ArticleGenes & cancer2010
Synthetic Lethality Induced by Loss of PKC δ and Mutated Ras.
Article in Genes & cancer, 2010. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 7 papers.
What it found
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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.
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.
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Who cites it
7 citing papers in PubMed, 10 citations in OpenAlex.
- Suppression of PKC causes oncogenic stress for triggering apoptosis in cancer cells.Oncotarget · 2017Article
- Protein kinase Cδ is a therapeutic target in malignant melanoma with NRAS mutation.ACS chemical biology · 2014Article
- Protein kinase C-δ inactivation inhibits the proliferation and survival of cancer stem cells in culture and in vivo.BMC cancer · 2014Article
- Induction of mitotic catastrophe by PKC inhibition in Nf1-deficient cells.Cell cycle (Georgetown, Tex.) · 2014Article
- Primarily screening and analyzing ESTs differentially expressed in rats' primary liver cancer.Chinese journal of cancer research = Chung-kuo yen cheng yen chiu · 2013Article
- Regulation of Transcriptional Networks by PKC Isozymes: Identification of c-Rel as a Key Transcription Factor for PKC-Regulated Genes.PloS one · 2013Article
- Differential sensitization of different prostate cancer cells to apoptosis.Genes & cancer · 2010Article
Corrections and comments
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Authors and funding
5 authors at 1 institution in 1 country.
Funding
Abstract
Synthetic lethal interaction between oncogenic Ha-ras and loss of PKC has been demonstrated. Recently, the authors reported that the concurrent knockdown of PKC α and β, via upregulating PKC δ, sensitizes cells with aberrant Ras signaling to apoptosis. As a continuation of the study, using shRNA, the authors demonstrate that loss of PKC δ causes a lethal reaction in NIH3T3/Hras or prostate cancer DU145 cells that overexpress JNK. In this apoptotic process, PKC α and β are upregulated and then associated with RACK1 (an adaptor for activated PKC) and JNK. Immunoblotting analysis shows that JNK is phosphorylated, accompanied with caspase 8 cleavage. The inhibition of JNK abrogates this apoptotic process triggered by PKC δ knockdown. Interestingly, without blocking PKC δ, the concurrent overexpression of wt- or CAT-PKC α and β is insufficient to induce apoptosis in the cells. Together with the authors' previous findings, the data suggest that PKC α/β and δ function oppositely to maintain a balance that supports cells expressing v-ras to survive and prevents them from being eliminated through oncogenic stress-induced apoptosis.
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Registered trials
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.