRan MaKey Laboratory for Experimental Teratology of Ministry of Education, Department of Pathology, School of Basic Medical Sciences, Cheeloo College of Medicine, Shandong University, Jinan Wen Hua Xi Road 44, Jinan, 250012, Shandong, China.
WenJie ZhuKey Laboratory for Experimental Teratology of Ministry of Education, Department of Pathology, School of Basic Medical Sciences, Cheeloo College of Medicine, Shandong University, Jinan Wen Hua Xi Road 44, Jinan, 250012, Shandong, China. 15266203531@163.com.
P GaoKey Laboratory for Experimental Teratology of Ministry of Education, Department of Pathology, School of Basic Medical Sciences, Cheeloo College of Medicine, Shandong University, Jinan Wen Hua Xi Road 44, Jinan, 250012, Shandong, China. gaopeng@sdu.edu.cn.ORCID http://orcid.org/0000-0002-4721-0887
Shandong University · CNQingdao University · CN

Funding

Key Technologies Research and Development Program 2017YFC1308600National Natural Science Foundation of China 81372856National Natural Science Foundation of China 81672842Project of Science and Technology of Yantai 2020YD025
6 · The paper itself

Abstract

KIF26B is a member of the kinesin superfamily that is up-regulated in various tumors, including breast cancer (BC), which can promote tumor progression. This study aimed to investigate the potential function of KIF26B in BC, and the underlying mechanisms, focusing mainly on cell proliferation. KIF26B expression was examined in BC tissue samples obtained from 99 patients. Then, we performed MTS, EdU and flow cytometry assays to detect cell proliferation, and western blotting to measure the expression of cell cycle-related proteins in MDA-MB-231 and MDA-MB-468 cells following KIF26B knockdown. Promoter analysis was used to study the upstream regulatory mechanism of KIF26B. KIF26B was upregulated in BC tissues. High expression of KIF26B was associated with clinicopathological parameters, such as positive lymph node metastasis, higher tumor grade, and higher proliferative index in BC. Furthermore, knockdown of KIF26B expression inhibited MDA-MB-231 and MDA-MB-468 cell proliferation, arresting cells in the G

Indexed as

Breast NeoplasmsCell CycleCell Line, TumorCell ProliferationDisease-Free Survivalets-Domain Protein Elk-1FemaleGene Expression Regulation, NeoplasticHumansKinesinsMiddle AgedPromoter Regions, GeneticProto-Oncogene Proteins c-mycTranscriptional ActivationELK1 protein, humanets-Domain Protein Elk-1KIF26B protein, humanKinesinsMYC protein, humanProto-Oncogene Proteins c-mycBreast cancerCell cycleELK1KIF26BProliferationWnt/β-catenin

Identifiers

PMID34817735
OpenAlexW3165530859

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.