Evidence map›Paper›PMID 35985176›Full record

ArticleNeoplasia (New York, N.Y.)2022

Hypoxia induces docetaxel resistance in triple-negative breast cancer via the HIF-1α/miR-494/Survivin signaling pathway.

Hongchang Li, Xianhao Sun, Jindong Li, Weiyan Liu, Gaofeng Pan, Anwei Mao, Jiazhe Liu, Qing Zhang, Longhua Rao, Xiaofeng Xie and 1 more

Erratum issuedOpen access · goldAbstract read
In one paragraph

Article in Neoplasia (New York, N.Y.), 2022. 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 23 papers.

0numbers the graph read from it
0cells of the map it votes in
23citing papers in PubMed
4.5field-weighted citation impact, top 4% 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

23 citing papers in PubMed, 49 citations in OpenAlex.

  1. Review
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  4. HIF-1 and HIF-2 in cancer: structure, regulation, and therapeutic prospects.Cellular and molecular life sciences : CMLS · 2025
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4 · The record

Corrections and comments

5 · Who and what money

Authors and funding

11 authors at 3 institutions in 1 country.

Hongchang LiDepartment of General Surgery, Institute of Fudan Minhang Academic Health System, Minhang Hospital, Fudan University. 170 Xinsong Rd, Shanghai, China.
Xianhao SunDepartment of General Surgery, Institute of Fudan Minhang Academic Health System, Minhang Hospital, Fudan University. 170 Xinsong Rd, Shanghai, China.
Jindong LiDepartment of General Surgery, Institute of Fudan Minhang Academic Health System, Minhang Hospital, Fudan University. 170 Xinsong Rd, Shanghai, China.
Weiyan LiuDepartment of General Surgery, Institute of Fudan Minhang Academic Health System, Minhang Hospital, Fudan University. 170 Xinsong Rd, Shanghai, China.
Gaofeng PanDepartment of General Surgery, Institute of Fudan Minhang Academic Health System, Minhang Hospital, Fudan University. 170 Xinsong Rd, Shanghai, China.
Anwei MaoDepartment of General Surgery, Institute of Fudan Minhang Academic Health System, Minhang Hospital, Fudan University. 170 Xinsong Rd, Shanghai, China.
Jiazhe LiuDepartment of General Surgery, Institute of Fudan Minhang Academic Health System, Minhang Hospital, Fudan University. 170 Xinsong Rd, Shanghai, China.
Qing ZhangDepartment of General Surgery, Institute of Fudan Minhang Academic Health System, Minhang Hospital, Fudan University. 170 Xinsong Rd, Shanghai, China.
Longhua RaoDepartment of General Surgery, Institute of Fudan Minhang Academic Health System, Minhang Hospital, Fudan University. 170 Xinsong Rd, Shanghai, China. Electronic address: raolonghua@fudan.edu.cn.
Xiaofeng XieDepartment of General Surgery, Shuguang Hospital Affiliated to Shanghai University of Traditional Chinese Medicine, 528 Zhangheng Rd, Shanghai, China. Electronic address: xiexf@shutcm.edu.cn.
Xia ShengDepartment of Pathology, Institute of Fudan-Minhang Academic Health System, Minhang Hospital, Fudan University. 170 Xinsong Rd, Shanghai, China. Electronic address: shengxia_021@fudan.edu.cn.
Fudan University · CNMinhang District Central Hospital · CNShanghai University of Traditional Chinese Medicine · CN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Cytotoxic chemotherapy is the major strategy to prevent and reduce triple-negative breast cancer (TNBC) progression and metastasis. Hypoxia increases chemoresistance and is associated with a poor prognosis for patients with cancer. Based on accumulating evidence, microRNAs (miRNAs) play an important role in acquired drug resistance. However, the role of miRNAs in hypoxia-induced TNBC drug resistance remains to be clarified. Here, we found that hypoxia induced TNBC docetaxel resistance by decreasing the miR-494 level. Modulating miR-494 expression altered the sensitivity of TNBC cells to DTX under hypoxic conditions. Furthermore, we identified Survivin as a direct miR-494 target. Hypoxia upregulated survivin expression. In a clinical study, the HIF-1α/miR-494/Survivin signaling pathway was also active in primary human TNBC, and miR-494 expression negatively correlated with HIF-1α and survivin expression. Finally, in a xenograft model, both miR-494 overexpression and the HIF-1α inhibitor PX-478 increased the sensitivity of TNBC to DTX by suppressing the HIF-1α/miR-494/Survivin signaling pathway in vivo. In conclusion, treatments targeting the HIF-1α/miR-494/Survivin signaling pathway potentially reverse hypoxia-induced drug resistance in TNBC.

Indexed as

MicroRNAsTriple Negative Breast NeoplasmsCell Line, TumorDocetaxelGene Expression Regulation, NeoplasticHumansHypoxiaHypoxia-Inducible Factor 1, alpha SubunitSignal TransductionSurvivinDocetaxelHypoxia-Inducible Factor 1, alpha SubunitMicroRNAsMIRN494 microRNA, humanSurvivinDrug-resistanceHIF-1αmiR-494SurvivinTNBC

Identifiers

PMID35985176
PMCPMC9403568
OpenAlexW4292289506

What OpenQuestion holds

Textmetadata
LicenceCC BY-NC-ND
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.