Evidence map›Paper›PMID 22333579›Full record

ArticleCell cycle (Georgetown, Tex.)2012

The selective inhibition of nuclear PKCζ restores the effectiveness of chemotherapeutic agents in chemoresistant cells.

Alessandro Rimessi, Erika Zecchini, Roberta Siviero, Carlotta Giorgi, Sara Leo, Rosario Rizzuto, Paolo Pinton

Open access · bronzeAbstract read
In one paragraph

Article in Cell cycle (Georgetown, Tex.), 2012. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 12 papers.

0numbers the graph read from it
0cells of the map it votes in
12citing papers in PubMed
0.7field-weighted citation impact, top 31% 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

12 citing papers in PubMed, 11 citations in OpenAlex.

  1. Article
  2. High Expression ofCancer genomics & proteomics · 2025
    Article
  3. Review
  4. Pharmacological and Genetic Inhibition of Caveolin-1 Promotes Epithelialization and Wound Closure.Molecular therapy : the journal of the American Society of Gene Therapy · 2019
    Article
  5. A novel and selective inhibitor of PKC ζ potently inhibits human breast cancer metastasis in vitro and in mice.Tumour biology : the journal of the International Society for Oncodevelopmental Biology and Medicine · 2016
    Article
  6. Review
  7. Article
  8. Article
  9. Review
  10. Review
  11. Cancer diagnosis & prognosis
    Article
  12. Co-expression ofCancer genomics & proteomics
    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 2 countries.

Alessandro RimessiDepartment of Experimental and Diagnostic Medicine, Section of General Pathology, Interdisciplinary Center for the Study of Inflammation (ICSI), Laboratory for Technologies of Advanced Therapies (LTTA), University of Ferrara, Ferrara, Italy.
Erika Zecchini
Roberta Siviero
Carlotta Giorgi
Sara Leo
Rosario Rizzuto
Paolo Pinton
University of Ferrara · ITUniversity of Padua · IT

Funding

TRANSLOCATION OF p66Shc: KINETICS, FUNCTION, APOPTOSISP01AG025532 · NIA · UNIVERSITY OF CALIFORNIA AT DAVIS · PI KIM, KYOUNGMI · 2007 to 2017
$12.1M
NIA NIH HHS 1P01AG025532-01A1NIA NIH HHS P01 AG025532Telethon GPP10005
6 · The paper itself

Abstract

The atypical protein kinase C (PKC) isoform zeta (PKCζ) has been implicated in the intracellular transduction of mitogenic and apoptotic signals by acting on different signaling pathways. The key role of these processes in tumorigenesis suggests a possible involvement of PKCζ in this event. PKCζ is activated by cytotoxic treatments, inhibits apoptotic cell death and reduces the sensitivity of cancer cells to chemotherapeutic agents. Here, using pharmacological and DNA recombinant approaches, we show that oxidative stress triggers nuclear translocation of PKCζ and induces resistance to apoptotic agents. Accordingly, chemoresistant cells show accumulation of PKCζ within the nucleus, and a nuclear-targeted PKCζ transfected in tumor cells decreases sensitivity to apoptosis. We thus developed a novel recombinant protein capable of selectively inhibiting the nuclear fraction of PKCζ that restored the susceptibility to apoptosis in cells in which PKCζ was enriched in the nuclear fraction, including chemoresistant cells. These findings establish the importance of PKCζ as a possible target to increase the effectiveness of anticancer therapies and highlight potential sites of intervention.

Indexed as

Antineoplastic AgentsApoptosisDoxorubicinDrug Resistance, NeoplasmHeLa CellsHumansHydrogen PeroxideOxidative StressProtein Kinase CProtein Kinase C zetaReactive Oxygen SpeciesTransfectionAntineoplastic AgentsDoxorubicinHydrogen PeroxideProtein Kinase CProtein Kinase C zetaReactive Oxygen Species

Identifiers

PMID22333579
PMCPMC3323800
OpenAlexW2132485444

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.