ArticleAdvanced pharmaceutical bulletin2014
Nucleostemin depletion induces post-g1 arrest apoptosis in chronic myelogenous leukemia k562 cells.
Article in Advanced pharmaceutical bulletin, 2014. 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.
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Who cites it
7 citing papers in PubMed, 15 citations in OpenAlex.
- Proteomic Investigation of the Role of Nucleostemin in Nucleophosmin-Mutated OCI-AML 3 Cell Line.International journal of molecular sciences · 2022Article
- Association of Nucleostemin Polymorphisms with Chronic Hepatitis B Virus Infection in Chinese Han Population.Genetic testing and molecular biomarkers · 2022Article
- Silencing of Nucleostemin by siRNA Induces Apoptosis in MCF-7 and MDA-MB-468 Cell Lines.Iranian journal of pharmaceutical research : IJPR · 2020Article
- Article
- Differential expression of nucleostemin in the cytoplasm and nuclei of normal and cancerous cell lines.Turkish journal of biology = Turk biyoloji dergisi · 2018Article
- Cellular and Molecular Preconditions for Retinal Pigment Epithelium (RPE) Natural Reprogramming during Retinal Regeneration in Urodela.Biomedicines · 2016Review
- Gene expression profiling of NB4 cells following knockdown of nucleostemin using DNA microarrays.Molecular medicine reports · 2016Article
Corrections and comments
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Authors and funding
6 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
purposeDespite significant improvements in treatment of chronic myelogenous leukemia (CML), the emergence of leukemic stem cell (LSC) concept questioned efficacy of current therapeutical protocols. Remaining issue on CML includes finding and targeting of the key genes responsible for self-renewal and proliferation of LSCs. Nucleostemin (NS) is a new protein localized in the nucleolus of most stem cells and tumor cells which regulates their self-renewal and cell cycle progression. The aim of this study was to investigate effects of NS knocking down in K562 cell line as an in vitro model of CML.
methodsNS gene silencing was performed using a specific small interfering RNA (NS-siRNA). The gene expression level of NS was evaluated by RT-PCR. The viability and growth rate of K562 cells were determined by trypan blue exclusion test. Cell cycle distribution of the cells was analyzed by flow cytometry.
resultsOur results showed that NS knocking down inhibited proliferation and viability of K562 cells in a time-dependent manner. Cell cycle studies revealed that NS depletion resulted in G(1) cell cycle arrest at short times of transfection (24 h) followed with apoptosis at longer times (48 and 72 h), suggest that post-G1 arrest apoptosis is occurred in K562 cells.
conclusionOverall, these results point to essential role of NS in K562 cells, thus, this gene might be considered as a promising target for treatment of CML.
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