Evidence map›Paper›PMID 15608672›Full record

ArticleOncogene2005

Differential regulation of survivin expression and apoptosis by vitamin D3 compounds in two isogenic MCF-7 breast cancer cell sublines.

Fengzhi Li, Xiang Ling, Huayi Huang, Lisa Brattain, Pasha Apontes, Jianguo Wu, Lise Binderup, Michael G Brattain

Open access · bronzeAbstract readComparative Study
In one paragraph

Article in Oncogene, 2005. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 24 papers.

0numbers the graph read from it
0cells of the map it votes in
24citing papers in PubMed
1.7field-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

24 citing papers in PubMed, 58 citations in OpenAlex.

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  16. Vitamin D and differentiation in cancer.Critical reviews in clinical laboratory sciences · 2009
    Review
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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 3 institutions in 2 countries.

Fengzhi LiDepartment of Pharmacology and Therapeutics, Grace Cancer Drug Center, Roswell Park Cancer Institute, Buffalo, NY 14263, USA. fengzhi.li@roswellpark.org
Xiang Ling
Huayi Huang
Lisa Brattain
Pasha Apontes
Jianguo Wu
Lise Binderup
Michael G Brattain
Roswell Park Comprehensive Cancer Center · USGrace (United States) · USLeo Pharma (Denmark) · DK

Funding

Two-Spirit Films in Indigenous Cancer HealthP30CA016056 · NCI · ROSWELL PARK CANCER INSTITUTE CORP · PI MARK G FRATTINI · 1985 to 2026
$116.6M
MECHANISM OF ACTION OF DIFFERENTIATION AGENTSR37CA038173 · NCI · UNIVERSITY OF NEBRASKA MEDICAL CENTER · PI BRATTAIN, MICHAEL G · 2001 to 2008
$3.1M
AUTOCRINE TGF BETA AND CELL DEATHR01CA072001 · NCI · UNIVERSITY OF TOLEDO HEALTH SCI CAMPUS · PI BRATTAIN, MICHAEL G · 1997 to 2011
$2.8M
MECHANISM OF ACTION OF DIFFERENTIATION AGENTSR01CA038173 · NCI · UNIVERSITY OF TOLEDO HEALTH SCI CAMPUS · PI BRATTAIN, MICHAEL G · 1986 to 2014
$1.8M
Survivin expression and cancer cell drug resistanceR01CA109481 · NCI · ROSWELL PARK CANCER INSTITUTE CORP · PI LI, FENGZHI · 2004 to 2008
$1.2M
NCI NIH HHS CA16056NCI NIH HHS P30 CA016056NCI NIH HHS R01 CA038173NCI NIH HHS R01 CA072001NCI NIH HHS R01 CA109481NCI NIH HHS R01 CA38173NCI NIH HHS R01 CA72001NCI NIH HHS R37 CA038173
6 · The paper itself

Abstract

Although both the antiapoptotic function of survivin and vitamin D3 (VD3)-mediated cell growth inhibition and apoptosis have been extensively studied, it is not known whether survivin plays a role in VD3 compound-mediated cell growth inhibition and apoptosis induction. Using an isogenic model of MCF-7 breast adenocarcinoma cells (MCF-7E and MCF-7L sublines that are sensitive and resistant to VD3 compounds), we found that VD3 compounds effectively downregulated survivin in VD3-sensitive MCF-7E cells, which was associated with VD3-induced apoptosis. In contrast, VD3 compounds failed to downregulate survivin in VD3-resistant MCF-7L cells, which showed resistant to VD3-induced apoptosis. However, inhibition of survivin expression by small interfering RNA (siRNA) induced cell death per se and further sensitized VD3-induced apoptosis in MCF-7L cells, indicating that the inability of these cells to respond to VD3 is due to the failure to downregulate survivin. Forced expression of survivin not only blocked VD3-mediated G1 cell accumulation but also increased S and G2/M cell populations. VD3 treatment rapidly triggered the activation of p38 MAPK signaling in MCF-7E cells but not in MCF-7L cells. Moreover, inhibition of p38 activation diminished VD3-mediated survivin inhibition and partially rescued VD3-induced cell death. We further showed that VD3 increased the expression of TGF(beta)1 and TGF(beta) receptor 2, and that blocking the function of TGF(beta) receptor 2 diminished VD3 compound-mediated survivin downregulation. Thus, we propose that the VD3 compound-induced growth inhibition and apoptosis induction are at least partially dependent on survivin downregulation via VD3-induced TGFbeta signaling and the activation of p38 MAPK pathway. Targeting survivin through these pathways may lead to novel applications for cancer therapeutics.

Indexed as

AdenocarcinomaApoptosisBreast NeoplasmsCell Line, TumorCholecalciferolDown-RegulationFemaleGene Expression Regulation, NeoplasticHumansInhibitor of Apoptosis ProteinsMicrotubule-Associated ProteinsNeoplasm Proteinsp38 Mitogen-Activated Protein KinasesPhosphorylationRNA, Small InterferingSurvivinBIRC5 protein, humanCholecalciferolInhibitor of Apoptosis ProteinsMicrotubule-Associated ProteinsNeoplasm Proteinsp38 Mitogen-Activated Protein KinasesRNA, Small InterferingSurvivinTransforming Growth Factor beta

Identifiers

PMID15608672
PMCPMC2820410
OpenAlexW2113325440

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.