Evidence map›Paper›PMID 37318676›Full record

ArticleDiscover oncology2023

AURKB activates EMT through PI3K/AKT signaling axis to promote ICC progression.

Peng Ma, Ying Hao, Wei Wang, Yue-Feng Zhang, Kai-Huan Yu, Wei-Xing Wang

Open access · goldAbstract read
In one paragraph

Article in Discover oncology, 2023. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 9 papers.

0numbers the graph read from it
0cells of the map it votes in
9citing papers in PubMed
5.4field-weighted citation impact, top 4% 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

9 citing papers in PubMed, 17 citations in OpenAlex.

  1. AURKB drives aggressive phenotype and clinicopathological progression in cholangiocarcinoma.Clinical & translational oncology : official publication of the Federation of Spanish Oncology Societies and of the National Cancer Institute of Mexico · 2026
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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

6 authors at 2 institutions in 1 country.

Peng Ma *Deportment of Hepatobiliary Surgery, Renmin Hospital, Wuhan University, Wuhan, 430060, Hubei Province, People's Republic of China.
Ying Hao *Deportment of Hepatobiliary Surgery, Renmin Hospital, Wuhan University, Wuhan, 430060, Hubei Province, People's Republic of China.
Wei Wang *Deportment of Hepatobiliary Surgery, Renmin Hospital, Wuhan University, Wuhan, 430060, Hubei Province, People's Republic of China.
Yue-Feng ZhangDeportment of Hepatobiliary Surgery, Renmin Hospital, Wuhan University, Wuhan, 430060, Hubei Province, People's Republic of China.
Kai-Huan YuDeportment of Hepatobiliary Surgery, Renmin Hospital, Wuhan University, Wuhan, 430060, Hubei Province, People's Republic of China. 13517282628@163.com.
Wei-Xing WangDeportment of Hepatobiliary Surgery, Renmin Hospital, Wuhan University, Wuhan, 430060, Hubei Province, People's Republic of China. sate.llite@163.com.
Renmin Hospital of Wuhan University · CNWuhan University · CN

Funding

Opening Project of Hubei Key Laboratory 2021KFY007
6 · The paper itself

Abstract

Intrahepatic cholangiocarcinoma (ICC) is a fatal disease and the molecular mechanism of its progression remains unknown. Aurora Kinase B (AURKB) is a central regulator of chromosome separation and cytokinesis and is abnormally expressed in a variety of cancer cells. This research aimed to explore the effect of AURKB in occurrence and metastasis of ICC. We found that AURKB showed a progressive up-regulation pattern from normal bile duct tissue to ICC with high invasion. Our data showed that AURKB significantly promoted ICC cell proliferation, induced epithelial-mesenchymal transition (EMT), migration and invasion through gain- and loss- of function experiments. In vivo results consistently showed that AURKB up-regulation not only promoted tumor growth, but also promoted tumor metastasis. Importantly, we discovered that AURKB regulates the expressions of EMT-related genes via PI3K/AKT signaling axis. Herein, our results suggest that AURKB induced EMT through the activation of PI3K/AKT signaling pathway is critical to the progression of ICC, which may be a prospective therapeutic treatment for overcoming ICC metastasis and progression.

Identifiers

PMID37318676
PMCPMC10272048
OpenAlexW4380730346

What OpenQuestion holds

Textmetadata
LicenceCC BY
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.