Evidence map›Paper›PMID 31340867›Full record

ArticleJournal of hematology & oncology2019

The long noncoding RNA H19 promotes tamoxifen resistance in breast cancer via autophagy.

Ji Wang, Shuduo Xie, Jingjing Yang, Hanchu Xiong, Yunlu Jia, Yulu Zhou, Yongxia Chen, Xiaogang Ying, Cong Chen, Chenyang Ye and 2 more

Open 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. Cited by 166 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
166citing papers in PubMed, 1 pooled it
10.6field-weighted citation impact, top 1% 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

166 citing papers in PubMed, 1 synthesis or guideline pooled it, 273 citations in OpenAlex.

  1. Pooled it
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  5. International journal of molecular sciences · 2026
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  12. The Biological Role and Clinical Significance of BECLIN-1 in Cancer.International journal of molecular sciences · 2025
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  18. Decoding the Epigenome of Breast Cancer.International journal of molecular sciences · 2025
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  20. Review

106 more citing papers are in PubMed but not listed here.

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

12 authors at 2 institutions in 1 country.

Ji WangDepartment of Surgical Oncology, Sir Run Run Shaw Hospital, Zhejiang University School of Medicine, No.3 Eastern Qingchun Road, Hangzhou, 310016, Zhejiang, China.
Shuduo XieDepartment of Surgical Oncology, Sir Run Run Shaw Hospital, Zhejiang University School of Medicine, No.3 Eastern Qingchun Road, Hangzhou, 310016, Zhejiang, China.
Jingjing YangDepartment of Surgical Oncology, Sir Run Run Shaw Hospital, Zhejiang University School of Medicine, No.3 Eastern Qingchun Road, Hangzhou, 310016, Zhejiang, China.
Hanchu XiongDepartment of Surgical Oncology, Sir Run Run Shaw Hospital, Zhejiang University School of Medicine, No.3 Eastern Qingchun Road, Hangzhou, 310016, Zhejiang, China.
Yunlu JiaDepartment of Surgical Oncology, Sir Run Run Shaw Hospital, Zhejiang University School of Medicine, No.3 Eastern Qingchun Road, Hangzhou, 310016, Zhejiang, China.
Yulu ZhouDepartment of Surgical Oncology, Sir Run Run Shaw Hospital, Zhejiang University School of Medicine, No.3 Eastern Qingchun Road, Hangzhou, 310016, Zhejiang, China.
Yongxia ChenDepartment of Surgical Oncology, Sir Run Run Shaw Hospital, Zhejiang University School of Medicine, No.3 Eastern Qingchun Road, Hangzhou, 310016, Zhejiang, China.
Xiaogang YingDepartment of Surgical Oncology, Sir Run Run Shaw Hospital, Zhejiang University School of Medicine, No.3 Eastern Qingchun Road, Hangzhou, 310016, Zhejiang, China.
Cong ChenDepartment of Surgical Oncology, Sir Run Run Shaw Hospital, Zhejiang University School of Medicine, No.3 Eastern Qingchun Road, Hangzhou, 310016, Zhejiang, China.
Chenyang YeCancer Institute (Key Laboratory of Cancer Prevention & Intervention, National Ministry of Education), Second Affiliated Hospital, Zhejiang University School of Medicine, Hangzhou, 310009, China.
Linbo WangDepartment of Surgical Oncology, Sir Run Run Shaw Hospital, Zhejiang University School of Medicine, No.3 Eastern Qingchun Road, Hangzhou, 310016, Zhejiang, China. linbowang@zju.edu.cn.
Jichun ZhouDepartment of Surgical Oncology, Sir Run Run Shaw Hospital, Zhejiang University School of Medicine, No.3 Eastern Qingchun Road, Hangzhou, 310016, Zhejiang, China. jichun-zhou@zju.edu.cn.
Zhejiang University · CNSir Run Run Shaw Hospital · CN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

backgroundTamoxifen resistance remains a clinical challenge for hormone receptor-positive breast cancer. Recently, dysregulations in autophagy have been suggested as a potential mechanism for tamoxifen resistance. Although the long noncoding RNA H19 is involved in various stages of tumorigenesis, its role in tamoxifen resistance remains unknown. Here, we assessed the role of H19 in the development of tamoxifen-resistant breast cancer.

methodsQuantitative real-time PCR analyzed expression of H19 in tamoxifen-resistant breast cancer tissues. Knockdown of H19 was used to assess the sensitivity to tamoxifen in vitro and in vivo. Both knockdown and overexpression of H19 were used to analyze the status of autophagy. Real-time quantitative methylation-specific polymerase chain reaction, chromatin immunoprecipitation, immunofluorescence, and Western blot were used to explore the tamoxifen resistance mechanism of H19.

resultsIn this study, we observed that the expression of H19 was substantially upregulated in tamoxifen-resistant breast cancer cell line and tumor tissues, and knockdown of H19 enhanced the sensitivity to tamoxifen both in vitro and in vivo. Furthermore, knockdown of H19 significantly inhibited autophagy in MCF7 tamoxifen-resistant (MCF7/TAMR) cells. Conversely, overexpression of H19 promoted autophagy. Interestingly, overexpression of H19 in MCF7 tamoxifen-sensitive cells could recapitulate tamoxifen resistance. Moreover, an increase in methylation in the promoter region of Beclin1 was observed in MCF7/TAMR-shH19 cells. In the double knockdown groups, both shH19+shSAHH and shH19+shDNMT3B rescued the Beclin1 promoter region methylation levels and reactivated autophagy functions. A chromatin immunoprecipitation assay further validated that DNMT3B binds to the Beclin1 promoter region and the knockdown of H19 increases this binding.

conclusionsOur findings demonstrate that H19 induces autophagy activation via the H19/SAHH/DNMT3B axis, which could contribute to tamoxifen resistance in breast cancer.

Indexed as

AdenosylhomocysteinaseAnimalsApoptosisAutophagyBeclin-1Breast NeoplasmsCell Line, TumorCell ProliferationDNA (Cytosine-5-)-MethyltransferasesDNA MethylationDNA Methyltransferase 3ADoxycyclineDrug Resistance, NeoplasmFemaleHumansMCF-7 CellsAdenosylhomocysteinaseAHCY protein, humanBeclin-1BECN1 protein, humanDNA (Cytosine-5-)-MethyltransferasesDNA Methyltransferase 3ADNMT3A protein, humanDoxycyclineH19 long non-coding RNARNA, Long NoncodingTamoxifenAutophagyBeclin1Breast cancerLncRNA H19MethylationTamoxifen resistance

Identifiers

PMID31340867
PMCPMC6657081
OpenAlexW2964233401

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.