Evidence map›Paper›PMID 27385212›Full record

ArticleOncotarget2016

Halofuginone and artemisinin synergistically arrest cancer cells at the G1/G0 phase by upregulating p21Cip1 and p27Kip1.

Guoqing Chen, Ruihong Gong, Xianli Shi, Dajian Yang, Ge Zhang, Aiping Lu, Jianbo Yue, Zhaoxiang Bian

Open access · diamondAbstract read
In one paragraph

Article in Oncotarget, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 18 papers.

0numbers the graph read from it
0cells of the map it votes in
18citing papers in PubMed
2.5field-weighted citation impact, top 11% 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

18 citing papers in PubMed, 37 citations in OpenAlex.

  1. Review
  2. New uses of halofuginone to treat cancer.Journal of pharmaceutical analysis · 2025
    Review
  3. Review
  4. Article
  5. Article
  6. The anti-inflammatory activity of the compounds isolated fromSaudi journal of biological sciences · 2023
    Article
  7. Article
  8. Review
  9. Article
  10. Article
  11. Review
  12. Article
  13. Antitumor Research on Artemisinin and Its Bioactive Derivatives.Natural products and bioprospecting · 2018
    Review
  14. Article
  15. Article
  16. Article
  17. Review
  18. Article
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 at 3 institutions in 2 countries.

Guoqing ChenSchool of Chinese Medicine, Hong Kong Baptist University, Hong Kong, China.
Ruihong GongSchool of Chinese Medicine, Hong Kong Baptist University, Hong Kong, China.
Xianli ShiDepartment of Biomedical Sciences, City University of Hong Kong, Hong Kong, China.
Dajian YangChongqing Academy of Chinese Materia Medica, Chongqing, China.
Ge ZhangSchool of Chinese Medicine, Hong Kong Baptist University, Hong Kong, China.
Aiping LuSchool of Chinese Medicine, Hong Kong Baptist University, Hong Kong, China.
Jianbo YueDepartment of Biomedical Sciences, City University of Hong Kong, Hong Kong, China.
Zhaoxiang BianSchool of Chinese Medicine, Hong Kong Baptist University, Hong Kong, China.
Hong Kong Baptist University · HKChongqing Academy of Chinese Materia Medica · CNCity University of Hong Kong · HK

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Combinational drug therapy is one of the most promising strategies in modern anticancer research. Traditional Chinese medicine (TCM) formulas represent a wealth of complex combinations proven successful over centuries of clinical application. One such formula used to treat a variety of diseases, including cancer, contains two herbs, whose main active components are Halofuginone (HF) and Artemisinin (ATS). Here we studied the anticancer synergism of HF and ATS in various cancer cell lines and in a xenograft nude mice model. We found that the HF-ATS combination arrested more cells at the G1/G0 phase than either one alone, with the concomitant increased levels of CDK2 inhibitors, p21Cip1 and p27Kip1. By knocking down p21Cip1 and p27Kip1 separately or simultaneously in HCT116 cells and MCF-7 cells, we found that p21Cip1 was required for HF induced G1/G0 arrest, whereas p21Cip1 and p27Kip1 were both required for ATS or HF-ATS combination-mediated cell cycle arrest. Moreover, HF-ATS combination synergistically inhibited tumor growth in xenograft nude mice, and this was associated with the increased levels of p21Cip1 and p27Kip1. Collectively, these data indicate that the upregulation of p21Cip1 and p27Kip1 contributes to the synergistic anticancer effect of the HF-ATS combination.

Indexed as

AnimalsAntineoplastic Combined Chemotherapy ProtocolsArtemisininsCell Cycle CheckpointsCell Line, TumorCell ProliferationCyclin-Dependent Kinase Inhibitor p21Cyclin-Dependent Kinase Inhibitor p27Drug SynergismFemaleG1 PhaseGene Expression Regulation, NeoplasticHCT116 CellsHumansMCF-7 CellsMiceartemisininArtemisininsCDKN1A protein, humanCDKN1B protein, humanCyclin-Dependent Kinase Inhibitor p21Cyclin-Dependent Kinase Inhibitor p27halofuginonePiperidinesQuinazolinonesartemisinincell cyclecell proliferationhalofuginonesynergy

Identifiers

PMID27385212
PMCPMC5226584
OpenAlexW2463508229

What OpenQuestion holds

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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.