ArticleCell death & disease2014
Survivin-2B promotes autophagy by accumulating IKK alpha in the nucleus of selenite-treated NB4 cells.
Article in Cell death & disease, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 13 papers.
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Who cites it
13 citing papers in PubMed, 21 citations in OpenAlex.
- Regulation of autophagy by the p53 family and the implications for cancer therapies.Discover oncology · 2026Review
- Deciphering the dual role of autophagy in gastric cancer and gastroesophageal junction cancer: from tumor suppression to cancer progression.Discover oncology · 2025Review
- Decreased BIRC5-206 promotes epithelial-mesenchymal transition in nasopharyngeal carcinoma through sponging miR-145-5p.Open medicine (Warsaw, Poland) · 2024Article
- Nanomedicine for autophagy modulation in cancer therapy: a clinical perspective.Cell & bioscience · 2023Review
- Selenite-induced ROS/AMPK/FoxO3a/GABARAPL-1 signaling pathway modulates autophagy that antagonize apoptosis in colorectal cancer cells.Discover oncology · 2021Article
- Role of constitutive nitric oxide synthases in the dynamic regulation of the autophagy response of keratinocytes upon UVB exposure.Photochemical & photobiological sciences : Official journal of the European Photochemistry Association and the European Society for Photobiology · 2020Article
- Article
- Proteome Analysis of Human Follicular Thyroid Cancer Cells Exposed to the Random Positioning Machine.International journal of molecular sciences · 2017Article
- Survivin splice variants and their diagnostic significance.Tumour biology : the journal of the International Society for Oncodevelopmental Biology and Medicine · 2015Review
- Suppressed diversity of survivin splicing in active rheumatoid arthritis.Arthritis research & therapy · 2015Article
- Role of autophagy in chronic kidney diseases.International journal of clinical and experimental medicine · 2015Review
- ROS inhibit autophagy by downregulating ULK1 mediated by the phosphorylation of p53 in selenite-treated NB4 cells.Cell death & disease · 2014Article
- Survivin is essential for fertile egg production and female fertility in mice.Cell death & disease · 2014Article
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Authors and funding
11 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Survivin-2B, a known splice variant of survivin, has been reported to promote cell death in some cancer cells, although it keeps prosurvival function in others, and the mechanisms are unclear. In this report, we discovered that selenite, an antitumor agent, switched protective autophagy to apoptosis in NB4 cells. In this process, the level of survivin-2B was decreased and the interaction between IKK alpha and survivin-2B in the nucleus was attenuated, which further led to the decrease of nuclear IKK alpha. As a result, P73, a known transcript factor of UVRAG, was downregulated. Therefore, the expression of UVRAG, one of the initiators of autophagy, was inhibited. The regulatory status of survivin-2B was also proved in NB4 cells after different chemicals' exposure and in other tumor cell lines (Jurkat, HCT116). Finally, experiments in vivo confirmed that the alterations of survivin-2B, IKK alpha, P73 and UVRAG were the same as that in vitro. Taken together, survivin-2B promoted autophagy and further regulated cell death by accumulating and stabilizing IKK alpha in the nucleus.
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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.