The art of killing: double stroke with apoptin and survivin as a novel approach in cancer therapy

Panigrahi, Soumya; Klonisch, Thomas; Łos, Marek

doi:10.4161/cbt.7.7.6492

Cited by 7 publications

(6 citation statements)

References 20 publications

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“…Shephedrin destabilises the above interaction, thus depleting survivin, and selectively induces apoptosis only in tumour cells but not in normal cells, by both caspase dependent and independent mechanisms 183. shRNA mediated inhibition of survivin expression combined with the introduction of apoptin, a viral protein that selectively kills cancer cells, has recently been tested, and the data reveal synergistic effects of both treatments 184 185. Apart from the above approaches, anti-survivin hammerhead ribozymes have been developed that can effectively downregulate survivin’s expression, and hence potentiate cancer cell apoptosis 186 – 188…”

Section: Caspases and Caspase Inhibitors: Potential Clinical Applicatmentioning

confidence: 99%

Apoptosis and cancer: mutations within caspase genes

Ghavami

Hashemi

Ande

et al. 2009

Journal of Medical Genetics

610

437

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Section: Caspases and Caspase Inhibitors: Potential Clinical Applicatmentioning

confidence: 99%

Apoptosis and cancer: mutations within caspase genes

Ghavami

Hashemi

Ande

et al. 2009

Journal of Medical Genetics

610

437

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“…Recent studies demonstrate that downregulation of survivin together with the expression of apoptin significantly increases the percentage of apoptotic cells compared to the effects seen upon survivin loss or apoptin expression alone [62,63]. Survivin belongs to the family of inhibitors of apoptosis proteins (IAP) and is highly expressed in several tumors.…”

Section: Clinical Perspectives Of Apoptinmentioning

confidence: 99%

Apoptin, a tumor-selective killer

Łos

Panigrahi

Rashedi

et al. 2009

Biochimica et Biophysica Acta (BBA) - Molecular Cell Research

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Apoptin, a small protein from chicken anemia virus, has attracted great attention, because it specifically kills tumor cells while leaving normal cells unharmed. The subcellular localization of apoptin appears to be crucial for this tumor-selective activity. In normal cells, apoptin resides in the cytoplasm, whereas in cancerous cells it translocates into the nucleus. The nuclear translocation of apoptin is largely controlled by its phosphorylation. In tumor cells, apoptin causes the nuclear accumulation of survival kinases including Akt and is phosphorylated by CDK2. Thereby, apoptin redirects survival signals into cell death responses. Apoptin also binds as a multimeric complex to DNA and interacts with several nuclear targets, such as the anaphase-promoting complex, resulting in a G2/M phase arrest. The proapoptotic signal of apoptin is then transduced from the nucleus to cytoplasm by Nur77, which triggers a p53-independent mitochondrial death pathway. In this review, we summarize recent discoveries of apoptin's mechanism of action that might provide intriguing insights for the development of novel tumor-selective anticancer drugs.

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“…Apoptin, a protein derived from chicken anemia virus, has received significant attention as a selective killer of cancer cells ( 7 ). Gene expression differences between normal and tumor cells may account for the sensitivity of tumor cells to apoptin.…”

Section: Introductionmentioning

confidence: 99%

Antitumor effects of a dual cancer-specific oncolytic adenovirus on colorectal cancer in vitro and in vivo

Yang

Sun

et al. 2014

Experimental and Therapeutic Medicine

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The efficacy and specificity of treatment are major challenges for cancer gene therapy. Oncolytic virotherapy is an attractive drug delivery platform for cancer gene therapy. In the present study, the dual-specific antitumor oncolytic adenovirus, Ad-Apoptin-hTERT-E1a, was used to infect SW1116 human colorectal carcinoma (CRC) cell lines and CT26 mouse-CRC-cell bearing BALB/c mouse models for testing antitumor effects in vitro and in vivo. The in vitro assays revealed that infection with Ad-Apoptin-hTERT-E1a induced a significant cytotoxic effect on the CRC cell line, SW1116; however, the normal human cell line, GES, was only slightly inhibited by the recombinant adenovirus. Acridine orange and ethidium bromide staining and an annexin V assay indicated that infection of SW1116 cells with Ad-Apoptin-hTERT-E1a resulted in a significant induction of apoptosis. Furthermore, western blotting and flow cytometry revealed a decrease in the mitochondrial membrane potential (MMP), the release of cytochrome c and the activation of caspase 3, 6 and 7 in Ad-Apoptin-hTERT-E1a-infected SW1116 cells. In the animal models, Ad-Apoptin-hTERT-E1a was shown to significantly inhibit tumor growth and extend the survival times of the animals. Therefore, the experimental results indicated that Ad-Apoptin-hTERT-E1a has potential for application in tumor gene therapy.

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The art of killing: double stroke with apoptin and survivin as a novel approach in cancer therapy

Cited by 7 publications

References 20 publications

Apoptosis and cancer: mutations within caspase genes

Apoptosis and cancer: mutations within caspase genes

Apoptin, a tumor-selective killer

Antitumor effects of a dual cancer-specific oncolytic adenovirus on colorectal cancer in vitro and in vivo

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