Evidence map›Paper›PMID 32547216›Full record

ArticleCancer management and research2020

TOP2A Promotes Cell Migration, Invasion and Epithelial-Mesenchymal Transition in Cervical Cancer via Activating the PI3K/AKT Signaling.

Bi Wang, Yaping Shen, Yin Zou, Zhengjun Qi, Guijia Huang, Shan Xia, Rui Gao, Fenghu Li, Zhi Huang

Open access · goldAbstract read
In one paragraph

Article in Cancer management and research, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 28 papers.

0numbers the graph read from it
0cells of the map it votes in
28citing papers in PubMed
1.7field-weighted citation impact, top 16% 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

28 citing papers in PubMed, 36 citations in OpenAlex.

  1. Article
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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

9 authors at 2 institutions in 1 country.

Bi Wang *Key Laboratory of Endemic and Ethnic Diseases, Ministry of Education, Guizhou Medical University, Guiyang, Guizhou, People's Republic of China.
Yaping Shen *Department of Interventional Radiology, The Affiliated Baiyun Hospital of Guizhou Medical University, Guiyang, Guizhou, People's Republic of China.
Yin ZouDepartment of Oncology, The Second Affiliated Hospital of Guizhou Medical University, Guiyang, Guizhou, People's Republic of China.
Zhengjun QiDepartment of Oncology, The Second Affiliated Hospital of Guizhou Medical University, Guiyang, Guizhou, People's Republic of China.
Guijia HuangDepartment of Oncology, The Second Affiliated Hospital of Guizhou Medical University, Guiyang, Guizhou, People's Republic of China.
Shan XiaDepartment of Gynecologic Oncology, The Affiliated Cancer Hospital of Guizhou Medical University, Guiyang, Guizhou, People's Republic of China.
Rui GaoGuiyang Customs Guizhou International Travel Healthcare Center, Guiyang, Guizhou, People's Republic of China.
Fenghu LiDepartment of Gynecologic Oncology, The Affiliated Cancer Hospital of Guizhou Medical University, Guiyang, Guizhou, People's Republic of China.
Zhi HuangDepartment of Interventional Radiology, The Affiliated Hospital of Guizhou Medical University, Guiyang, Guizhou, People's Republic of China.ORCID 0000-0001-9020-897X
Guiyang Medical University · CNShenzhen International Travel Health Care Center · CN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

BACKGROUND/

objectiveTopoisomerases type IIA (TOP2A) was identified to present with a high-expression pattern in cervical cancer. However, TOP2A role in the progression of cervical cancer remains unknown. Here, we aimed to explore the effect and reveal the underlying mechanism of TOP2A in the migration, invasion and epithelial-mesenchymal transition (EMT) of cervical cancer. MATERIALS AND

methodsThe expression profiles of TOP2A in 20 paired cervical cancer tissues and the paracancerous normal tissues were detected by using Western blotting assay. Transwell chambers were used to test cell migration and invasion abilities. Cell morphology and the expressions of E-cadherin and N-cadherin were detected to assess cell EMT. LY294002 was used to inhibit the activation of PI3K/AKT signaling.

resultsCompared with the paracancerous normal tissues, TOP2A was overexpressed in 85% (17/20) cervical cancer tissues. Repression of TOP2A expression in SiHa cells significantly weakened cell migration and invasion abilities, reduced cell numbers in shuttle shape and increased E-cadherin expression while decreased E-cadherin expression. To the opposite, overexpression of TOP2A in Hela cells induced opposite results. In addition, the expression of p-AKT was increased when TOP2A was overexpressed in Hela cells, and p-AKT expression was decreased when TOP2A was silenced in SiHa cells. Moreover, suppression of the PI3K/AKT signaling with LY294002 treatment apparently rescued TOP2A-mediated promotions in cell migration, invasion and EMT in Hela cells.

conclusionThis study reveals that TOP2A is abnormally overexpressed in cervical cancer tissues, and TOP2A overexpression leads to cell migration, invasion and EMT via activating PI3K/AKT signaling.

Indexed as

cell morphologyepithelial–mesenchymal transitionmigrationPI3K/AKT signalingtopoisomerases type IIA

Identifiers

PMID32547216
PMCPMC7251484
OpenAlexW3026197278

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LicenceCC BY-NC
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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.