Evidence map›Paper›PMID 25737737›Full record

ArticleEvidence-based complementary and alternative medicine : eCAM2015

Shikonin Induces Apoptosis, Necrosis, and Premature Senescence of Human A549 Lung Cancer Cells through Upregulation of p53 Expression.

Yueh-Chiao Yeh, Tsun-Jui Liu, Hui-Chin Lai

Open access · hybridAbstract read
In one paragraph

Article in Evidence-based complementary and alternative medicine : eCAM, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 20 papers.

0numbers the graph read from it
0cells of the map it votes in
20citing papers in PubMed
1.9field-weighted citation impact, top 17% 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

20 citing papers in PubMed, 45 citations in OpenAlex.

  1. Article
  2. Article
  3. Article
  4. Review
  5. Review
  6. Article
  7. Review
  8. Article
  9. Article
  10. Article
  11. Onosma bracteata Wall. induces GEnvironmental science and pollution research international · 2021
    Article
  12. Article
  13. Targeting Metabolic Pathways of Myeloid Cells Improves Cancer Immunotherapy.Frontiers in cell and developmental biology · 2021
    Review
  14. Observational
  15. The Effects ofMolecules (Basel, Switzerland) · 2020
    Article
  16. Pathobiological Mechanisms of Endothelial Dysfunction Induced byInternational journal of medical sciences · 2020
    Article
  17. Article
  18. Article
  19. Article
  20. 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

3 authors at 3 institutions in 1 country.

Yueh-Chiao YehDepartment of Natural Biotechnology, Nanhua University, Sec. 1, No. 55, Nanhua Road, Dalin, Chiayi 62249, Taiwan.
Tsun-Jui LiuCardiovascular Center and Department of Anesthesiology, Taichung Veterans General Hospital, Sec. 4, No. 1650 Taiwan Boulevard, Taichung 40705, Taiwan ; Department of Medicine and Cardiovascular Research Center, National Yang-Ming University School of Medicine, Sec. 2, No. 155, Linong Street, Taipei 11221, Taiwan.
Hui-Chin LaiCardiovascular Center and Department of Anesthesiology, Taichung Veterans General Hospital, Sec. 4, No. 1650 Taiwan Boulevard, Taichung 40705, Taiwan ; Department of Medicine and Cardiovascular Research Center, National Yang-Ming University School of Medicine, Sec. 2, No. 155, Linong Street, Taipei 11221, Taiwan.
Nanhua University · TWNational Yang Ming Chiao Tung University · TWTaichung Veterans General Hospital · TW

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Shikonin, a natural naphthoquinone pigment isolated from Lithospermum erythrorhizon, has been reported to suppress growth of various cancer cells. This study was aimed to investigate whether this chemical could also inhibit cell growth of lung cancer cells and, if so, works via what molecular mechanism. To fulfill this, A549 lung cancer cells were treated with shikonin and then subjected to microscopic, biochemical, flow cytometric, and molecular analyses. Compared with the controls, shikonin significantly induced cell apoptosis and reduced proliferation in a dose-dependent manner. Specially, lower concentrations of shikonin (1-2.5 μg/mL) cause viability reduction; apoptosis and cellular senescence induction is associated with upregulated expressions of cell cycle- and apoptotic signaling-regulatory proteins, while higher concentrations (5-10 μg/mL) precipitate both apoptosis and necrosis. Treatment of cells with pifithrin-α, a specific inhibitor of p53, suppressed shikonin-induced apoptosis and premature senescence, suggesting the role of p53 in mediating the actions of shikonin on regulation of lung cancer cell proliferation. These results indicate the potential and dose-related cytotoxic actions of shikonin on A549 lung cancer cells via p53-mediated cell fate pathways and raise shikonin a promising adjuvant chemotherapeutic agent for treatment of lung cancer in clinical practice.

Identifiers

PMID25737737
PMCPMC4337265
OpenAlexW2044952996

What OpenQuestion holds

Textmetadata
LicenceCC BY
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.