Evidence map›Paper›PMID 30728351›Full record

ArticleCell death & disease2019

LncRNA H19 overexpression induces bortezomib resistance in multiple myeloma by targeting MCL-1 via miR-29b-3p.

Yafang Pan, Yu Zhang, Wenwen Liu, Yan Huang, Xianjuan Shen, Rongrong Jing, Jiang Pu, Xudong Wang, Shaoqing Ju, Hui Cong and 1 more

Abstract read
In one paragraph

Article in Cell death & disease, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 67 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
67citing papers in PubMed, 1 pooled it
–field-weighted citation impact
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

67 citing papers in PubMed, 1 synthesis or guideline pooled it.

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  18. The miR-29-3p family suppresses inflammatory osteolysis.Journal of cellular physiology · 2024
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7 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

11 authors.

Yafang PanDepartment of Laboratory Medicine, Affiliated hospital of Nantong University, Nantong, Jiangsu, 226001, China.
Yu ZhangDepartment of Laboratory Medicine, Affiliated hospital of Nantong University, Nantong, Jiangsu, 226001, China.
Wenwen LiuDepartment of Laboratory Medicine, Affiliated hospital of Nantong University, Nantong, Jiangsu, 226001, China.
Yan HuangDepartment of General Surgery, Affiliated Hospital of Nantong University, Nantong, Jiangsu, 226001, China.
Xianjuan ShenDepartment of Laboratory Medicine, Affiliated hospital of Nantong University, Nantong, Jiangsu, 226001, China.
Rongrong JingDepartment of Laboratory Medicine, Affiliated hospital of Nantong University, Nantong, Jiangsu, 226001, China.
Jiang PuDepartment of Laboratory Medicine, Affiliated hospital of Nantong University, Nantong, Jiangsu, 226001, China.
Xudong WangDepartment of Laboratory Medicine, Affiliated hospital of Nantong University, Nantong, Jiangsu, 226001, China.
Shaoqing JuDepartment of Laboratory Medicine, Affiliated hospital of Nantong University, Nantong, Jiangsu, 226001, China.
Hui CongDepartment of Laboratory Medicine, Affiliated hospital of Nantong University, Nantong, Jiangsu, 226001, China. huicjs@163.com.
Hongmei ChenDepartment of General Surgery, Affiliated Hospital of Nantong University, Nantong, Jiangsu, 226001, China. chm1923@163.com.

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Radiotherapy, chemotherapy, autologous/allogeneic stem cell transplantation, and targeted drug therapy are currently available therapeutic options for multiple myeloma (MM), but the clinical outcome remains unsatisfactory owing to frequent occurrence of drug resistance. Anti apoptosis is one of the main mechanisms to mediate drug resistance. Studies have shown that MCL-1 plays a key role in the growth of cancer cells "escaping" drug attacks, but the underlying mechanism remains unclear. Our previous study demonstrated that lncRNA H19 was highly expressed in the serum of MM patients. Bioinformatics predicts that miR-29b-3p is the downstream target gene, and MCL-1 is the downstream target protein of miR-29b-3p. Therefore, we speculated that MCL-1 may be involved in the occurrence of drug resistance through epigenetics. On the basis of these previous findings, the present study was intended to explore the biological function of H19, interactions between the downstream target genes, and the effect of H19 on BTZ resistance of myeloma cells. In addition, in vivo experiments we have also confirmed that H19 promoted tumor growth and may develop resistance to bortezomib partly. It was found that H19 reduced cell sensitivity to the chemotherapeutic drug BTZ by working as a miRNA sponge to inhibit the expression of miR-29b-3p, enhance MCL-1 transcriptional translation and inhibit apoptosis. These findings may help gain insights into the molecular mechanism of acquired BTZ resistance and develop new drug targets for the clinical treatment of MM.

Indexed as

AnimalsAntineoplastic AgentsApoptosisBortezomibCell Line, TumorCell MovementCell ProliferationHumansMaleMiceMice, Inbred BALB CMice, NudeMicroRNAsMultiple MyelomaMyeloid Cell Leukemia Sequence 1 ProteinRNA, Long NoncodingAntineoplastic AgentsBortezomibH19 long non-coding RNAMCL1 protein, humanMicroRNAsMIRN29a microRNA, humanMyeloid Cell Leukemia Sequence 1 ProteinRNA, Long Noncoding

Identifiers

PMID30728351
PMCPMC6365572

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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.