Evidence map›Paper›PMID 31273338›Full record

ArticleOncogene2019

The MRVI1-AS1/ATF3 signaling loop sensitizes nasopharyngeal cancer cells to paclitaxel by regulating the Hippo-TAZ pathway.

Yuxing Zhu, Dong He, Hao Bo, Zexian Liu, Mengqing Xiao, Liang Xiang, Jianda Zhou, Yan Liu, Xiaoming Liu, Lian Gong and 9 more

Abstract read
PubMed Publisher
In one paragraph

Article in Oncogene, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 33 papers.

0numbers the graph read from it
0cells of the map it votes in
33citing papers in PubMed
4.3field-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

33 citing papers in PubMed, 60 citations in OpenAlex.

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  12. Regulation of Ferroptosis by Non-Coding RNAs in Head and Neck Cancers.International journal of molecular sciences · 2022
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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

19 authors at 4 institutions in 1 country.

Yuxing ZhuDepartment of Oncology, Third Xiangya Hospital of Central South University, 410013, Changsha, People's Republic of China.
Dong HeDepartment of Respiration, The Second People's Hospital of Hunan Province of Hunan University of Chinese Medicine, Changsha, 410000, People's Republic of China.
Hao BoInstitute of Reproductive and Stem Cell Engineering, Central South University, 410083, Changsha, Hunan, People's Republic of China.
Zexian LiuState Key Laboratory of Oncology in South China, Collaborative Innovation Center for Cancer Medicine, Sun Yat-sen University Cancer Center, 510060, Guangzhou, People's Republic of China.ORCID http://orcid.org/0000-0001-9698-0610
Mengqing XiaoDepartment of Oncology, Third Xiangya Hospital of Central South University, 410013, Changsha, People's Republic of China.
Liang XiangDepartment of Oncology, Third Xiangya Hospital of Central South University, 410013, Changsha, People's Republic of China.
Jianda ZhouDepartment of Plastic Surgery, Third Xiangya Hospital, Central South University, 410013, Changsha, Hunan, People's Republic of China.
Yan LiuDepartment of Plastic Surgery, Third Xiangya Hospital, Central South University, 410013, Changsha, Hunan, People's Republic of China.
Xiaoming LiuDepartment of Gastroenterology, Third Xiangya Hospital of Central South University, 410013, Changsha, People's Republic of China.
Lian GongDepartment of Oncology, Third Xiangya Hospital of Central South University, 410013, Changsha, People's Republic of China.
Yanni MaDepartment of Oncology, Third Xiangya Hospital of Central South University, 410013, Changsha, People's Republic of China.
Yanhong ZhouCancer Research Institute and Key Laboratory of Carcinogenesis of Ministry of Health, Central South University, 410078, Changsha, People's Republic of China.
Ming ZhouCancer Research Institute and Key Laboratory of Carcinogenesis of Ministry of Health, Central South University, 410078, Changsha, People's Republic of China.
Wei XiongCancer Research Institute and Key Laboratory of Carcinogenesis of Ministry of Health, Central South University, 410078, Changsha, People's Republic of China.
Fei YangSchool of Public Health, Central South University, 410078, Changsha, Hunan, People's Republic of China.
Xiaowei XingCenter for Medical Experiments, Third Xiangya Hospital, Central South University, 410013, Changsha, People's Republic of China.ORCID http://orcid.org/0000-0002-5648-8864
Ruhong LiYan'an Affiliated Hospital of Kunming Medical University, 650051, Kunming, People's Republic of China.
Wei LiDepartment of Otolaryngology-Head Neck Surgery, Third Xiangya Hospital, Central South University, 410013, Changsha, Hunan, People's Republic of China.
Ke CaoDepartment of Oncology, Third Xiangya Hospital of Central South University, 410013, Changsha, People's Republic of China. csucaoke@163.com.ORCID http://orcid.org/0000-0001-5392-2306
Central South University · CNHunan University · CNKunming Medical University · CNSun Yat-sen University · CN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Long non-coding RNA (lncRNA) plays an important role in malignant tumor occurrence, development, and chemoresistance, but the mechanism of how they affect nasopharyngeal cancer (NPC) paclitaxel chemosensitivity is unclear. In this study, lncRNA array of CNE-1 and HNE-2 paclitaxel-resistant cells and their parental strains revealed that the paclitaxel-resistant strains had significantly lower MRVI1-AS1 (murine retrovirus integration site 1 homolog antisense RNA 1) expression than the parental strains, and that MRVI1-AS1 overexpression in vitro and in vivo increased paclitaxel chemosensitivity. Further, MRVI1-AS1 upregulated ATF3 (activating transcription factor 3) by simultaneously inhibiting miR-513a-5p (microRNA-513a-5p) and miR-27b-3p expression levels to increase NPC paclitaxel chemosensitivity. Chromatin immunoprecipitation and quantitative real-time PCR showed that ATF3 could feed-back MRVI1-AS1 regulation positively. Furthermore, MRVI1-AS1 and ATF3 could form a positive feedback loop, which promoted the expression of RASSF1 (Ras association domain family member 1), a Hippo-TAZ (tafazzin) signaling pathway regulatory factor, thereby inhibiting TAZ expression. The MTT (3-[4,5-dimethylthiazol-2-yl]-2,5 diphenyltetrazolium bromide) assay and flow cytometry showed that the decreased TAZ increased NPC cell paclitaxel chemosensitivity. Overall, the results indicate that the MRVI1-AS1/ATF3 signaling pathway can increase NPC paclitaxel chemosensitivity by modulating the Hippo-TAZ signaling pathway. Therefore, targeting the loop may be a new NPC treatment strategy.

Indexed as

A549 CellsActivating Transcription Factor 3AcyltransferasesCell Line, TumorDrug Resistance, NeoplasmGene Expression Regulation, NeoplasticHEK293 CellsHippo Signaling PathwayHumansMCF-7 CellsMembrane ProteinsNasopharyngeal CarcinomaNasopharyngeal NeoplasmsPaclitaxelPhosphoproteinsProtein Serine-Threonine KinasesActivating Transcription Factor 3AcyltransferasesATF3 protein, humanIRAG1 protein, humanMembrane ProteinsPaclitaxelPhosphoproteinsProtein Serine-Threonine KinasesRNA, AntisenseTAFAZZIN protein, humanTranscription Factors

Identifiers

PMID31273338
OpenAlexW2972703949

What OpenQuestion holds

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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.