Evidence map›Paper›PMID 17873911›Full record

ArticleOncogene2008

BH3-only protein BIK induces caspase-independent cell death with autophagic features in Bcl-2 null cells.

R Rashmi, S G Pillai, S Vijayalingam, J Ryerse, G Chinnadurai

Open access · greenAbstract read
In one paragraph

Article in Oncogene, 2008. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 30 papers.

0numbers the graph read from it
0cells of the map it votes in
30citing papers in PubMed
4.7field-weighted citation impact, top 5% 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

30 citing papers in PubMed, 63 citations in OpenAlex.

  1. Review
  2. Article
  3. Article
  4. Article
  5. Article
  6. Article
  7. Article
  8. Article
  9. Breast cancer cell line MDA-MB-231 miRNA profile expression after BIK interference: BIK involvement in autophagy.Tumour biology : the journal of the International Society for Oncodevelopmental Biology and Medicine · 2016
    Article
  10. Article
  11. Article
  12. Article
  13. Review
  14. Article
  15. Article
  16. Article
  17. BIK/NBK gene as potential marker of prognostic and therapeutic target in breast cancer patients.Clinical & translational oncology : official publication of the Federation of Spanish Oncology Societies and of the National Cancer Institute of Mexico · 2012
    Article
  18. Article
  19. Article
  20. Autophagy in tumor suppression and cancer therapy.Critical reviews in eukaryotic gene expression · 2011
    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

5 authors at 1 institution in 1 country.

R RashmiInstitute for Molecular Virology, Saint Louis University Health Sciences Center, St Louis, MO 63110, USA.
S G Pillai
S Vijayalingam
J Ryerse
G Chinnadurai
Saint Louis University · US

Funding

PROMOTION OF CELL SURVIVAL BY ADENOVIRUS E1B 19K PROTEINR01CA033616 · NCI · SAINT LOUIS UNIVERSITY · PI CHINNADURAI, GOVINDASWAMY · 1985 to 2015
$4.0M
ONCOGENIC AND CHEMORESISTANCE BY BCL 2R01CA073803 · NCI · SAINT LOUIS UNIVERSITY · PI CHINNADURAI, GOVINDASWAMY · 1998 to 2008
$2.0M
BH3-only protein BNIP3 in tumor progressionR21CA116262 · NCI · SAINT LOUIS UNIVERSITY · PI CHINNADURAI, GOVINDASWAMY · 2005 to 2006
$250k
NCI NIH HHS CA-116262NCI NIH HHS CA-33616NCI NIH HHS CA-73803NCI NIH HHS R01 CA033616NCI NIH HHS R01 CA073803NCI NIH HHS R21 CA116262
6 · The paper itself

Abstract

The BH3-only protein BIK normally induces apoptotic cell death. Here, we have investigated the role of BCL-2 in BIK-induced cell death using Bcl-2+/+ and Bcl-2-/- mouse embryo fibroblasts. Ectopic expression of BIK in Bcl-2-/- cells resulted in enhanced cell death compared to Bcl-2+/+ cells. In these cells, while caspase-8 was activated, there was no significant activation of caspase-9 and 3. There was no detectable mitochondrial to cytosolic release of cytochrome-c. However, there was significant redistribution of AIF from mitochondria to the nucleus. The extent of BIK-induced cell death was augmented by treatment with the pancaspase inhibitor, zVAD-fmk. The Bcl-2 null cells expressing BIK exhibited autophagic features such as cytosolic vacuoles, punctate distribution of LC3 and enhanced expression of Beclin-1. The survival of BIK-expressing Bcl-2-/- cells was enhanced in the presence of PI3 kinase inhibitors 3-methyladenine and Wortmannin and also by depletion of Atg5 and Beclin-1. Death of BIK-expressing Bcl-2-/- cells treated with zVAD-fmk was increased under caspase-8 depletion. Our results suggest enhanced expression of BIK in the Bcl-2 deficient cells leads to cell death with autophagic features and the extent of such cell death could be increased by inhibition of caspases.

Indexed as

ApoptosisGenes, bcl-2Adaptor Proteins, Signal TransducingAnimalsApoptosis Regulatory ProteinsAutophagyCaspasesCell Line, TransformedCells, CulturedMiceMitochondrial ProteinsProtein Structure, TertiaryProto-Oncogene Proteins c-bcl-2Adaptor Proteins, Signal TransducingApoptosis Regulatory ProteinsBik protein, mouseCaspasesMitochondrial ProteinsProto-Oncogene Proteins c-bcl-2

Identifiers

PMID17873911
PMCPMC2928058
OpenAlexW2014840658

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.