Evidence map›Paper›PMID 39220482›Full record

ArticleACS omega2024

Lonidamine Increases the Cytotoxic Effect of 1-[(4-Amino-2-methyl-5-pyrimidinyl)methyl]-3-(2-chloroethyl)-3-nitrosourea via Energy Inhibition, Disrupting Redox Homeostasis, and Downregulating MGMT Expression in Human Lung Cancer Cell Line.

Tengjiao Fan, Lin Shen, Yaxin Huang, Xin Wang, Lijiao Zhao, Rugang Zhong, Peng Wang, Guohui Sun

Abstract read
In one paragraph

Article in ACS omega, 2024. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 2 papers.

0numbers the graph read from it
0cells of the map it votes in
2citing papers in PubMed
–field-weighted citation impact
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

2 citing papers in PubMed.

  1. Article
  2. Review
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.

Tengjiao FanDepartment of Medical Technology, Beijing Pharmaceutical University of Staff and Workers, Beijing 100079, P. R. China.
Lin ShenDepartment of Dermatology, the First Medical Center of PLA General Hospital, Beijing 100853, P. R. China.
Yaxin HuangBeijing Key Laboratory of Environment & Viral Oncology, College of Chemistry and Life Science, Beijing University of Technology, Beijing 100124, P. R. China.
Xin WangDepartment of Clinical Trials Center, National Cancer Center/National Clinical Research Center for Cancer/Cancer Hospital, Chinese Academy of Medical Sciences and Peking Union Medical College, Beijing 100029, P. R. China.
Lijiao ZhaoBeijing Key Laboratory of Environment & Viral Oncology, College of Chemistry and Life Science, Beijing University of Technology, Beijing 100124, P. R. China.ORCID https://orcid.org/0000-0002-4876-323X
Rugang ZhongBeijing Key Laboratory of Environment & Viral Oncology, College of Chemistry and Life Science, Beijing University of Technology, Beijing 100124, P. R. China.
Peng WangDepartment of Neurosurgery, the First Medical Center of Chinese PLA General Hospital, Beijing 100853, P. R. China.
Guohui SunBeijing Key Laboratory of Environment & Viral Oncology, College of Chemistry and Life Science, Beijing University of Technology, Beijing 100124, P. R. China.ORCID https://orcid.org/0000-0003-2259-5431

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Lung cancer ranks as the second most diagnosed cancer and the leading cause of cancer-related deaths worldwide. Novel chemotherapeutic strategies are crucial to efficiently target tumor cells while minimizing toxicity to normal cells. In this study, we proposed a combination strategy using energy blocker lonidamine (LND) and cytotoxic drug nimustine (ACNU, 1-[(4-amino-2-methyl-5-pyrimidinyl)methyl]-3-(2-chloroethyl)-3-nitrosourea) to enhance the killing of a human lung cancer cell line and investigated the potential chemo-sensitizing mechanism of LND. LND was found to remarkably increase the cytotoxicity of ACNU to A549 and H1299 cells without significantly affecting normal lung BEAS2B cells. The combination of LND and ACNU also produced significant effects on cell apoptosis, colony formation, cell migration, and invasion assays compared to single drug treatment. Mechanistically, LND decreased intracellular ATP levels by inhibiting glycolysis and inducing mitochondrial dysfunction. Furthermore, the combination of LND and ACNU could intensify cellular oxidative stress, decrease cellular GSH contents, and increase reactive oxygen species (ROS) production. Notably, LND alone dramatically downregulated the expression of DNA repair protein MGMT (O

Identifiers

PMID39220482
PMCPMC11360010

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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.