Evidence map›Paper›PMID 30832689›Full record

ArticleJournal of hematology & oncology2019

Transcriptional factor six2 promotes the competitive endogenous RNA network between CYP4Z1 and pseudogene CYP4Z2P responsible for maintaining the stemness of breast cancer cells.

Lufeng Zheng, Qianqian Guo, Chenxi Xiang, Shijia Liu, Yuzhang Jiang, Lanlan Gao, Haiwei Ni, Ting Wang, Qiong Zhao, Hai Liu and 4 more

Erratum issuedOpen access · goldAbstract read
In one paragraph

Article in Journal of hematology & oncology, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. An erratum has been issued. Cited by 36 papers.

0numbers the graph read from it
0cells of the map it votes in
36citing papers in PubMed
3.8field-weighted citation impact, top 6% 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

36 citing papers in PubMed, 73 citations in OpenAlex.

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4 · The record

Corrections and comments

5 · Who and what money

Authors and funding

14 authors at 5 institutions in 1 country.

Lufeng ZhengJiangsu Key Laboratory of Carcinogenesis and Intervention, School of Life Science and Technology, China Pharmaceutical University, 24 Tong Jia Xiang, Nanjing, 210009, China.
Qianqian GuoJiangsu Key Laboratory of Carcinogenesis and Intervention, School of Life Science and Technology, China Pharmaceutical University, 24 Tong Jia Xiang, Nanjing, 210009, China.
Chenxi XiangDepartment of Pathology, The Affiliated Hospital of Xuzhou Medical University, Xuzhou, 221002, Jiangsu, China.
Shijia LiuDepartment of Pharmacy, Jiangsu Province Hospital of TCM, Nanjing, 210023, China.
Yuzhang JiangDepartment of Clinical Laboratory, Huai An First People's Hospital, Huai An, 223300, China.
Lanlan GaoJiangsu Key Laboratory of Carcinogenesis and Intervention, School of Life Science and Technology, China Pharmaceutical University, 24 Tong Jia Xiang, Nanjing, 210009, China.
Haiwei NiJiangsu Key Laboratory of Carcinogenesis and Intervention, School of Life Science and Technology, China Pharmaceutical University, 24 Tong Jia Xiang, Nanjing, 210009, China.
Ting WangJiangsu Key Laboratory of Carcinogenesis and Intervention, School of Life Science and Technology, China Pharmaceutical University, 24 Tong Jia Xiang, Nanjing, 210009, China.
Qiong ZhaoJiangsu Key Laboratory of Carcinogenesis and Intervention, School of Life Science and Technology, China Pharmaceutical University, 24 Tong Jia Xiang, Nanjing, 210009, China.
Hai LiuJiangsu Key Laboratory of Carcinogenesis and Intervention, School of Life Science and Technology, China Pharmaceutical University, 24 Tong Jia Xiang, Nanjing, 210009, China.
Yingying XingJiangsu Key Laboratory of Carcinogenesis and Intervention, School of Life Science and Technology, China Pharmaceutical University, 24 Tong Jia Xiang, Nanjing, 210009, China.
Yaohui WangDepartment of Pathology, Jiangsu Province Hospital of TCM, Nanjing, 210023, China.
Xiaoman LiJiangsu Key Laboratory for Pharmacology and Safety Evaluation of Chinese Materia Medica, School of Pharmacy, Nanjing University of Chinese Medicine, Nanjing, 210023, China. xiaoman1205@163.com.
Tao XiJiangsu Key Laboratory of Carcinogenesis and Intervention, School of Life Science and Technology, China Pharmaceutical University, 24 Tong Jia Xiang, Nanjing, 210009, China. xitao18@hotmail.com.ORCID 0000-0001-8065-2639
China Pharmaceutical University · CNJiangsu Province Hospital · CNHuaian First People’s Hospital · CNNanjing University of Chinese Medicine · CNXuzhou Medical College · CN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

backgroundThe expression of CYP4Z1 and the pseudogene CYP4Z2P has been shown to be specifically increased in breast cancer by our group and others. Additionally, we previously revealed the roles of the competitive endogenous RNA (ceRNA) network mediated by these genes (ceRNET_CC) in breast cancer angiogenesis, apoptosis, and tamoxifen resistance. However, the roles of ceRNET_CC in regulating the stemness of breast cancer cells and the mechanisms through which ceRNET_CC is regulated remain unclear.

methodsTranscriptional factor six2, CYP4Z1-3'UTR, and CYP4Z2P-3'UTR were stably overexpressed or knocked down in breast cancer cells via lentivirus infection. ChIP-sequencing and RNA-sequencing analysis were performed to reveal the mechanism through which ceRNET_CC is regulated and the transcriptome change mediated by ceRNET_CC. Clinical samples were used to validate the correlation between six2 and ceRNET_CC. Finally, the effects of the six2/ceRNET_CC axis on the stemness of breast cancer cells and chemotherapy sensitivity were evaluated by in vitro and in vivo experiments.

resultsWe revealed that ceRNET_CC promoted the stemness of breast cancer cells. Mechanistically, six2 activated ceRNET_CC by directly binding to their promoters, thus activating the downstream PI3K/Akt and ERK1/2 pathways. Finally, we demonstrated that the six2/ceRNET_CC axis was involved in chemoresistance.

conclusionsOur results uncover the mechanism through which ceRNET_CC is regulated, identify novel roles for the six2/ceRNET_CC axis in regulating the stemness of breast cancer cells, and propose the possibility of targeting the six2/ceRNET_CC axis to inhibit breast cancer stem cell (CSC) traits.

Indexed as

AnimalsBreast NeoplasmsCell Line, TumorCytochrome P450 Family 4FemaleHEK293 CellsHeterograftsHomeodomain ProteinsHumansMCF-7 CellsMiceMice, Inbred BALB CMice, NudeNeoplastic Stem CellsNerve Tissue ProteinsPseudogenesCYP4Z1 protein, humanCytochrome P450 Family 4Homeodomain ProteinsNerve Tissue ProteinsSIX2 protein, humanTranscription FactorsBreast cancerceRNET_CCChemoresistanceCYP4Z1Pseudogene CYP4Z2PSix2Stemness

Identifiers

PMID30832689
PMCPMC6399913
OpenAlexW4229551140

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.