ArticleOncogene2002
Mitochondrial dysfunction is an essential step for killing of non-small cell lung carcinomas resistant to conventional treatment.
Article in Oncogene, 2002. 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 36 papers.
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.
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
36 citing papers in PubMed, 98 citations in OpenAlex.
- A Mini Review on Molecules Inducing Caspase-Independent Cell Death: A New Route to Cancer Therapy.Molecules (Basel, Switzerland) · 2022Review
- Sulfur dioxide induces apoptosis via reactive oxygen species generation in rat cardiomyocytes.Environmental science and pollution research international · 2019Article
- Gene expression profiling of breast cancer cell lines treated with proton and electron radiations.The British journal of radiology · 2018Article
- Visfatin induces the apoptosis of endothelial progenitor cells via the induction of pro-inflammatory mediators through the NF-κB pathway.International journal of molecular medicine · 2017Article
- Apoptosis-inducing factor and calpain upregulation in glutamate-induced injury of rat spiral ganglion neurons.Molecular medicine reports · 2015Article
- Comprehensive review on betulin as a potent anticancer agent.BioMed research international · 2015Review
- Genes associated with sodium fluoride-induced human osteoblast apoptosis.International journal of clinical and experimental medicine · 2015Article
- Ameloblastic carcinoma of the mandible: Report of a case and review.Journal of oral and maxillofacial pathology : JOMFP · 2014Review
- Differential sensitivity to apoptosome apparatus activation in non-small cell lung carcinoma and the lung.International journal of oncology · 2014Article
- Inhibition of Ephrin B3-mediated survival signaling contributes to increased cell death response of non-small cell lung carcinoma cells after combined treatment with ionizing radiation and PKC 412.Cell death & disease · 2013Article
- The Yin and Yang of redox regulation.Redox report : communications in free radical research · 2013Review
- Role of glutathione in cancer progression and chemoresistance.Oxidative medicine and cellular longevity · 2013Review
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- Article
- Thioredoxin reductase 1 knockdown enhances selenazolidine cytotoxicity in human lung cancer cells via mitochondrial dysfunction.Biochemical pharmacology · 2011Article
- Critical role for hyperpolarization-activated cyclic nucleotide-gated channel 2 in the AIF-mediated apoptosis.The EMBO journal · 2010Article
- Delayed activation of caspase-independent apoptosis during heart failure in transgenic mice overexpressing caspase inhibitor CrmA.American journal of physiology. Heart and circulatory physiology · 2010Article
- Dasatinib synergizes with JSI-124 to inhibit growth and migration and induce apoptosis of malignant human glioma cells.Journal of carcinogenesis · 2010Article
- Opposing effects of hMOF and SIRT1 on H4K16 acetylation and the sensitivity to the topoisomerase II inhibitor etoposide.Oncogene · 2010Article
- Proinsulin C-peptide regulates ribosomal RNA expression.The Journal of biological chemistry · 2010Article
Corrections and comments
- Erratum issued
Authors and funding
6 authors at 3 institutions in 2 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Apoptosis, a tightly controlled multi-step mechanism of cell death, is important for anti-cancer therapy-based elimination of tumor cells. However, this process is not always efficient. Small cell lung carcinoma (SCLC) and non-small cell lung carcinoma (NSCLC) cells display different susceptibility to undergo apoptosis induced by anticancer treatment. In contrast to SCLC, NSCLC cells are cross-resistant to a broad spectrum of apoptotic stimuli, including receptor stimulation, cytotoxic drugs and gamma-radiation. Since resistance of tumor cells to treatment often accounts for the failure of traditional forms of cancer therapy, in the present study attempts to find a potent broad-range apoptosis inductor, which can kill therapy-resistant NSCLC cells were undertaken and the mechanism of apoptosis induction by this drug was investigated in detail. We found that staurosporine (STS) had cell killing effect on both types of lung carcinomas. Release of cytochrome c, activation of apical and effector caspases followed by cleavage of their nuclear substrates and morphological changes specific for apoptosis were observed in STS-treated cells. In contrast to treatment with radiation or chemotherapy drugs, STS induces mitochondrial dysfunction followed by translocation of AIF into the nuclei. These events preceded the activation of nuclear apoptosis. Thus, in lung carcinomas two cell death pathways, caspase-dependent and caspase-independent, coexist. In NSCLC cells, where the caspase-dependent pathway is less efficient, the triggering of an AIF-mediated caspase-independent mechanism circumvents the resistance of these cells to treatment.
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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.