Evidence map›Paper›PMID 39171468›Full record

ArticleCurrent cancer drug targets2025

Mitochondrial Deoxyguanosine Kinase Induces 5-Fluorouracil Chemotherapy Sensitivity through Autophagy.

Lu Dong, Sifan Liu, Wenjing Sun, Siying Liu, Nan Zhang, Shutian Zhang

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Article in Current cancer drug targets, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Not yet cited in PubMed.

0numbers the graph read from it
0cells of the map it votes in
0citing papers in PubMed
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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

0 citing papers in PubMed.

No citing paper in PubMed yet.

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.

Lu DongSchool of Clinical Medicine, Shandong Second Medical University, Weifang, 261000, China.
Sifan LiuDepartment of Gastroenterology, Beijing Friendship Hospital, Capital Medical University, State Key Laboratory for Digestive Health, National Clinical Research Center for Digestive Diseases, Beijing Digestive Disease Center, Beijing Key Laboratory for Precancerous Lesion of Digestive Diseases, Beijing, 100050, China.
Wenjing SunSchool of Clinical Medicine, Shandong Second Medical University, Weifang, 261000, China.
Siying LiuDepartment of Gastroenterology, Beijing Friendship Hospital, Capital Medical University, State Key Laboratory for Digestive Health, National Clinical Research Center for Digestive Diseases, Beijing Digestive Disease Center, Beijing Key Laboratory for Precancerous Lesion of Digestive Diseases, Beijing, 100050, China.
Nan ZhangDepartment of Gastroenterology, Beijing Friendship Hospital, Capital Medical University, State Key Laboratory for Digestive Health, National Clinical Research Center for Digestive Diseases, Beijing Digestive Disease Center, Beijing Key Laboratory for Precancerous Lesion of Digestive Diseases, Beijing, 100050, China.
Shutian ZhangDepartment of Gastroenterology, Beijing Friendship Hospital, Capital Medical University, State Key Laboratory for Digestive Health, National Clinical Research Center for Digestive Diseases, Beijing Digestive Disease Center, Beijing Key Laboratory for Precancerous Lesion of Digestive Diseases, Beijing, 100050, China.

Funding

Beijing Hospitals Authority Youth Programme QML20230104National Natural Science Foundation of China 82103198, 82027801Research Foundation of Beijing Friendship Hospital, Capital Medical University YYZZ202108
6 · The paper itself

Abstract

aimsThe purpose of this study was to investigate the role of DGUOK in the progression of colorectal cancer (CRC) and its impact on the sensitivity of CRC cells to 5-FU treatment.

methodsWe conducted bioinformatics analysis and qRT-PCR to evaluate DGUOK expression in CRC tissues/cells. Cell viability of CRC cells treated with 5-FU was assessed using CCK-8 and colony formation assays. Autophagy levels were determined through immunofluorescence assays and Western blot analysis. Additionally, the influence of p-p38 on autophagy was investigated

resultsOur findings indicate that DGUOK is upregulated in CRC tissues compared to normal tissues, correlating with increased cell proliferation and migration. Functionally, inhibition of DGUOK enhances autophagy, thereby decreasing the sensitivity of CRC cells to 5-FU. This effect is partly mediated by DGUOK's impact on the mitogen-activated protein kinase (MAPK) pathway, specifically promoting the phosphorylation of p38 MAPK, a crucial regulator in autophagy pathways.

conclusionThese results suggest that DGUOK could serve as a novel marker for predicting the efficacy of 5-FU in CRC treatment.

Indexed as

Antimetabolites, AntineoplasticAutophagyColorectal NeoplasmsDrug Resistance, NeoplasmFluorouracilMitochondriaCell Line, TumorCell MovementCell ProliferationCell SurvivalGene Expression Regulation, NeoplasticHumansp38 Mitogen-Activated Protein KinasesAntimetabolites, AntineoplasticFluorouracilp38 Mitogen-Activated Protein Kinases5-fluorouracilautophagychemotherapy sensitivity.Colorectal cancerdeoxyguanosine kinasep38 MAPK

Identifiers

PMID39171468

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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.