Evidence map›Paper›PMID 34740994›Full record

ArticleAging2021

LncRNA OTUD6B-AS1 promotes paclitaxel resistance in triple negative breast cancer by regulation of miR-26a-5p/MTDH pathway-mediated autophagy and genomic instability.

Peng-Ping Li, Rong-Guo Li, Yu-Qing Huang, Jin-Pian Lu, Wei-Jun Zhang, Zhen-Yu Wang

Open access · hybridAbstract read
PubMed Full text at PMC Publisher
In one paragraph

Article in Aging, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 51 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
51citing papers in PubMed, 1 pooled it
14.2field-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

51 citing papers in PubMed, 1 synthesis or guideline pooled it, 109 citations in OpenAlex.

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  16. LncRNAs in modulating cancer cell resistance to paclitaxel (PTX) therapy.Medical oncology (Northwood, London, England) · 2024
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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

6 authors at 2 institutions in 1 country.

Peng-Ping LiDepartment of Breast-Thyroid Surgery, Department of General Surgery, The First Hospital of Xiaoshan District, Hangzhou, Zhejiang Province 311000, China.
Rong-Guo LiDepartment of Breast-Thyroid Surgery, Department of General Surgery, The First Hospital of Xiaoshan District, Hangzhou, Zhejiang Province 311000, China.
Yu-Qing HuangDepartment of Breast-Thyroid Surgery, Department of General Surgery, The First Hospital of Xiaoshan District, Hangzhou, Zhejiang Province 311000, China.
Jin-Pian LuThe Second Affiliated Hospital of Zhejiang Chinese Medical University, Hangzhou, Zhejiang Province 310000, China.
Wei-Jun ZhangDepartment of Breast-Thyroid Surgery, Department of General Surgery, The First Hospital of Xiaoshan District, Hangzhou, Zhejiang Province 311000, China.
Zhen-Yu WangDepartment of Breast-Thyroid Surgery, Department of General Surgery, The First Hospital of Xiaoshan District, Hangzhou, Zhejiang Province 311000, China.
The First People's Hospital of Xiaoshan District, Hangzhou · CNZhejiang Chinese Medical University · CN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Genomic instability (GIN) is pivotal in regulating tumor drug resistance, which blocked the treatment of triple negative breast cancer (TNBC). Although recent studies implied that non-coding RNA (ncRNA)-mediated autophagy abolishment promoted tumorigenesis by up-regulation of GIN, autophagy was known as a risk factor in tumor drug resistance. However, previous study also pointed that up-regulation of autophagy promoted GIN. Therefore, the relationship between autophagy and GIN is not clear, and more work is needed. And, if an ncRNA is identified to be a co-regulator of autophagy and GIN, it will be a potential therapy target of chemotherapy resistance in TNBC. In our study, we recognized both autophagy-GIN-associated microRNA (mi-26a-5p) by big data analysis, which was prognosis-correlated in breast cancer. Next, we identified the up-stream regulators (long non-coding RNA, lncRNA) and down-stream targets of miR-26a-5p by bioinformatics analysis (online public databases). Finally, we established lncRNA OTUD6B-AS1/miR-26a-5p/MTDH signaling pathway, and verified their functions by cytological, molecular biological and zoological experiments. In general, our study found (1) miR-26a-5p was a protective factor of breast cancer, while OTUD6B-AS1 and MTDH were risk factors; (2) OTUD6B-AS1 was the up-stream regulator of miR-26a-5p verified by luciferase; (3) up-regulation of miR-26a-5p and down-regulation of MTDH promoted cellular cytotoxicity of paclitaxel (PTX)

Indexed as

Triple Negative Breast NeoplasmsAnimalsAntineoplastic AgentsAutophagyCell Line, TumorDrug Resistance, NeoplasmFemaleGenomic InstabilityHumansMembrane ProteinsMiceMice, NudeMicroRNAsPaclitaxelRNA-Binding ProteinsRNA, Long NoncodingAntineoplastic AgentsMembrane ProteinsMicroRNAsMIRN26 microRNA, humanMTDH protein, humanPaclitaxelRNA-Binding ProteinsRNA, Long Noncodingautophagychemotherapy resistanceDNA damage response (DDR)genomic instability (GIN)triple negative breast cancer (TNBC)

Identifiers

PMID34740994
PMCPMC8610138
OpenAlexW3209399935

What Socratic 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 Socratic graph.