Evidence map›Paper›PMID 34830434›Full record

ArticleInternational journal of molecular sciences2021

Impact of Sodium Dichloroacetate Alone and in Combination Therapies on Lung Tumor Growth and Metastasis.

Aya Al-Azawi, Shahrazad Sulaiman, Kholoud Arafat, Javed Yasin, Abderrahim Nemmar, Samir Attoub

Abstract read
In one paragraph

Article in International journal of molecular sciences, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 13 papers.

0numbers the graph read from it
0cells of the map it votes in
13citing 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

13 citing papers in PubMed.

  1. Review
  2. Article
  3. Review
  4. Article
  5. Dichloroacetate and Salinomycin as Therapeutic Agents in Cancer.Medical sciences (Basel, Switzerland) · 2025
    Review
  6. Article
  7. Dichloroacetate for Cancer Treatment: Some Facts and Many Doubts.Pharmaceuticals (Basel, Switzerland) · 2024
    Review
  8. Review
  9. Article
  10. PD-1 Independent Role of PD-L1 in Triple-Negative Breast Cancer Progression.International journal of molecular sciences · 2023
    Article
  11. Article
  12. Article
  13. 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

6 authors.

Aya Al-AzawiDepartment of Pharmacology & Therapeutics, College of Medicine & Health Sciences, United Arab Emirates University, Al-Ain 17666, United Arab Emirates.
Shahrazad SulaimanDepartment of Pharmacology & Therapeutics, College of Medicine & Health Sciences, United Arab Emirates University, Al-Ain 17666, United Arab Emirates.
Kholoud ArafatDepartment of Pharmacology & Therapeutics, College of Medicine & Health Sciences, United Arab Emirates University, Al-Ain 17666, United Arab Emirates.
Javed YasinDepartment of Medicine, College of Medicine & Health Sciences, United Arab Emirates University, Al-Ain 17666, United Arab Emirates.ORCID 0000-0002-5867-2833
Abderrahim NemmarDepartment of Physiology, College of Medicine & Health Sciences, United Arab Emirates University, Al-Ain 17666, United Arab Emirates.ORCID 0000-0002-0699-1015
Samir AttoubDepartment of Pharmacology & Therapeutics, College of Medicine & Health Sciences, United Arab Emirates University, Al-Ain 17666, United Arab Emirates.

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Metabolic reprogramming has been recognized as an essential emerging cancer hallmark. Dichloroacetate (DCA), an inhibitor of pyruvate dehydrogenase kinase (PDK), has been reported to have anti-cancer effects by reversing tumor-associated glycolysis. This study was performed to explore the anti-cancer potential of DCA in lung cancer alone and in combination with chemo- and targeted therapies using two non-small cell lung cancer (NSCLC) cell lines, namely, A549 and LNM35. DCA markedly caused a concentration- and time-dependent decrease in the viability and colony growth of A549 and LNM35 cells in vitro. DCA also reduced the growth of tumor xenografts in both a chick embryo chorioallantoic membrane and nude mice models in vivo. Furthermore, DCA decreased the angiogenic capacity of human umbilical vein endothelial cells in vitro. On the other hand, DCA did not inhibit the in vitro cellular migration and invasion and the in vivo incidence and growth of axillary lymph nodes metastases in nude mice. Treatment with DCA did not show any toxicity in chick embryos and nude mice. Finally, we demonstrated that DCA significantly enhanced the anti-cancer effect of cisplatin in LNM35. In addition, the combination of DCA with gefitinib or erlotinib leads to additive effects on the inhibition of LNM35 colony growth after seven days of treatment and to synergistic effects on the inhibition of A549 colony growth after 14 days of treatment. Collectively, this study demonstrates that DCA is a safe and promising therapeutic agent for lung cancer.

Indexed as

A549 CellsAnimalsCellular ReprogrammingDichloroacetic AcidGlycolysisHumansLung NeoplasmsMiceNeoplasm MetastasisPyruvate Dehydrogenase Acetyl-Transferring KinaseXenograft Model Antitumor AssaysDichloroacetic AcidPyruvate Dehydrogenase Acetyl-Transferring Kinaseangiogenesisdichloroacetateerlotinibgefitiniblung cancerpyruvate dehydrogenase kinase inhibitortumor growth

Identifiers

PMID34830434
PMCPMC8624089

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Registered trials

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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.