Evidence map›Paper›PMID 32252682›Full record

ArticleBMC cancer2020

Overexpression of SLC6A1 associates with drug resistance and poor prognosis in prostate cancer.

Chaojiang Chen, Zhiduan Cai, Yangjia Zhuo, Ming Xi, Zhuoyuan Lin, Funeng Jiang, Zezhen Liu, Yueping Wan, Yu Zheng, Jianxin Li and 3 more

Open access · goldAbstract read
In one paragraph

Article in BMC cancer, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 14 papers.

0numbers the graph read from it
0cells of the map it votes in
14citing papers in PubMed
1.6field-weighted citation impact, top 13% 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

14 citing papers in PubMed, 16 citations in OpenAlex.

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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

13 authors at 5 institutions in 1 country.

Chaojiang ChenGuangdong Provincial Institute of Nephrology, Nanfang Hospital, Southern Medical University, Guangzhou, 510515, China.
Zhiduan CaiGuangdong Provincial Institute of Nephrology, Nanfang Hospital, Southern Medical University, Guangzhou, 510515, China.
Yangjia ZhuoDepartment of Urology, Guangdong Key Laboratory of Clinical Molecular Medicine and Diagnostics, Guangzhou First People's Hospital, School of Medicine, South China University of Technology, Guangzhou, 510180, China.
Ming XiDepartment of Urology, Huadu District People's Hospital, Southern Medical University, Guangzhou, 510800, China.
Zhuoyuan LinDepartment of Urology, The Second Affiliated Hospital of Guangzhou Medical University, Guangzhou Medical University, Guangzhou, China.
Funeng JiangDepartment of Urology, Guangdong Key Laboratory of Clinical Molecular Medicine and Diagnostics, Guangzhou First People's Hospital, School of Medicine, South China University of Technology, Guangzhou, 510180, China.
Zezhen LiuGuangdong Provincial Institute of Nephrology, Nanfang Hospital, Southern Medical University, Guangzhou, 510515, China.
Yueping WanDepartment of Urology, Huadu District People's Hospital, Southern Medical University, Guangzhou, 510800, China.
Yu ZhengDepartment of Urology, The Second Affiliated Hospital of Guangzhou Medical University, Guangzhou Medical University, Guangzhou, China.
Jianxin LiDepartment of Urology, The Second Affiliated Hospital of Guangzhou Medical University, Guangzhou Medical University, Guangzhou, China.
Xing ZhouDepartment of Urology, The Second Affiliated Hospital of Guangzhou Medical University, Guangzhou Medical University, Guangzhou, China.
Jianguo ZhuDepartment of Urology, Guizhou Provincial People's Hospital, The Affiliated Hospital of Guizhou Medical University, Guiyang, 550002, China. doctorzhujianguo@163.com.
Weide ZhongGuangdong Provincial Institute of Nephrology, Nanfang Hospital, Southern Medical University, Guangzhou, 510515, China. zhongwd2009@live.cn.
Guangzhou Medical University · CNSouthern Medical University · CNSecond Affiliated Hospital of Guangzhou Medical University · CNSouth China University of Technology · CNAffiliated Hospital of Guizhou Medical University · CN

Funding

Guangzhou Municipal Science and Technology Project 201607010398Guangzhou Municipal Science and Technology Project 201803040001 ,201707010291Medical Scientific Research Foundation of Guangdong Province A2018302National Natural Science Foundation of China 81571427, 81660426National Natural Science Foundation of China 81802555Natural Science Foundation of Guangdong Province 2017A030310149Science and Technology Planning Project of Shenzhen Municipality (CN) HD15CXY005Science and Technology Project of Guangdong Province 2016A020215018, 2014A020212471Science and Technology Project of Guizhou Province in 2017 [2017]5803The General Guiding Project of Guangzhou Health and Family Planning Commission 20171A011303
6 · The paper itself

Abstract

backgroundSolute Carrier Family 6 Member 1 (SLC6A1) has been identified as a cancer-promoting gene in various human cancers, such as clear cell renal cell carcinoma and ovarian cancer. However, its roles in prostate cancer (PCa) has not been fully elucidated. The aim of this study was to investigate the expression and clinical significance of SLC6A1 in PCa tissues and its effect on drug resistance to docetaxel in PCa.

methodsExpression patterns of SLC6A1 protein in PCa tissues were examined by immunohistochemistry based on Tissue microarray. Associations of SLC6A1 protein expression with various clinicopathological features and patients' prognosis of PCa were also statistically evaluated based on TCGA data. Roles of SLC6A1 deregulation in prostate carcinogenesis and drug resistance was further determined in vitro and in vivo experiments.

resultsBased on TCGA Dataset, SLC6A1 expression was markedly higher in patients with high Gleason score, advanced clinical stage and positive biochemical recurrence than those with control features (all P < 0.05). Both unvariate and multivariate analyses demonstrated that SLC6A1 expression was significantly associated with biochemical recurrence-free survival in PCa patients. In addition, enforced expression of SLC6A1 effectively promoted cell proliferation, migration and invasion of PCa cells in vitro. Moreover, the inhibition of SLC6A1 suppressed the tumor growth in vivo. Additionally, immunohistochemical notches of PCNA and MMP-9 in the low-expression cluster were pointedly lower compared to those of NC group. Finally, the cell viability revealed that the overexpression of SLC6A1 obviously promoted the PCa cell resistant to docetaxel (DTX), and the transplanted tumor in the overexpression group had no significant reduction compared with the untreated group.

conclusionsOur data suggest that SLC6A1 overexpression may be associated with aggressive progression and short biochemical recurrence-free survival of PCa, and may be related to the resistance to docetaxel therapy.

Indexed as

Drug Resistance, NeoplasmAgedAnimalsAntineoplastic AgentsBiomarkers, TumorCell Line, TumorCell ProliferationComputational BiologyDatabases, GeneticDisease ProgressionDocetaxelGABA Plasma Membrane Transport ProteinsGene Expression Regulation, NeoplasticHumansMaleMiceAntineoplastic AgentsBiomarkers, TumorDocetaxelGABA Plasma Membrane Transport ProteinsSLC6A1 protein, humanChemotherapy resistancePrognosisProstate cancerSolute carrier family 6 member 1

Identifiers

PMID32252682
PMCPMC7137497
OpenAlexW3014536322

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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.