Evidence map›Paper›PMID 28765935›Full record

ArticleOncology reports2017

FBW7 increases the chemosensitivity of pancreatic cancer cells to gemcitabine through upregulation of ENT1.

Qiangsheng Hu, Yi Qin, Bo Zhang, Chen Liang, Shunrong Ji, Si Shi, Wenyan Xu, Jinfeng Xiang, Dingkong Liang, Quanxing Ni and 2 more

Open access · hybridAbstract read
In one paragraph

Article in Oncology reports, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 20 papers.

0numbers the graph read from it
0cells of the map it votes in
20citing papers in PubMed
1.5field-weighted citation impact, top 15% 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

20 citing papers in PubMed, 30 citations in OpenAlex.

  1. Review
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  5. Molecular insights and clinical implications for the tumor suppressor role of SCFBiochimica et biophysica acta. Reviews on cancer · 2024
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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

12 authors at 1 institution in 1 country.

Qiangsheng HuDepartment of Pancreatic Surgery, Fudan University Shanghai Cancer Center, Shanghai 200032, P.R. China.
Yi QinDepartment of Pancreatic Surgery, Fudan University Shanghai Cancer Center, Shanghai 200032, P.R. China.
Bo ZhangDepartment of Pancreatic Surgery, Fudan University Shanghai Cancer Center, Shanghai 200032, P.R. China.
Chen LiangDepartment of Pancreatic Surgery, Fudan University Shanghai Cancer Center, Shanghai 200032, P.R. China.
Shunrong JiDepartment of Pancreatic Surgery, Fudan University Shanghai Cancer Center, Shanghai 200032, P.R. China.
Si ShiDepartment of Pancreatic Surgery, Fudan University Shanghai Cancer Center, Shanghai 200032, P.R. China.
Wenyan XuDepartment of Pancreatic Surgery, Fudan University Shanghai Cancer Center, Shanghai 200032, P.R. China.
Jinfeng XiangDepartment of Pancreatic Surgery, Fudan University Shanghai Cancer Center, Shanghai 200032, P.R. China.
Dingkong LiangDepartment of Pancreatic Surgery, Fudan University Shanghai Cancer Center, Shanghai 200032, P.R. China.
Quanxing NiDepartment of Pancreatic Surgery, Fudan University Shanghai Cancer Center, Shanghai 200032, P.R. China.
Xianjun YuDepartment of Pancreatic Surgery, Fudan University Shanghai Cancer Center, Shanghai 200032, P.R. China.
Jin XuDepartment of Pancreatic Surgery, Fudan University Shanghai Cancer Center, Shanghai 200032, P.R. China.
Fudan University Shanghai Cancer Center · CN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

F-box and WD repeat domain-containing 7 (FBW7) has been characterized as a tumor suppressor, and its mutation or decreased expression has been observed in many types of human cancers. Our recent studies have uncovered that in pancreatic cancer, the KRAS mutation decreased FBW7 expression through phosphorylation and subsequent ubiquitination. Moreover, FBW7 inhibited aerobic glycolysis in pancreatic cancer via induction of thioredoxin-interacting protein (TXNIP), a mitochondrial localized tumor suppressor. The roles of FBW7 in anti-apoptosis and drug resistance via proteosomal degradation of myeloid cell leukemia-1 (MCL-1), which is an anti-apoptotic factor have been reported. However, the role of FBW7 in the chemotherapeutic resistance of pancreatic cancer to gemcitabine has seldom been reported. In the present study, we demonstrated that overexpression of FBW7 in pancreatic cancer cells rendered increased sensitivity to gemcitabine. Mechanistically, FBW7 promoted gemcitabine sensitivity via upregulation of equilibrative nucleoside transporter 1 (ENT1) at the protein level rather than the transcriptional level. In depth analysis demonstrated that the ENT1 protein level could be increased by lysosome inhibition. Taken together, our results demonstrated that FBW7 could be a target for improving the therapeutic efficacy of gemcitabine by induction of ENT1.

Indexed as

Antimetabolites, AntineoplasticCell Line, TumorDeoxycytidineDrug Resistance, NeoplasmEquilibrative Nucleoside Transporter 1F-Box-WD Repeat-Containing Protein 7GemcitabineHumansLysosomesMyeloid Cell Leukemia Sequence 1 ProteinPancreatic NeoplasmsUp-RegulationAntimetabolites, AntineoplasticDeoxycytidineEquilibrative Nucleoside Transporter 1F-Box-WD Repeat-Containing Protein 7FBXW7 protein, humanGemcitabineMCL1 protein, humanMyeloid Cell Leukemia Sequence 1 ProteinSLC29A1 protein, human

Identifiers

PMID28765935
PMCPMC5652962
OpenAlexW2741282735

What OpenQuestion holds

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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.