Evidence map›Paper›PMID 30961661›Full record

ArticleJournal of experimental & clinical cancer research : CR2019

GTSE1 is involved in breast cancer progression in p53 mutation-dependent manner.

Fen Lin, Yu-Jie Xie, Xin-Ke Zhang, Tie-Jun Huang, Hong-Fa Xu, Yan Mei, Hu Liang, Hao Hu, Si-Ting Lin, Fei-Fei Luo and 4 more

Open access · goldAbstract read
In one paragraph

Article in Journal of experimental & clinical cancer research : CR, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 43 papers.

0numbers the graph read from it
0cells of the map it votes in
43citing papers in PubMed
4.0field-weighted citation impact, top 5% 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

43 citing papers in PubMed, 69 citations in OpenAlex.

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  8. GTSE1-driven ZEB1 stabilization promotes pulmonary fibrosis through the epithelial-to-mesenchymal transition.Molecular therapy : the journal of the American Society of Gene Therapy · 2024
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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

14 authors at 5 institutions in 1 country.

Fen LinState Key Laboratory of Oncology in South China and Collaborative Innovation Center for Cancer Medicine, Sun Yat-sen University Cancer Center, Guangzhou, 510060, People's Republic of China.
Yu-Jie XieState Key Laboratory of Oncology in South China and Collaborative Innovation Center for Cancer Medicine, Sun Yat-sen University Cancer Center, Guangzhou, 510060, People's Republic of China.
Xin-Ke ZhangDepartment of pathology, Sun Yat-sen University Cancer Center, Guangzhou, 510060, People's Republic of China.
Tie-Jun HuangDepartment of Nuclear Medicine, The Second People's Hospital of Shenzhen, Shenzhen, People's Republic of China.
Hong-Fa XuZhuhai Precision Medicine Center, Zhuhai People's Hospital Affiliated with Jinan University, Zhuhai, Guangdong, 519000, People's Republic of China.
Yan MeiState Key Laboratory of Oncology in South China and Collaborative Innovation Center for Cancer Medicine, Sun Yat-sen University Cancer Center, Guangzhou, 510060, People's Republic of China.
Hu LiangState Key Laboratory of Oncology in South China and Collaborative Innovation Center for Cancer Medicine, Sun Yat-sen University Cancer Center, Guangzhou, 510060, People's Republic of China.
Hao HuDepartment of Traditional Chinese Medicine, The First Affiliated Hospital of Sun Yat-Sen University, Guangzhou, 510060, People's Republic of China.
Si-Ting LinState Key Laboratory of Oncology in South China and Collaborative Innovation Center for Cancer Medicine, Sun Yat-sen University Cancer Center, Guangzhou, 510060, People's Republic of China.
Fei-Fei LuoState Key Laboratory of Oncology in South China and Collaborative Innovation Center for Cancer Medicine, Sun Yat-sen University Cancer Center, Guangzhou, 510060, People's Republic of China.
Yan-Hong LangState Key Laboratory of Oncology in South China and Collaborative Innovation Center for Cancer Medicine, Sun Yat-sen University Cancer Center, Guangzhou, 510060, People's Republic of China.
Li-Xia PengState Key Laboratory of Oncology in South China and Collaborative Innovation Center for Cancer Medicine, Sun Yat-sen University Cancer Center, Guangzhou, 510060, People's Republic of China.
Chao-Nan QianState Key Laboratory of Oncology in South China and Collaborative Innovation Center for Cancer Medicine, Sun Yat-sen University Cancer Center, Guangzhou, 510060, People's Republic of China. qianchn@sysucc.org.cn.
Bi-Jun HuangState Key Laboratory of Oncology in South China and Collaborative Innovation Center for Cancer Medicine, Sun Yat-sen University Cancer Center, Guangzhou, 510060, People's Republic of China. huangbj@sysucc.org.cn.
Sun Yat-sen University · CNSun Yat-sen University Cancer Center · CNJinan University · CNShenzhen Second People's Hospital · CNThe First Affiliated Hospital, Sun Yat-sen University · CN

Funding

National Natural Science Foundation of China 31170151National Natural Science Foundation of China 81572901National Natural Science Foundation of China 81773162Natural Science Foundation of Guangdong Province 2017A030313866Science and Technology Planning Project of Guangdong Province 2014A020209024Science and Technology Planning Project of Guangdong Province 2014B020212017
6 · The paper itself

Abstract

backgroundWith the rapid development of the high throughput detection techniques, tumor-related Omics data has become an important source for studying the mechanism of tumor progression including breast cancer, one of the major malignancies worldwide. A previous study has shown that the G2 and S phase-expressed-1 (GTSE1) can act as an oncogene in several human cancers. However, its functional roles in breast cancer remain elusive.

methodIn this study, we analyzed breast cancer data downloaded from The Cancer Genome Atlas (TCGA) databases and other online database including the Oncomine, bc-GenExMiner and PROGgeneV2 database to identify the molecules contributing to the progression of breast cancer. The GTSE1 expression levels were investigated using qRT-PCR, immunoblotting and IHC. The biological function of GTSE1 in the growth, migration and invasion of breast cancer was examined in MDA-MB-231, MDA-MB-468 and MCF7 cell lines. The in vitro cell proliferative, migratory and invasive abilities were evaluated by MTS, colony formation and transwell assay, respectively. The role of GTSE1 in the growth and metastasis of breast cancer were revealed by in vivo investigation using BALB/c nude mice.

resultsWe showed that the expression level of GTSE1 was upregulated in breast cancer specimens and cell lines, especially in triple negative breast cancer (TNBC) and p53 mutated breast cancer cell lines. Importantly, high GTSE1 expression was positively correlated with histological grade and poor survival. We demonstrated that GTSE1 could promote breast cancer cell growth by activating the AKT pathway and enhance metastasis by regulating the Epithelial-Mesenchymal transition (EMT) pathway. Furthermore, it could cause multidrug resistance in breast cancer cells. Interestingly, we found that GTSE1 could regulate the p53 function to alter the cell cycle distribution dependent on the mutation state of p53.

conclusionOur results reveal that GTSE1 played a key role in the progression of breast cancer, indicating that GTSE1 could serve as a novel biomarker to aid in the assessment of the prognosis of breast cancer.

Indexed as

AnimalsBreast NeoplasmsCell CycleCell DifferentiationCell Line, TumorDisease ProgressionDrug Resistance, NeoplasmFemaleHeterograftsHumansMCF-7 CellsMiceMice, Inbred BALB CMice, NudeMicrotubule-Associated ProteinsMutationGTSE1 protein, humanMicrotubule-Associated ProteinsProto-Oncogene Proteins c-aktTP53 protein, humanTumor Suppressor Protein p53Breast cancerCell cycleGTSE1p53Prognosis

Identifiers

PMID30961661
PMCPMC6454633
OpenAlexW2944729792

What OpenQuestion holds

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LicenceCC BY
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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.