Evidence map›Paper›PMID 29472793›Full record

ArticleSaudi journal of biological sciences2018

Dihydroartemisinin inhibits colon cancer cell viability by inducing apoptosis through up-regulation of PPARγ expression.

Zhen-Hai Lu, Jian-Hong Peng, Rong-Xin Zhang, Fulong Wang, Hui-Ping Sun, Yu-Jing Fang, De-Sen Wan, Zhi-Zhong Pan

Abstract read
In one paragraph

Article in Saudi journal of biological sciences, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 14 papers.

0numbers the graph read from it
0cells of the map it votes in
14citing 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

14 citing papers in PubMed.

  1. Article
  2. Dual function of activated PPARγ by ligands on tumor growth and immunotherapy.Medical oncology (Northwood, London, England) · 2024
    Review
  3. Review
  4. Review
  5. Review
  6. Article
  7. Novel dihydroartemisinin derivative Mito-DHABMC pharmacology & toxicology · 2022
    Article
  8. Article
  9. Article
  10. Dihydroartemisinin: A Potential Natural Anticancer Drug.International journal of biological sciences · 2021
    Review
  11. Review
  12. Article
  13. Article
  14. Therapeutic potential of PPARγ natural agonists in liver diseases.Journal of cellular and molecular medicine · 2020
    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.

Zhen-Hai LuDepartment of Colorectal Surgery, Sun Yat-sen University Cancer Cente, State Key Laboratory of Oncology in South China, Collaborative Innovation Center of Cancer Medicine, Guangzhou 510060, Guangdong, China.
Jian-Hong PengDepartment of Colorectal Surgery, Sun Yat-sen University Cancer Cente, State Key Laboratory of Oncology in South China, Collaborative Innovation Center of Cancer Medicine, Guangzhou 510060, Guangdong, China.
Rong-Xin ZhangDepartment of Colorectal Surgery, Sun Yat-sen University Cancer Cente, State Key Laboratory of Oncology in South China, Collaborative Innovation Center of Cancer Medicine, Guangzhou 510060, Guangdong, China.
Fulong WangDepartment of Colorectal Surgery, Sun Yat-sen University Cancer Cente, State Key Laboratory of Oncology in South China, Collaborative Innovation Center of Cancer Medicine, Guangzhou 510060, Guangdong, China.
Hui-Ping SunDepartment of Colorectal Surgery, Sun Yat-sen University Cancer Cente, State Key Laboratory of Oncology in South China, Collaborative Innovation Center of Cancer Medicine, Guangzhou 510060, Guangdong, China.
Yu-Jing FangDepartment of Colorectal Surgery, Sun Yat-sen University Cancer Cente, State Key Laboratory of Oncology in South China, Collaborative Innovation Center of Cancer Medicine, Guangzhou 510060, Guangdong, China.
De-Sen WanDepartment of Colorectal Surgery, Sun Yat-sen University Cancer Cente, State Key Laboratory of Oncology in South China, Collaborative Innovation Center of Cancer Medicine, Guangzhou 510060, Guangdong, China.
Zhi-Zhong PanDepartment of Colorectal Surgery, Sun Yat-sen University Cancer Cente, State Key Laboratory of Oncology in South China, Collaborative Innovation Center of Cancer Medicine, Guangzhou 510060, Guangdong, China.

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

The present study was aimed to investigate the effect of dihydroartemisinin on the colon cancer cell proliferation and apoptosis. The results from MTT assay revealed a concentration and time dependent relation between the inhibition of SW 948 cell viability and dihydroartemisinin addition. The viability of SW 948 cells was reduced to 45 and 24% on treatment with 30 and 50 µM, respectively concentrations of dihydroartemisinin after 48 h. Morphological examination of SW 948 cells showed attainment of rounded shape and cluster formation on treatment with dihydroartemisinin. Western blot analysis showed a significant increase in the activation of caspase-3 and expression of cleaved PARP by dihydroartemisinin treatment. The activation of PPARγ was increased significantly in SW 948 cells by treatment with dihydroartemisinin. Compared to control, the migration potential of SW 948 cells was reduced significantly (p < 0.005) and the expression levels of MMP-2 and -9 inhibited by dihydroartemisinin at 50 µM concentration. In the dihydroartemisinin treatment group colon tumor formation was significantly inhibited on treatment with 20 mg/kg doses of dihydroartemisinin after 30 days. Therefore, dihydroartemisinin inhibits colon cancer growth by inducing apoptosis and increasing the expression of PPARγ. Thus dihydroartemisinin can be used for the treatment of colon cancer.

Indexed as

ApoptosisCondensationDihydroartemisininMatrix metalloproteinViability

Identifiers

PMID29472793
PMCPMC5816000

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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.