Evidence map›Paper›PMID 32244823›Full record

ArticleCancers2020

CD44s Induces miR-629-3p Expression in Association with Cisplatin Resistance in Head and Neck Cancer Cells.

Junichiro Chikuda, Kurataka Otsuka, Iwao Shimomura, Kagenori Ito, Hiroaki Miyazaki, Ryou-U Takahashi, Masahiro Nagasaki, Yoshiki Mukudai, Takahiro Ochiya, Toshikazu Shimane and 2 more

Open access · goldAbstract read
In one paragraph

Article in Cancers, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 8 papers.

0numbers the graph read from it
0cells of the map it votes in
8citing papers in PubMed
1.2field-weighted citation impact, top 24% 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

8 citing papers in PubMed, 20 citations in OpenAlex.

  1. Article
  2. Article
  3. Article
  4. Article
  5. Article
  6. Review
  7. Article
  8. 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

12 authors at 3 institutions in 1 country.

Junichiro ChikudaDivision of Cellular Signaling, National Cancer Center Research Institute, Tokyo 104-0045, Japan.
Kurataka OtsukaDivision of Cellular Signaling, National Cancer Center Research Institute, Tokyo 104-0045, Japan.
Iwao ShimomuraDivision of Cellular Signaling, National Cancer Center Research Institute, Tokyo 104-0045, Japan.
Kagenori ItoDivision of Cellular Signaling, National Cancer Center Research Institute, Tokyo 104-0045, Japan.ORCID 0000-0002-4970-1727
Hiroaki MiyazakiDivision of Cellular Signaling, National Cancer Center Research Institute, Tokyo 104-0045, Japan.
Ryou-U TakahashiDivision of Cellular Signaling, National Cancer Center Research Institute, Tokyo 104-0045, Japan.ORCID 0000-0002-9192-2929
Masahiro NagasakiDepartment of Oral and Maxillofacial Surgery, Showa University School of Dentistry, Tokyo 145-8515, Japan.
Yoshiki MukudaiDepartment of Oral and Maxillofacial Surgery, Showa University School of Dentistry, Tokyo 145-8515, Japan.ORCID 0000-0002-9600-4430
Takahiro OchiyaDivision of Cellular Signaling, National Cancer Center Research Institute, Tokyo 104-0045, Japan.
Toshikazu ShimaneHead and Neck Oncology Center, Showa University, Tokyo 142-8555, Japan.
Tatsuo ShirotaDepartment of Oral and Maxillofacial Surgery, Showa University School of Dentistry, Tokyo 145-8515, Japan.
Yusuke YamamotoDivision of Cellular Signaling, National Cancer Center Research Institute, Tokyo 104-0045, Japan.ORCID 0000-0002-5262-8479
Showa University · JPHiroshima University · JPTokyo Medical University · JP

Funding

Japan Agency for Medical Research and Development 16ae0101011h0003Japan Society for the Promotion of Science 17H04991Japan Society for the Promotion of Science 17K17110
6 · The paper itself

Abstract

Cisplatin (cis-diamminedichloroplatinum II [CDDP] ) is a well-known chemotherapeutic drug that has been used for the treatment of various types of human cancers, including head and neck cancer. Cisplatin exerts anticancer effects by causing DNA damage, replication defects, transcriptional inhibition, cell cycle arrest, and the induction of apoptosis. However, drug resistance is one of the most serious problems with cancer chemotherapy, and it causes expected therapeutic effects to not always be achieved. Here, we analyzed global microRNA (miRNA) expression in CD44 standard form (CD44s)-expressing SAS cells, and we identified miR-629-3p as being responsible for acquiring anticancer drug resistance in head and neck cancer. The introduction of miR-629-3p expression inhibited apoptotic cell death under cisplatin treatment conditions, and it promoted cell migration. Among the computationally predicted target genes of miR-629-3p, we found that a number of gene expressions were suppressed by the transfection with miR-629-3p. Using a xenografting model, we showed that miR-629-3p conferred cisplatin resistance to SAS cells. Clinically, increased miR-629-3p expression tended to be associated with decreased survival in head and neck cancer patients. In conclusion, our data suggest that the increased expression of miR-629-3p provides a mechanism of cisplatin resistance in head and neck cancer and may serve as a therapeutic target to reverse chemotherapy resistance.

Indexed as

apoptosiscancer stem cellcisplatin resistancemigrationmiR-629-3pSAS cell

Identifiers

PMID32244823
PMCPMC7226407
OpenAlexW3014296170

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.