ArticleCancer research2012
Chk2 phosphorylation of survivin-DeltaEx3 contributes to a DNA damage-sensing checkpoint in cancer.
Article in Cancer research, 2012. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 12 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
12 citing papers in PubMed, 17 citations in OpenAlex.
- Targeted Hyperbranched Nanoparticles for Delivery of Doxorubicin in Breast Cancer Brain Metastasis.Molecular pharmaceutics · 2023Article
- Characterization and mechanisms of radioresistant lung squamous cell carcinoma cell lines.Thoracic cancer · 2023Article
- Synthetic Antibodies Detect Distinct Cellular States of Chromosome Passenger Complex Proteins.Journal of molecular biology · 2022Article
- Inhibition of survivin induces spindle disorganization, chromosome misalignment, and DNA damage during mouse embryo development.Cell cycle (Georgetown, Tex.) · 2020Article
- Article
- Protein Sam68 regulates the alternative splicing of survivin DEx3.The Journal of biological chemistry · 2017Article
- Survivin splice variants and their diagnostic significance.Tumour biology : the journal of the International Society for Oncodevelopmental Biology and Medicine · 2015Review
- Survivin family proteins as novel molecular determinants of doxorubicin resistance in organotypic human breast tumors.Breast cancer research : BCR · 2014Article
- Article
- Clinico-pathologic relevance of Survivin splice variant expression in cancer.Cancer letters · 2013Review
- MEK1/2 inhibition enhances the radiosensitivity of cancer cells by downregulating survival and growth signals mediated by EGFR ligands.International journal of oncology · 2013Article
- Chemotherapy induced DNA damage response: convergence of drugs and pathways.Cancer biology & therapy · 2013Review
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
13 authors at 5 institutions in 3 countries.
Funding
Abstract
Survivin is an oncogene that functions in cancer cell cytoprotection and mitosis. Here we report that differential expression in cancer cells of a C-terminal splice variant of survivin, termed survivin-ΔEx3, is tightly associated with aggressive disease and markers of unfavorable prognosis. In contrast to other survivin variants, survivin-ΔEx3 localized exclusively to nuclei in tumor cells and was phosphorylated at multiple residues by the checkpoint kinase Chk2 during DNA damage. Mutagenesis of the Chk2 phosphorylation sites enhanced the stability of survivin-ΔEx3 in tumor cells, inhibited the expression of phosphorylated H2AX (γH2AX) in response to double-strand DNA breaks, and impaired growth after DNA damage. DNA damage induced Chk2 phosphorylation, stabilization of p53, induction of the cyclin-dependent kinase inhibitor p21, and homologous recombination-induced repair were not affected. In vivo, active Chk2 was detected at the earliest stages of the colorectal adenoma-to-carcinoma transition, persisted in advanced tumors, and correlated with increased survivin expression. Together, our findings suggest that Chk2-mediated phosphorylation of survivin-ΔEx3 contributes to a DNA damage-sensing checkpoint that may affect cancer cell sensitivity to genotoxic therapies.
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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.