Evidence map›Paper›PMID 29117108›Full record

ArticleInternational journal of molecular sciences2017

Effect of AICAR and 5-Fluorouracil on X-ray Repair, Cross-Complementing Group 1 Expression, and Consequent Cytotoxicity Regulation in Human HCT-116 Colorectal Cancer Cells.

Ko-Chao Lee, Chien-Tsong Lin, Shun-Fu Chang, Cheng-Nan Chen, Jing-Lan Liu, Wen-Shih Huang

Open access · goldAbstract read
In one paragraph

Article in International journal of molecular sciences, 2017. 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
0.4field-weighted citation impact, top 36% 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, 10 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

6 authors at 4 institutions in 1 country.

Ko-Chao LeeDepartment of Colorectal Surgery, Department of Surgery, Chang Gung Memorial Hospital, Kaohsiung Medical Center, Kaohsiung 833, Taiwan. kmch4329@gmail.com.
Chien-Tsong LinCenter for General Education, National Formosa University, Yunlin 632, Taiwan. mite402@yahoo.com.tw.
Shun-Fu ChangDepartment of Medical Research and Development, Chang Gung Memorial Hospital Chiayi Branch, Chiayi 613, Taiwan. sfchang@cgmh.org.tw.
Cheng-Nan ChenDepartment of Biochemical Science and Technology, National Chiayi University, Chiayi 600, Taiwan. cnchen@mail.ncyu.edu.tw.
Jing-Lan LiuDepartment of Pathology, Chang Gung Memorial Hospital Chiayi Branch, Chiayi 600, Taiwan. b8801046@gmail.com.
Wen-Shih HuangGraduate Institute of Clinical Medical Sciences, College of Medicine, Chang Gung University, Taoyuan 333, Taiwan. wen1204@adm.cgmh.org.tw.
Chiayi Chang Gung Memorial Hospital · TWNational Chiayi University · TWChang Gung University · TWKaohsiung Chang Gung Memorial Hospital · TW

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Colorectal cancer (CRC) is one of the leading causes of cancer mortality and 5-Fluorouracil (5-FU) is the most common chemotherapy agent of CRC. A high level of X-ray repair cross complementing group 1 (XRCC1) in cancer cells has been associated with the drug resistance occurrence. Moreover, the activation of adenosine monophosphate (AMP)-activated protein kinase (AMPK) has been indicated to regulate the cancer cell survival. Thus, this study was aimed to examine whether XRCC1 plays a role in the 5-FU/AMPK agonist (AICAR)-induced cytotoxic effect on CRC and the underlying mechanisms. Human HCT-116 colorectal cells were used in this study. It was shown that 5-FU increases the XRCC1 expression in HCT-116 cells and then affects the cell survival through CXCR4/Akt signaling. Moreover, 5-FU combined with AICAR further result in more survival inhibition in HCT-116 cells, accompanied with reduced CXCR4/Akt signaling activity and XRCC1 expression. These results elucidate the role and mechanism of XRCC1 in the drug resistance of HCT-116 cells to 5-FU. We also demonstrate the synergistic inhibitory effect of AMPK on 5-FU-inhibited HCT-116 cell survival under the 5-FU and AICAR co-treatment. Thus, our findings may provide a new notion for the future drug regimen incorporating 5-FU and AMPK agonists for the CRC treatment.

Indexed as

Aminoimidazole CarboxamideAMP-Activated Protein Kinase KinasesAntineoplastic AgentsApoptosisCell ProliferationCell SurvivalColorectal NeoplasmsDrug Resistance, NeoplasmDrug SynergismDrug Therapy, CombinationFluorouracilHCT116 CellsHumansProtein KinasesReceptors, CXCR4RibonucleotidesAICA ribonucleotideAminoimidazole CarboxamideAMP-Activated Protein Kinase KinasesAntineoplastic AgentsCXCR4 protein, humanFluorouracilProtein KinasesReceptors, CXCR4RibonucleotidesX-ray Repair Cross Complementing Protein 1XRCC1 protein, human5-fluorouracilAICARAMP-activated protein kinasecolorectal cancerX-ray repair cross complementing group 1

Identifiers

PMID29117108
PMCPMC5713332
OpenAlexW2767344670

What OpenQuestion holds

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LicenceCC BY
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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.