Evidence map›Paper›PMID 28832761›Full record

ArticleBrazilian journal of medical and biological research = Revista brasileira de pesquisas medicas e biologica2017

Salinomycin enhances doxorubicin sensitivity through reversing the epithelial-mesenchymal transition of cholangiocarcinoma cells by regulating ARK5.

Z Yu, H Cheng, H Zhu, M Cao, C Lu, S Bao, Y Pan, Y Li

Open access · goldAbstract read
In one paragraph

Article in Brazilian journal of medical and biological research = Revista brasileira de pesquisas medicas e biologica, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 9 papers.

0numbers the graph read from it
0cells of the map it votes in
9citing papers in PubMed
4.0field-weighted citation impact, top 6% 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

9 citing papers in PubMed, 23 citations in OpenAlex.

  1. Article
  2. Article
  3. Article
  4. Role of ARK5 in cancer and other diseases (Review).Experimental and therapeutic medicine · 2021
    Review
  5. Article
  6. Review
  7. Article
  8. Article
  9. Article
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

8 authors at 4 institutions in 1 country.

Z YuDepartment of General Surgery, Qingdao Clinic Medical College, Nanjing Medical University, Qingdao, China.
H ChengDepartment of General Surgery, The Afflicted Drum Tower Hospital, Nanjing University Medical School, Nanjing, China.
H ZhuDepartment of Gastroenterology, The Afflicted Drum Tower Hospital, Nanjing University Medical School, Nanjing, China.
M CaoDepartment of General Surgery, The Afflicted Drum Tower Hospital, Nanjing University Medical School, Nanjing, China.
C LuDepartment of General Surgery, The Afflicted Drum Tower Hospital, Nanjing University Medical School, Nanjing, China.
S BaoDepartment of General Surgery, The Afflicted Drum Tower Hospital, Nanjing University Medical School, Nanjing, China.
Y PanDepartment of General Surgery, The Afflicted Drum Tower Hospital, Nanjing University Medical School, Nanjing, China.
Y LiDepartment of General Surgery, Qingdao Clinic Medical College, Nanjing Medical University, Qingdao, China.
Nanjing University · CNNanjing Drum Tower Hospital · CNNanjing Medical University · CNThe First People’s Hospital of Lianyungang · CN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Chemotherapy response rates in patients with cholangiocarcinoma remain low, primarily due to the development of drug resistance. Epithelial-mesenchymal transition (EMT) of cancer cells is widely accepted to be important for metastasis and progression, but it has also been linked to the development of chemoresistance. Salinomycin (an antibiotic) has shown some potential as a chemotherapeutic agent as it selectively kills cancer stem cells, and has been hypothesized to block the EMT process. In this study, we investigated whether salinomycin could reverse the chemoresistance of cholangiocarcinoma cells to the chemotherapy drug doxorubicin. We found that combined salinomycin with doxorubicin treatment resulted in a significant decrease in cell viability compared with doxorubicin or salinomycin treatment alone in two cholangiocarcinoma cell lines (RBE and Huh-28). The dosages of both drugs that were required to produce a cytotoxic effect decreased, indicating that these two drugs have a synergistic effect. In terms of mechanism, salinomycin reversed doxorubicin-induced EMT of cholangiocarcinoma cells, as shown morphologically and through the detection of EMT markers. Moreover, we showed that salinomycin treatment downregulated the AMP-activated protein kinase family member 5 (ARK5) expression, which regulates the EMT process of cholangiocarcinoma. Our results indicated that salinomycin reversed the EMT process in cholangiocarcinoma cells by inhibiting ARK5 expression and enhanced the chemosensitivity of cholangiocarcinoma cells to doxorubicin. Therefore, a combined treatment of salinomycin with doxorubicin could be used to enhance doxorubicin sensitivity in patients with cholangiocarcinoma.

Indexed as

AMP-Activated Protein KinasesAntibiotics, AntineoplasticCell Line, TumorCell SurvivalCholangiocarcinomaDoxorubicinDrug SynergismEpithelial-Mesenchymal TransitionGene Expression Regulation, NeoplasticHumansPolyether PolyketidesPyransAMP-Activated Protein KinasesAntibiotics, AntineoplasticDoxorubicinPolyether PolyketidesPyranssalinomycin

Identifiers

PMID28832761
PMCPMC5561806
OpenAlexW2746190369

What OpenQuestion holds

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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.