Evidence map›Paper›PMID 27431500›Full record

ArticleProstate cancer and prostatic diseases2016

Berbamine inhibited the growth of prostate cancer cells in vivo and in vitro via triggering intrinsic pathway of apoptosis.

Y Zhao, J J Lv, J Chen, X B Jin, M W Wang, Z H Su, L Y Wang, H Y Zhang

Abstract read
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In one paragraph

Article in Prostate cancer and prostatic diseases, 2016. 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
3.4field-weighted citation impact, top 9% 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

19 citing papers in PubMed, 39 citations in OpenAlex.

  1. Article
  2. Review
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  5. Regulation of Cell-Signaling Pathways by Berbamine in Different Cancers.International journal of molecular sciences · 2022
    Review
  6. Article
  7. Cyclometalated Ru(II) β-carboline complexes induce cell cycle arrest and apoptosis in human HeLa cervical cancer cells via suppressing ERK and Akt signaling.Journal of biological inorganic chemistry : JBIC : a publication of the Society of Biological Inorganic Chemistry · 2021
    Article
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  14. Prostate cancer and prostatic diseases Best of China, 2018.Prostate cancer and prostatic diseases · 2019
    Article
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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 2 institutions in 2 countries.

Y ZhaoMinimally Invasive Urology Center, Shandong Provincial Hospital affiliated with Shandong University, Jinan, China.
J J LvDepartment of Urology, Shandong Provincial Hospital affiliated with Shandong University, Jinan, China.
J ChenMinimally Invasive Urology Center, Shandong Provincial Hospital affiliated with Shandong University, Jinan, China.
X B JinMinimally Invasive Urology Center, Shandong Provincial Hospital affiliated with Shandong University, Jinan, China.
M W WangMinimally Invasive Urology Center, Shandong Provincial Hospital affiliated with Shandong University, Jinan, China.
Z H SuDepartment of Pathology, Shandong Provincial Hospital affiliated with Shandong University, Jinan, China.
L Y WangCenter of Electron Microscopy, School of Medicine, Shandong University, Jinan, China.
H Y ZhangMinimally Invasive Urology Center, Shandong Provincial Hospital affiliated with Shandong University, Jinan, China.
Shandong University · CNShandong Provincial Hospital · CN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

backgroundBerbamine (BBM) has been reported with antitumor activities. BBM inhibited the growth of prostate cancer (PCa) cells and caused vacuolization of mitochondria in preliminary study. We hypothesized BBM could enhance apoptosis of PCa cells through mitochondrial pathway.

methodsGrowth of PC-3 and LNCaP cells treated by BBM was determined by cell viability assay. The morphology of mitochondria was observed by electron microscopy. Apoptosis was quantified by flow cytometry. Expressions of bax/bcl-2, active caspase-9 and active caspase-3 were examined by western blot and real-time PCR. Methazolamide, an inhibitor of cytochrome c, was added to examine its blockade effect on BBM. PC-3 cells were injected subcutaneously into athymic mice, and BBM or saline was administrated intravenously. Diameters of induced tumors were compared, and ratios of apoptotic cells in tumor tissues were calculated.

resultsBBM inhibited viability of cultured PC-3 and LNCaP cells in dose- and time-dependent manners. Flow cytometry showed BBM induced apoptosis in cultured cells. Mitochondria showed swelling, vacuolization and fused mitochondrial cristae. Western blot and real-time PCR analysis both showed increases of bax/bcl-2, active caspase-9 and active caspase-3. Methazolamide impeded effect of BBM on inducing apoptosis of cultured cells, and activations of caspase-9 and caspase-3 were also inhibited. Growth of tumors by grafted PC-3 cells was significantly slower in BBM group. Ratios of apoptotic cells in tumors were significantly higher in BBM group. Expressions of active caspase-9 and active caspase-3 in tumors were significantly upregulated by BBM.

conclusionsBBM exhibited strong anti-PCa activities in vitro and in vivo relying on activating caspase-3 via intrinsic pathway of apoptosis, holding a great promise to develop new strategies for PCa.

Indexed as

AnimalsApoptosisbcl-2-Associated X ProteinBenzylisoquinolinesCaspase 3Caspase 9Cell ProliferationCell SurvivalHumansMaleMiceMice, NudeMitochondriaProstateProstatic NeoplasmsProto-Oncogene Proteins c-bcl-2bcl-2-Associated X ProteinBenzylisoquinolinesberbamineCaspase 3Caspase 9Proto-Oncogene Proteins c-bcl-2

Identifiers

PMID27431500
OpenAlexW2484753938

What OpenQuestion holds

Textmetadata
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.