Evidence map›Paper›PMID 27577078›Full record

ArticleOncotarget2016

miR-223 increases gallbladder cancer cell sensitivity to docetaxel by downregulating STMN1.

Wei Lu, Yunping Hu, Qiang Ma, Linzhu Zhou, Lin Jiang, Zhizhen Li, Shuai Zhao, Yuzhen Xu, Weibin Shi, Sheng Li and 1 more

Open access · diamondAbstract read
In one paragraph

Article in Oncotarget, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 10 papers.

0numbers the graph read from it
0cells of the map it votes in
10citing papers in PubMed
1.2field-weighted citation impact, top 23% 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

10 citing papers in PubMed, 24 citations in OpenAlex.

  1. Review
  2. Review
  3. Article
  4. Overview of current targeted therapy in gallbladder cancer.Signal transduction and targeted therapy · 2020
    Review
  5. Article
  6. Article
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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

11 authors at 4 institutions in 1 country.

Wei LuDepartment of General Surgery, Xinhua Hospital, Affiliated to Shanghai Jiao Tong University, School of Medicine, Shanghai, China.
Yunping HuInstitute of Biliary Tract Diseases Research, Shanghai Jiao Tong University School of Medicine, Shanghai, China.
Qiang MaInstitute of Biliary Tract Diseases Research, Shanghai Jiao Tong University School of Medicine, Shanghai, China.
Linzhu ZhouInstitute of Chemistry, Shanghai Jiao Tong University, Shanghai, China.
Lin JiangInstitute of Biliary Tract Diseases Research, Shanghai Jiao Tong University School of Medicine, Shanghai, China.
Zhizhen LiInstitute of Biliary Tract Diseases Research, Shanghai Jiao Tong University School of Medicine, Shanghai, China.
Shuai ZhaoInstitute of Biliary Tract Diseases Research, Shanghai Jiao Tong University School of Medicine, Shanghai, China.
Yuzhen XuDepartment of Gastrointestinal Surgery, Xu Zhou Center Hospital, Affiliated to Medical College of Southeast University, Jiangsu, China.
Weibin ShiDepartment of General Surgery, Xinhua Hospital, Affiliated to Shanghai Jiao Tong University, School of Medicine, Shanghai, China.
Sheng LiDepartment of Biochemistry, Dalian Medical University, Liaoning, China.
Yingbin LiuDepartment of General Surgery, Xinhua Hospital, Affiliated to Shanghai Jiao Tong University, School of Medicine, Shanghai, China.
Shanghai Jiao Tong University · CNXinHua Hospital · CNDalian Medical University · CNInstitute of Chemistry · CN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

backgroundMicroRNAs (miRs) are involved in cancer carcinogenesis, and certain regulatory miRs could provide promising therapeutic methods for refractory malignancies, such as gallbladder cancer (GBC). miR-223 was found to play a pivotal role in enhancing chemotherapeutic effects, therefore evoking interest in the role of miR-223 in GBC.

resultsmiR-223 was decreased in GBC tissues and cell lines, and ectopic miR- 223 expression exhibited multiple anti-tumorigenic effects in GBC cells, including decreased proliferation, migration and invasion in vitro. However, treatment with a miR-223 inhibitor increased cell viability. We determined that STMN1 was negatively correlated with and regulated by miR-223 in GBC. miR-223 increased GBC sensitivity to docetaxel in vitro and in vivo, and the induced sensitivity to docetaxel was suppressed by the restoration of STMN1 expression.

methodsWe examined miR-223 expression in GBC tissue and GBC cell lines using qRT-PCR. The effects of modulated miR-223 expression in GBC cells were assayed using Cell Counting Kit-8 (CCK8), flow cytometry, and wound-healing and invasion assays. Susceptibility to docetaxel was evaluated in miR-223/STMN1-modulated GBC cells and xenograft tumor models. The protein expression of relevant genes was examined by Western blotting.

conclusionsThese findings indicated that miR-223 might serve as an onco-suppressor that enhances susceptibility to docetaxel by downregulating STMN1 in GBC, highlighting its promising therapeutic value.

Indexed as

Gene Expression Regulation, NeoplasticAnimalsAntineoplastic AgentsCell Line, TumorCell ProliferationCell SurvivalDocetaxelDown-RegulationFlow CytometryGallbladderGallbladder NeoplasmsGenes, Tumor SuppressorHumansImmunohistochemistryMiceMice, NudeAntineoplastic AgentsDocetaxelMicroRNAsMIR223, humanStathminSTMN1 protein, humanTaxoidsgallbladder cancermalignancymiR-223STMN1

Identifiers

PMID27577078
PMCPMC5308733
OpenAlexW2511536337

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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.