Evidence map›Paper›PMID 33747225›Full record

ReviewOncology letters2021

Altered glycolysis results in drug-resistant in clinical tumor therapy.

Jinghui Peng, Yangyang Cui, Shipeng Xu, Xiaowei Wu, Yue Huang, Wenbin Zhou, Shui Wang, Ziyi Fu, Hui Xie

Open access · diamondAbstract readReview
In one paragraph

Review in Oncology letters, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 47 papers.

0numbers the graph read from it
0cells of the map it votes in
47citing papers in PubMed
4.6field-weighted citation impact, top 3% 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

47 citing papers in PubMed, 63 citations in OpenAlex.

  1. Review
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  7. Solute carrier family 16 member 3 is a target of nodakenetin in breast cancer.Naunyn-Schmiedeberg's archives of pharmacology · 2026
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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

9 authors at 3 institutions in 2 countries.

Jinghui PengDepartment of Breast Surgery, The First Affiliated Hospital, Nanjing Medical University, Nanjing, Jiangsu 210029, P.R. China.
Yangyang CuiDepartment of Breast Surgery, The First Affiliated Hospital, Nanjing Medical University, Nanjing, Jiangsu 210029, P.R. China.
Shipeng XuRobert H. Lurie Comprehensive Cancer Center, Northwestern University Feinberg School of Medicine, Chicago, IL 60611, USA.
Xiaowei WuDepartment of Breast Surgery, The First Affiliated Hospital, Nanjing Medical University, Nanjing, Jiangsu 210029, P.R. China.
Yue HuangDepartment of Breast Surgery, The First Affiliated Hospital, Nanjing Medical University, Nanjing, Jiangsu 210029, P.R. China.
Wenbin ZhouDepartment of Breast Surgery, The First Affiliated Hospital, Nanjing Medical University, Nanjing, Jiangsu 210029, P.R. China.
Shui WangDepartment of Breast Surgery, The First Affiliated Hospital, Nanjing Medical University, Nanjing, Jiangsu 210029, P.R. China.
Ziyi FuNanjing Maternal and Child Health Medical Institute, Obstetrics and Gynecology Hospital Affiliated to Nanjing Medical University, Nanjing Maternity and Child Health Care Hospital, Nanjing, Jiangsu 210004, P.R. China.
Hui XieDepartment of Breast Surgery, The First Affiliated Hospital, Nanjing Medical University, Nanjing, Jiangsu 210029, P.R. China.
Nanjing Medical University · CNNanjing Maternity and Child Health Care Hospital · CNNorthwestern University · US

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Cancer cells undergo metabolic reprogramming, including increased glucose metabolism, fatty acid synthesis and glutamine metabolic rates. These enhancements to three major metabolic pathways are closely associated with glycolysis, which is considered the central component of cancer cell metabolism. Increasing evidence suggests that dysfunctional glycolysis is commonly associated with drug resistance in cancer treatment, and aberrant glycolysis plays a significant role in drug-resistant cancer cells. Studies on the development of drugs targeting these abnormalities have led to improvements in the efficacy of tumor treatment. The present review discusses the changes in glycolysis targets that cause drug resistance in cancer cells, including hexokinase, pyruvate kinase, pyruvate dehydrogenase complex, glucose transporters, and lactate, as well the underlying molecular mechanisms and corresponding novel therapeutic strategies. In addition, the association between increased oxidative phosphorylation and drug resistance is introduced, which is caused by metabolic plasticity. Given that aberrant glycolysis has been identified as a common metabolic feature of drug-resistant tumor cells, targeting glycolysis may be a novel strategy to develop new drugs to benefit patients with drug-resistance.

Indexed as

cancerdrug resistanceglycolysismetabolismmicroenvironment

Identifiers

PMID33747225
PMCPMC7967983
OpenAlexW3135905016

What OpenQuestion holds

Textmetadata
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.