Evidence map›Paper›PMID 29344648›Full record

ArticleInternational journal of molecular medicine2018

Effect of midkine on gemcitabine resistance in biliary tract cancer.

Yongliang Lu, Bing Yan, Huihui Guo, Li Qiu, Xinrong Sun, Xiang Wang, Qian Shi, Ying Bao

Open access · hybridAbstract read
In one paragraph

Article in International journal of molecular medicine, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 14 papers.

0numbers the graph read from it
0cells of the map it votes in
14citing papers in PubMed
1.7field-weighted citation impact, top 18% 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

14 citing papers in PubMed, 24 citations in OpenAlex.

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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

8 authors at 1 institution in 1 country.

Yongliang LuDepartment of Medicine, Huzhou University, Huzhou, Zhejiang 313000, P.R. China.
Bing YanDepartment of Pharmacy, The First Affiliated Hospital of Huzhou University, The First People's Hospital of Huzhou, Huzhou, Zhejiang 313000, P.R. China.
Huihui GuoDepartment of Laboratory Medicine, The First Affiliated Hospital of Huzhou University, The First People's Hospital of Huzhou, Huzhou, Zhejiang 313000, P.R. China.
Li QiuDepartment of Pharmacy, The First Affiliated Hospital of Huzhou University, The First People's Hospital of Huzhou, Huzhou, Zhejiang 313000, P.R. China.
Xinrong SunDepartment of Surgery, The First Affiliated Hospital of Huzhou University, The First People's Hospital of Huzhou, Huzhou, Zhejiang 313000, P.R. China.
Xiang WangDepartment of Laboratory Medicine, The First Affiliated Hospital of Huzhou University, The First People's Hospital of Huzhou, Huzhou, Zhejiang 313000, P.R. China.
Qian ShiDepartment of Laboratory Medicine, The First Affiliated Hospital of Huzhou University, The First People's Hospital of Huzhou, Huzhou, Zhejiang 313000, P.R. China.
Ying BaoDepartment of Surgery, The First Affiliated Hospital of Huzhou University, The First People's Hospital of Huzhou, Huzhou, Zhejiang 313000, P.R. China.
Huzhou University · CN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Gemcitabine‑based chemotherapy is one of the most effective and commonly used chemotherapeutic regimens for biliary tract cancer (BTC). However, development of resistance to this drug limits its efficacy. The present study aimed to explore the effects of midkine (MDK) on the resistance of BTC cells to gemcitabine. Cell viability and proliferation were measured by a Cell Counting Kit‑8 assay and 5‑ethynyl‑2'‑deoxyuridine staining, respectively. Western blot analysis was used to detect the expression of E‑cadherin and vimentin. The results indicated that BTC cell lines were more resistant to gemcitabine plus MDK compared with gemcitabine alone. In terms of the underlying mechanism, MDK promoted the epithelial to mesenchymal transition (EMT) of BTC cells and the enhancing effect of MDK on gemcitabine resistance was abrogated when the EMT was blocked with small interfering (si)RNA targeting Twist. In addition, MDK promoted the expression of Notch‑1, while knockdown of Notch‑1 by siRNA blocked the EMT process in the BTC cell lines. Taken together, these results indicated that MDK promoted gemcitabine resistance of BTC through inducing EMT via upregulating Notch‑1. It was suggested that inhibition of the EMT is a promising strategy to overcome MDK‑induced drug resistance.

Indexed as

Drug Resistance, NeoplasmAntimetabolites, AntineoplasticBiliary Tract NeoplasmsCell Line, TumorCell ProliferationCell SurvivalDeoxycytidineEpithelial-Mesenchymal TransitionGemcitabineHumansIntercellular Signaling Peptides and ProteinsMidkineAntimetabolites, AntineoplasticDeoxycytidineGemcitabineIntercellular Signaling Peptides and ProteinsMDK protein, humanMidkine

Identifiers

PMID29344648
PMCPMC5810218
OpenAlexW2785185187

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.