Evidence map›Paper›PMID 27830724›Full record

ArticleScientific reports2016

Activation of AMPKα mediates additive effects of solamargine and metformin on suppressing MUC1 expression in castration-resistant prostate cancer cells.

SongTao Xiang, QiuHong Zhang, Qing Tang, Fang Zheng, JingJing Wu, LiJun Yang, Swei Sunny Hann

Open access · goldAbstract read
In one paragraph

Article in Scientific reports, 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
1.7field-weighted citation impact, top 15% 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, 35 citations in OpenAlex.

  1. Trial
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  4. Metformin: A Dual-Role Player in Cancer Treatment and Prevention.International journal of molecular sciences · 2024
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  14. Anticancer activity of glycoalkaloids fromFrontiers in pharmacology · 2022
    Review
  15. Probing the Antitumor Mechanism ofBioengineering (Basel, Switzerland) · 2019
    Article
  16. Article
  17. Article
  18. 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

7 authors at 1 institution in 1 country.

SongTao XiangDepartment of Urology Surgery, Guangdong Provincial Hospital of Chinese Medicine, The Second Clinical Medical Collage, Guangzhou University of Chinese Medicine, Guangzhou, Guangdong Province, 510120, China.
QiuHong ZhangDepartment of Urology Surgery, Guangdong Provincial Hospital of Chinese Medicine, The Second Clinical Medical Collage, Guangzhou University of Chinese Medicine, Guangzhou, Guangdong Province, 510120, China.
Qing TangDepartment of Medical Oncology, Guangzhou, University of Chinese Medicine, Guangzhou, Guangdong Province, 510120, China.
Fang ZhengDepartment of Medical Oncology, Guangzhou, University of Chinese Medicine, Guangzhou, Guangdong Province, 510120, China.
JingJing WuDepartment of Medical Oncology, Guangzhou, University of Chinese Medicine, Guangzhou, Guangdong Province, 510120, China.
LiJun YangDepartment of Medical Oncology, Guangzhou, University of Chinese Medicine, Guangzhou, Guangdong Province, 510120, China.
Swei Sunny HannDepartment of Medical Oncology, Guangzhou, University of Chinese Medicine, Guangzhou, Guangdong Province, 510120, China.
Guangzhou University of Chinese Medicine · CN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Prostate cancer is the second most common cause of cancer-related deaths worldwide. The mucin 1 (MUC1) oncoprotein is highly expressed in human prostate cancers with aggressive features. However, the role for MUC1 in occurrence and progression of castration-resistant prostate cancer (CRPC) remained elusive. In this study, we showed that solamargine, a major steroidal alkaloid glycoside, inhibited the growth of CRPC cells, which was enhanced in the presence of metformin. Furthermore, we found that solamargine increased phosphorylation of AMPKα, whereas reducing the protein expression and promoter activity of MUC1. A greater effect was observed in the presence of metformin. In addition, solamargine reduced NF-κB subunit p65 protein expression. Exogenously expressed p65 resisted solamargine-reduced MUC1 protein and promoter activity. Interestingly, exogenously expressed MUC1 attenuated solamargine-stimulated phosphorylation of AMPKα and, more importantly reversed solamargine-inhibited cell growth. Finally, solamargine increased phosphorylation of AMPKα, while inhibiting MUC1, p65 and tumor growth were observed in vivo. Overall, our results show that solamargine inhibits the growth of CRPC cells through AMPKα-mediated inhibition of p65, followed by reduction of MUC1 expression in vitro and in vivo. More importantly, metformin facilitates the antitumor effect of solamargine on CRPC cells.

Indexed as

AMP-Activated Protein KinasesAnimalsAntineoplastic AgentsCell Line, TumorDrug SynergismEnzyme ActivationFemaleGene ExpressionGene Expression Regulation, NeoplasticHumansInhibitory Concentration 50MaleMetforminMice, NudeMucin-1PhosphorylationAMP-Activated Protein KinasesAntineoplastic Agentsbeta-solamarineMetforminMUC1 protein, humanMucin-1RELA protein, humanRNA, MessengerSolanaceous AlkaloidsTranscription Factor RelA

Identifiers

PMID27830724
PMCPMC5103223
OpenAlexW2554359977

What OpenQuestion holds

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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.