Evidence map›Paper›PMID 24842234›Full record

ArticleMolecular cancer research : MCR2014

BaxΔ2 promotes apoptosis through caspase-8 activation in microsatellite-unstable colon cancer.

Honghong Zhang, Yuting Lin, Adriana Mañas, Yu Zhao, Mitchell F Denning, Li Ma, Jialing Xiang

Abstract read
In one paragraph

Article in Molecular cancer research : MCR, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 13 papers.

0numbers the graph read from it
0cells of the map it votes in
13citing papers in PubMed
0.9field-weighted citation impact, top 28% 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

13 citing papers in PubMed, 19 citations in OpenAlex.

  1. Review
  2. Article
  3. Article
  4. Article
  5. Review
  6. Article
  7. Article
  8. Article
  9. BaxΔ2 sensitizes colorectal cancer cells to proteasome inhibitor-induced cell death.Biochemical and biophysical research communications · 2018
    Article
  10. Article
  11. Differential Impacts of Alternative Splicing Networks on Apoptosis.International journal of molecular sciences · 2016
    Review
  12. Review
  13. 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

7 authors at 2 institutions in 1 country.

Honghong ZhangDepartment of Biological and Chemical Sciences;
Yuting LinDepartment of Biological and Chemical Sciences;
Adriana MañasDepartment of Biological and Chemical Sciences;
Yu ZhaoDepartment of Biological and Chemical Sciences;
Mitchell F DenningDepartment of Pathology, Loyola University Medical Center, Maywood, Illinois.
Li MaMumetel, LLC, University Technology Park, Illinois Institute of Technology, Chicago; and.
Jialing XiangDepartment of Biological and Chemical Sciences; xiang@iit.edu.
Illinois Institute of Technology · USLoyola University Medical Center · US

Funding

Differentially Regulating Apoptosis by AR: Activating Bax or Inhibiting JNK MAPKR01CA128114 · NCI · ILLINOIS INSTITUTE OF TECHNOLOGY · PI XIANG, JIALING · 2008 to 2012
$1.5M
Mechanism and Regulation of Baxdelta2 in Colorectal CancerR15CA195526 · NCI · ILLINOIS INSTITUTE OF TECHNOLOGY · PI XIANG, JIALING · 2016 to 2016
$458k
NCI NIH HHS R01 CA128114NCI NIH HHS R15 CA195526
6 · The paper itself

Abstract

unlabelledLoss of apoptotic Bax due to microsatellite mutation contributes to tumor development and chemoresistance. Recently, a Bax microsatellite mutation was uncovered in combination with a specific alternative splicing event that could generate a unique Bax isoform (BaxΔ2) in otherwise Bax-negative cells. Like the prototype Baxα, BaxΔ2 is a potent proapoptotic molecule. However, the proapoptotic mechanism and therapeutic implication of BaxΔ2 remain elusive. Here, the isolation and analysis of isogenic subcell lines are described that represent different Bax microsatellite statuses from colorectal cancer. Colon cancer cells harboring Bax microsatellite G7/G7 alleles are capable of producing low levels of endogenous BaxΔ2 transcripts and proteins. Interestingly, BaxΔ2-positive cells are selectively sensitive to a subgroup of chemotherapeutics compared with BaxΔ2-negative cells. Unlike other Bax isoforms, BaxΔ2 recruits caspase-8 into the proximity for activation, and the latter, in turn, activates caspase-3 and apoptosis independent of the mitochondrial pathway. These data suggest that the expression of BaxΔ2 may provide alternative apoptotic and chemotherapeutic advantages for Bax-negative tumors. IMPLICATIONS: "Bax-negative" colorectal tumors expressing a Bax isoform are sensitive to selective chemotherapeutics.

Indexed as

Apoptosisbcl-2-Associated X ProteinCaspase 3Caspase 8Colorectal NeoplasmsDrug Resistance, NeoplasmGene Expression Regulation, NeoplasticHumansMicrosatellite InstabilityProtein Isoformsbcl-2-Associated X ProteinCaspase 3Caspase 8Protein Isoforms

Identifiers

PMID24842234
PMCPMC12019869
OpenAlexW2028172012

What OpenQuestion holds

Textmetadata
LicenceTDM
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.