Evidence map›Paper›PMID 29845238›Full record

ArticleMolecular medicine reports2018

Matrine inhibits prostate cancer via activation of the unfolded protein response/endoplasmic reticulum stress signaling and reversal of epithelial to mesenchymal transition.

Junli Chang, Shaopu Hu, Wenyi Wang, Yimian Li, Wenlan Zhi, Sheng Lu, Qi Shi, Yongjun Wang, Yanping Yang

Abstract read
In one paragraph

Article in Molecular medicine reports, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 19 papers.

0numbers the graph read from it
0cells of the map it votes in
19citing 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

19 citing papers in PubMed.

  1. Computational and Experimental Analysis ofMolecules (Basel, Switzerland) · 2026
    Article
  2. Article
  3. Review
  4. Article
  5. Article
  6. Review
  7. Review
  8. Article
  9. Article
  10. Article
  11. Prostate cancer: Therapeutic prospect with herbal medicine.Current research in pharmacology and drug discovery · 2021
    Review
  12. Article
  13. Article
  14. Review
  15. Article
  16. Article
  17. UPR: An Upstream Signal to EMT Induction in Cancer.Journal of clinical medicine · 2019
    Review
  18. Article
  19. 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

9 authors.

Junli ChangDepartment Orthopedics and Traumatology, Longhua Hospital, Shanghai University of Traditional Chinese Medicine, Shanghai 200032, P.R. China.
Shaopu HuDepartment Orthopedics and Traumatology, Longhua Hospital, Shanghai University of Traditional Chinese Medicine, Shanghai 200032, P.R. China.
Wenyi WangDepartment Orthopedics and Traumatology, Longhua Hospital, Shanghai University of Traditional Chinese Medicine, Shanghai 200032, P.R. China.
Yimian LiDepartment Orthopedics and Traumatology, Longhua Hospital, Shanghai University of Traditional Chinese Medicine, Shanghai 200032, P.R. China.
Wenlan ZhiDepartment Orthopedics and Traumatology, Longhua Hospital, Shanghai University of Traditional Chinese Medicine, Shanghai 200032, P.R. China.
Sheng LuDepartment Orthopedics and Traumatology, Longhua Hospital, Shanghai University of Traditional Chinese Medicine, Shanghai 200032, P.R. China.
Qi ShiDepartment Orthopedics and Traumatology, Longhua Hospital, Shanghai University of Traditional Chinese Medicine, Shanghai 200032, P.R. China.
Yongjun WangDepartment Orthopedics and Traumatology, Longhua Hospital, Shanghai University of Traditional Chinese Medicine, Shanghai 200032, P.R. China.
Yanping YangDepartment Orthopedics and Traumatology, Longhua Hospital, Shanghai University of Traditional Chinese Medicine, Shanghai 200032, P.R. China.

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Prostate cancer is the second most commonly diagnosed malignancy and the sixth global primary cause of malignancy‑associated fatality. Increased invasiveness and motility in prostate cancer cells are associated with ubiquitin proteasome system‑regulated epithelial to mesenchymal transition (EMT). Impairment of the endoplasmic reticulum (ER) causes ER stress due to the accumulation of unfolded proteins and altered cell survival. In the current study, the effect and mechanism of matrine on cell apoptosis, viability, migration and invasion of human prostate cancer cells in vivo and in vitro through the unfolded protein response (UPR)/ER stress pathway were investigated. Matrine inhibited proteasomal chymotrypsin‑like (CT‑like) activity in the prostate carcinoma cellular proteasome. Upregulated vimentin and N‑cadherin and downregulated E‑cadherin were also observed in vitro and in vivo. In vitro analyses showed that matrine repressed cell motility, viability and invasion, arrested the cell cycle at the G0/G1 phase and induced prostate cancer cell apoptosis. Furthermore, matrine activated the UPR/ER stress signaling cascade in prostate cancer cells and tumor tissues of xenograft‑bearing nude mice. Results also demonstrated that the anti‑apoptotic protein Bcl‑2 was downregulated, the pro‑apoptotic protein Bak was upregulated and the cell growth and cell cycle‑related proteins c‑Myc, Cyclin B1, Cyclin D1 and CDK1 were downregulated. Moreover, matrine inhibited tumor growth and Ki‑67 expression in xenograft‑bearing nude mice. To the best of our knowledge, the present study indicated for the first time that matrine exerted marked anticancer functions in human prostate carcinoma in vivo and in vitro through activation of the proteasomal CT‑like activity inhibition mediated by the UPR/ER stress signaling pathway.

Indexed as

AlkaloidsCell Line, TumorEndoplasmic Reticulum StressEpithelial-Mesenchymal TransitionHumansMaleMatrinesProstatic NeoplasmsQuinolizinesUnfolded Protein ResponseAlkaloidsMatrinesQuinolizines

Identifiers

PMID29845238
PMCPMC6059727

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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.