Evidence map›Paper›PMID 31938099›Full record

ArticleInternational journal of clinical and experimental pathology2018

Endogenous SARI exerts oncogenic functions in human K562 leukemia cells by targeting the PI3K/Akt/mTOR and NF-κB signaling pathways.

Xiaodan Fu, Zhaolei Cui, Yan Chen, Yongjin Tang, Chuncai Wu, Jianping Xu, Donghong Lin

Open access · greenAbstract read
In one paragraph

Article in International journal of clinical and experimental pathology, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 1 paper.

0numbers the graph read from it
0cells of the map it votes in
1citing papers in PubMed
0.2field-weighted citation impact, top 42% 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

1 citing paper in PubMed, 1 citations in OpenAlex.

  1. Article
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 1 institution in 1 country.

Xiaodan FuDepartment of Pathology, The First Affiliated Hospital of Fujian Medical University Fuzhou, Fujian, P. R. China.
Zhaolei CuiLaboratory of Biochemistry and Molecular Biology Research, Fujian Provincial Key Laboratory of Tumor Biotherapy, Department of Clinical Laboratory, Fujian Cancer Hospital, Fujian Medical University Cancer Hospital Fuzhou, Fujian, P. R. China.
Yan ChenLaboratory of Biochemistry and Molecular Biology Research, Fujian Provincial Key Laboratory of Tumor Biotherapy, Department of Clinical Laboratory, Fujian Cancer Hospital, Fujian Medical University Cancer Hospital Fuzhou, Fujian, P. R. China.
Yongjin TangFaculty of Laboratory Medicine, School of Medical Technology and Engineering, Fujian Medical University Fuzhou, Fujian, P. R. China.
Chuncai WuFaculty of Laboratory Medicine, School of Medical Technology and Engineering, Fujian Medical University Fuzhou, Fujian, P. R. China.
Jianping XuFaculty of Laboratory Medicine, School of Medical Technology and Engineering, Fujian Medical University Fuzhou, Fujian, P. R. China.
Donghong LinFaculty of Laboratory Medicine, School of Medical Technology and Engineering, Fujian Medical University Fuzhou, Fujian, P. R. China.
Fujian Medical University · CN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Suppressor of activator protein-1, regulated by interferon (SARI), is a novel basic leucine zipper containing type I IFN-inducible early response protein that plays an important regulatory role in a wide variety of tumors, including leukemia. However, the functional role of SARI in myeloid leukemia is not thoroughly understood. In this study, we discovered that knock-down of SARI expression suppressed cell growth and colony formation, inhibited invasion, enhanced imatinib (STI571)-mediated apoptosis, and induced G0/G1 and G2/M arrest in human K562 myeloid leukemia cells. Moreover, using immunoblotting, we provide evidence that silencing of SARI resulted in declined expression of cyclinD1 and cyclinA2, as well as down-regulation of mTOR, c-myc p-mTOR, p-PI3K (p85), p-Akt, p70-S6K, p-p70-S6K and NF-κB (p65) that involved in the PI3K/Akt/mTOR and NF-κB signaling pathways. Taken together, our results demonstrate that SARI functions as an oncogenic role in K562 myeloid leukemia cells through regulating the PI3K/Akt/mTOR and NF-κB signaling pathways.

Indexed as

K562 cellmechanismmyeloid leukemiaSARI

Identifiers

PMID31938099
PMCPMC6957961
OpenAlexW3010582994

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.