Evidence map›Paper›PMID 28415683›Full record

ArticleOncotarget2017

Suppression of PKC causes oncogenic stress for triggering apoptosis in cancer cells.

Suthakar Ganapathy, Bo Peng, Ling Shen, Tianqi Yu, Jean Lafontant, Ping Li, Rui Xiong, Alexandros Makriyannis, Changyan Chen

Erratum issuedOpen access · diamondAbstract read
PubMed Full text at PMC Publisher
In one paragraph

Article in Oncotarget, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. An erratum has been issued. Cited by 6 papers.

0numbers the graph read from it
0cells of the map it votes in
6citing papers in PubMed
0.5field-weighted citation impact, top 38% 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

6 citing papers in PubMed, 7 citations in OpenAlex.

  1. Review
  2. Review
  3. Review
  4. Hypothalamic extended synaptotagmin-3 contributes to the development of dietary obesity and related metabolic disorders.Proceedings of the National Academy of Sciences of the United States of America · 2020
    Article
  5. Article
  6. Article
4 · The record

Corrections and comments

5 · Who and what money

Authors and funding

9 authors at 2 institutions in 3 countries.

Suthakar GanapathyCenter for Drug Discovery, Northeastern University, Boston, MA, USA.
Bo PengCenter for Drug Discovery, Northeastern University, Boston, MA, USA.
Ling ShenCenter for Drug Discovery, Northeastern University, Boston, MA, USA.
Tianqi YuCenter for Drug Discovery, Northeastern University, Boston, MA, USA.
Jean LafontantCenter for Drug Discovery, Northeastern University, Boston, MA, USA.
Ping LiThe First Affiliated Hospital, Zhengzhou University, Zhengzhou, China.
Rui XiongThe Institute of Clinic Sciences, Sahlgrenska Academy, Gothenburg, Sweden.
Alexandros MakriyannisCenter for Drug Discovery, Northeastern University, Boston, MA, USA.
Changyan ChenCenter for Drug Discovery, Northeastern University, Boston, MA, USA.
Northeastern University · USUniversity of Gothenburg · SE

Funding

Study of Ras-Mediated ApoptosisR01CA100498 · NCI · NORTHEASTERN UNIVERSITY · PI CHEN, CHANGYAN · 2004 to 2017
$2.5M
Study of Anti-Survival signals in NF1R01CA153354 · NCI · NORTHEASTERN UNIVERSITY · PI CHEN, CHANGYAN · 2012 to 2017
$1.6M
NCI NIH HHS R01 CA100498NCI NIH HHS R01 CA153354
6 · The paper itself

Abstract

Gain of functional mutations in ras occurs in more than 30% of human malignancies and in particular 90% of pancreatic cancer. Mutant ras, via activating multiple effector pathways, not only promote cell growth or survival, but also apoptosis, depending upon cell types or circumstances. In order to further study the mechanisms of apoptosis induced by oncogenic ras, we employed the ras loop mutant genes and demonstrated that Akt functioned downstream of Ras in human pancreatic cancer or HPNE cells ectopically expressing mutated K-ras for the induction of apoptosis after the concurrent suppression of PKC α and β. In this apoptotic process, the redox machinery was aberrantly switched on in the pancreatic cancer cells as well as prostate cancer DU145 cells. p73 was phosphorylated and translocated to the nucleus, accompanied with UPR activation and induction of apoptosis. The in vitro results were corroborated by the in vivo data. Thus, our study indicated that PKC α and β appeared coping with oncogenic Ras or mutated Akt to maintain the balance of the homeostasis in cancer cells. Once these PKC isoforms were suppressed, the redox state in the cancer cells was disrupted, which elicited persistent oncogenic stress and subsequent apoptotic crisis.

Indexed as

AnimalsApoptosisCell Line, TumorCell Transformation, NeoplasticDisease Models, AnimalGenes, rasHumansMiceMutationNeoplasmsOncogene ProteinsOxidative StressPhosphatidylinositol 3-KinasesPhosphorylationProtein IsoformsProtein Kinase COncogene ProteinsPhosphatidylinositol 3-KinasesProtein IsoformsProtein Kinase CProtein SubunitsProto-Oncogene Proteins c-aktReactive Oxygen SpeciesTumor Protein p73Aktapoptosisp73RasROS

Identifiers

PMID28415683
PMCPMC5458183
OpenAlexW2592536115

What OpenQuestion holds

Textmetadata
LicenceCC BY
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.