Evidence map›Paper›PMID 34552061›Full record

ArticleCell death & disease2021

MiR-9-3p regulates the biological functions and drug resistance of gemcitabine-treated breast cancer cells and affects tumor growth through targeting MTDH.

Yike Wang, Lifeng Dong, Fang Wan, Fangfang Chen, Dianlei Liu, Deqin Chen, Jingpei Long

Open access · goldAbstract read
In one paragraph

Article in Cell death & disease, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 16 papers.

0numbers the graph read from it
0cells of the map it votes in
16citing papers in PubMed
3.0field-weighted citation impact, top 8% 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

16 citing papers in PubMed, 27 citations in OpenAlex.

  1. Article
  2. Article
  3. Article
  4. Review
  5. Article
  6. Review
  7. Article
  8. Article
  9. Article
  10. Article
  11. Review
  12. Effects of hsa-miR-9-3p and hsa-miR-9-5p on Topoisomerase IIThe Journal of pharmacology and experimental therapeutics · 2023
    Article
  13. Article
  14. Article
  15. Article
  16. Review
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

7 authors at 1 institution in 1 country.

Yike WangDepartment of Surgery, Women's Hospital School of Medicine Zhejiang University, Hangzhou, Zhejiang, China.
Lifeng DongDepartment of Surgery, Women's Hospital School of Medicine Zhejiang University, Hangzhou, Zhejiang, China.
Fang WanDepartment of Surgery, Women's Hospital School of Medicine Zhejiang University, Hangzhou, Zhejiang, China.
Fangfang ChenDepartment of Surgery, Women's Hospital School of Medicine Zhejiang University, Hangzhou, Zhejiang, China.
Dianlei LiuDepartment of Surgery, Women's Hospital School of Medicine Zhejiang University, Hangzhou, Zhejiang, China.
Deqin ChenDepartment of Surgery, Women's Hospital School of Medicine Zhejiang University, Hangzhou, Zhejiang, China.
Jingpei LongDepartment of Surgery, Women's Hospital School of Medicine Zhejiang University, Hangzhou, Zhejiang, China. longjp@zju.edu.cn.
Women's Hospital, School of Medicine, Zhejiang University · CN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

This study explored the role of MTDH in regulating the sensitivity of breast cancer cell lines to gemcitabine (Gem) and the potential miRNAs targeting MTDH. The expression of MTDH in cancer tissues and cells was detected by immunohistochemical staining or qRT-PCR. The target genes for MTDH were predicted by bioinformatics and further confirmed by dual-luciferase reporter assay and qRT-PCR. Cancer cells were transfected with siMTDH, MTDH, miR-9-3p inhibitor, or mimics and treated by Gem, then CCK-8, colony formation assay, tube formation assay, flow cytometry, wound healing assay, and Transwell were performed to explore the effects of MTDH, miR-9-3p, and Gem on cancer cell growth, apoptosis, migration, and invasion. Expressions of VEGF, p53, cleaved caspase-3, MMP-2, MMP-9, E-Cadherin, N-Cadherin, and Vimentin were determined by Western blot. MTDH was high-expressed in cancer tissues and cells, and the cells with high-expressed MTDH were less sensitive to Gem, while silencing MTDH expression significantly promoted the effect of Gem on inducing apoptosis, inhibiting cell migration, invasion, and growth, and on regulating protein expressions of cancer cells. Moreover, miR-9-3p had a targeted binding relationship with MTDH, and overexpressed miR-9-3p greatly promoted the toxic effects of Gem on cancer cells and expressions of apoptosis-related proteins, whereas overexpressed MTDH partially reversed such effects of overexpressed miR-9-3p. The study proved that miR-9-3p regulates biological functions, drug resistance, and the growth of Gem-treated breast cancer cells through targeting MTDH.

Indexed as

AnimalsApoptosisBreast NeoplasmsCell Line, TumorCell MovementCell ProliferationCell SurvivalDeoxycytidineDrug Resistance, NeoplasmFemaleGemcitabineGene Expression Regulation, NeoplasticGene SilencingHEK293 CellsHumansMembrane ProteinsDeoxycytidineGemcitabineMembrane ProteinsMicroRNAsMIRN92 microRNA, humanMTDH protein, humanNeoplasm ProteinsRNA-Binding Proteins

Identifiers

PMID34552061
PMCPMC8458456
OpenAlexW3199574800

What OpenQuestion 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 OpenQuestion graph.