Evidence map›Paper›PMID 28421457›Full record

ArticleDigestive diseases and sciences2017

KLF15 Inhibits Cell Proliferation in Gastric Cancer Cells via Up-Regulating CDKN1A/p21 and CDKN1C/p57 Expression.

Chongqi Sun, Pei Ma, Yanfen Wang, Weitao Liu, Qinnan Chen, Yutian Pan, Chenhui Zhao, Yingchen Qian, Jie Liu, Wei Li and 1 more

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Article in Digestive diseases and sciences, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 27 papers.

0numbers the graph read from it
0cells of the map it votes in
27citing papers in PubMed
1.6field-weighted citation impact, top 17% 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

27 citing papers in PubMed, 51 citations in OpenAlex.

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  18. MiR-181a promotes cell proliferation and migration through targeting KLF15 in papillary thyroid cancer.Clinical & translational oncology : official publication of the Federation of Spanish Oncology Societies and of the National Cancer Institute of Mexico · 2022
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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 at 3 institutions in 1 country.

Chongqi SunDepartment of Oncology, The First Affiliated Hospital of Nanjing Medical University, No.300 Guangzhou Road, Nanjing, People's Republic of China.
Pei MaDepartment of Oncology, The First Affiliated Hospital of Nanjing Medical University, No.300 Guangzhou Road, Nanjing, People's Republic of China.
Yanfen WangDepartment of Pathology, Yangzhou No.1 People's Hospital, Yangzhou, People's Republic of China.
Weitao LiuDepartment of Pathology, Nanjing Medical University, Nanjing, People's Republic of China.
Qinnan ChenDepartment of Oncology, The Second Affiliated Hospital of Nanjing Medical University, Nanjing, People's Republic of China.
Yutian PanDepartment of Oncology, The First Affiliated Hospital of Nanjing Medical University, No.300 Guangzhou Road, Nanjing, People's Republic of China.
Chenhui ZhaoDepartment of Oncology, The First Affiliated Hospital of Nanjing Medical University, No.300 Guangzhou Road, Nanjing, People's Republic of China.
Yingchen QianDepartment of Pathology, Nanjing Medical University, Nanjing, People's Republic of China.
Jie LiuDepartment of Oncology, The First Affiliated Hospital of Nanjing Medical University, No.300 Guangzhou Road, Nanjing, People's Republic of China.
Wei LiDepartment of Oncology, The First Affiliated Hospital of Nanjing Medical University, No.300 Guangzhou Road, Nanjing, People's Republic of China. real.lw@163.com.
Yongqian ShuDepartment of Oncology, The First Affiliated Hospital of Nanjing Medical University, No.300 Guangzhou Road, Nanjing, People's Republic of China. yongqianshu@hotmail.com.
Nanjing Medical University · CNJiangsu Province Hospital · CNSecond Affiliated Hospital of Nanjing Medical University · CN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

backgroundKrüppel-like factors (KLFs) have been identified in multi-cancers and act as oncogenes or tumor suppressors. The function of KLF15, one member of KLFs, has not been well elucidated, especially in gastric cancer (GC).

aimsThis study was designed to investigate the prognostic value and biological functions of KLF15 in GC.

methodsKLF15 protein expression in GC patients was evaluated by immunohistochemistry assays in 50 paired GC tissues and adjacent normal tissues, and correlations between KLF15 expression and clinicopathological characteristics and prognosis were analyzed. Then, we investigated the over-expression of KLF15 on cell proliferation and its mechanism in GC cells.

resultsKLF15 expression levels were significantly down-regulated in GC tissues compared to adjacent normal tissues. And KLF15 expression was negatively correlated with clinical stage, lymphatic metastasis, and distant metastasis. Furthermore, KLF15 expression could predict prognosis in patients with GC. Moreover, over-expression of KLF15 could inhibit cell proliferation partly via regulating CDKN1A/p21 and CDKN1C/p57.

conclusionThese findings demonstrate that KLF15 plays a significant role in GC progression and could be a therapeutic target for GC.

Indexed as

AdenocarcinomaCell Line, TumorCell ProliferationCyclin-Dependent Kinase Inhibitor p21Cyclin-Dependent Kinase Inhibitor p57FemaleG1 Phase Cell Cycle CheckpointsGene Expression Regulation, NeoplasticHumansKi-67 AntigenKruppel-Like Transcription FactorsLymphatic MetastasisMaleMiddle AgedNeoplasm StagingNuclear ProteinsCDKN1A protein, humanCDKN1C protein, humanCyclin-Dependent Kinase Inhibitor p21Cyclin-Dependent Kinase Inhibitor p57Ki-67 AntigenKLF15 protein, humanKruppel-Like Transcription FactorsNuclear ProteinsCDKN1A/p21CDKN1C/p57Gastric cancerKrüppel-like factor 15 (KLF15)PrognosisProliferation

Identifiers

PMID28421457
OpenAlexW2607190720

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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.