In vitro Study of Nucleostemin as a Potential Therapeutic Target in Human Breast Carcinoma SKBR-3 Cells

Guo, Yu; Liao, Ya-Ping; Zhang, Ding; Xu, Li; Li, Na; Guan, Weijun; Liu, Changqing

doi:10.7314/apjcp.2014.15.5.2291

Cited by 4 publications

(4 citation statements)

References 19 publications

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“…Cells were cultured in DMEM or RPMI 1640 containing 10% FBS in a humidified 5% CO 2 incubator at 37°C (Sakamoto et al, 2013). The cell lines were confirmed to be free of mycoplasma contamination using the MycoAlert mycoplasma detection kit (Lonza) (Guo et al, 2014).…”

Section: Cell Culturementioning

confidence: 99%

Betaine Effects on Morphology, Proliferation, and p53-induced Apoptosis of HeLa Cervical Carcinoma Cells in Vitro

Guo

Xu²,

Ding³

et al. 2015

Asian Pacific Journal of Cancer Prevention

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Objectives: To investigate the effects of betaine on HeLa cell growth and apoptosis and molecular mechanisms. Materials and Methods: Concentrations of 0.1, 1.0, 5.0, 20.0, 100.0 mg/ml of betaine were used to evaluate the anticancer efficacy for HeLa cells respectively, and MCF-10A was also detected as a normal diploid cell control. Results: We found that proliferation of HeLa cells was inhibited significantly upon exposure to increasing betaine levels with the MTT test (p<0.05). The percentage of S phase cells in the low dose groups (< 5mg/ml) were distinctly higher than in high dose groups, and the rates of Sub-G1 phase were the opposite (p<0.01); A high concentration of betaine (>5.0mg/ml) significantly promoted the apoptosis of HeLa cells (p<0.01). SOD activities of the low dose groups were slightly higher than the control group (p<0.05) and there were obvious synchronicity and correlation among the expression of promoting apoptosis genes Bax, P53, Caspase 3 and apoptosis suppression gene Bcl-2. In response to an apoptosis-inducing stimulus, p53 and cyclin D1 could be activated with blockage of the cell cycle at G1/S or S/G2 checkpoints. Conclusions: Our data showed that betaine could promote HeLa cells proliferation in vitro at low concentrations.In contrast, high concentrations could significantly inhibit cell growth and migration, and induce apoptosis of HeLa cells through caspase 3 signaling and further promoted necrosis. This might imply that betaine exhibits tumoricidal effects and acts as a biological response modifier in cancer treatment by inducing apoptosis and cell cycle arrest in a dose and time-dependent manner.

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Section: Cell Culturementioning

confidence: 99%

Betaine Effects on Morphology, Proliferation, and p53-induced Apoptosis of HeLa Cervical Carcinoma Cells in Vitro

Guo

Xu²,

Ding³

et al. 2015

Asian Pacific Journal of Cancer Prevention

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“…In 2002, nucleostemin (NS) was detected in the nucleoli of early pluripotent cells, and was found to be associated with cell proliferation; it is also crucial for supporting the undifferentiated properties of self-renewal certain types of stem cell ( 1 , 2 ) as well as germ cell tumors ( 3 ). Furthermore, NS is abundantly expressed in numerous tumor types, including prostate cancer ( 4 ), esophageal cancer ( 5 ), breast carcinoma ( 6 ) and gastric adenocarcinoma ( 7 ). Elevated NS expression is associated with poor prognosis of patients with various types of cancer ( 8 , 9 ).…”

Section: Introductionmentioning

confidence: 99%

“…Elevated NS expression is associated with poor prognosis of patients with various types of cancer ( 8 , 9 ). Furthermore, knockdown of NS was shown to inhibit cell proliferation as well as induce cell cycle arrest and apoptosis ( 6 , 10 – 13 ). NS is therefore a potential biomarker for tumor diagnosis and prognosis ( 7 , 14 ).…”

Section: Introductionmentioning

confidence: 99%

Gene expression profiling of NB4 cells following knockdown of nucleostemin using DNA microarrays

Sun

Wei

et al. 2016

Molecular Medicine Reports

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Nucleostemin (NS) is mainly expressed in stem and tumor cells, and is necessary for the maintenance of their self-renewal and proliferation. Originally, NS was thought to exert its effects through inhibiting p53, while recent studies have revealed that NS is also able to function independently of p53. The present study performed a gene expression profiling analysis of p53-mutant NB4 leukeima cells following knockdown of NS in order to elucidate the p53-independent NS pathway. NS expression was silenced using lentivirus-mediated RNA interference technology, and gene expression profiling of NB4 cells was performed by DNA microarray analysis. A total of 1,953 genes were identified to be differentially expressed (fold change ≥2 or ≤0.5) following knockdown of NS expression. Furthermore, reverse-transcription quantitative polymerase chain reaction analysis was used to detect the expression of certain candidate genes, and the results were in agreement with the micaroarray data. Pathway analysis indicated that aberrant genes were enhanced in endoplasmic, c-Jun N-terminal kinase and mineral absorption pathways. The present study shed light on the mechanisms of the p54-independent NS pathway in NB4 cells and provided a foundation for the discovery of promising targets for the treatment of p53-mutant leukemia.

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“…NS is preferentially expressed in embryo-derived stem cells and human tumors (Fan et al 2006). Suppression of NS protein blocks cell cycle progression and promotes cell apoptosis in human breast carcinoma SKBR-3 cells (Guo et al 2014). NS was transiently re-expressed in the adult heart after acute myocardial infarction and other pathological challenges (Tjwa and Dimmeler 2008).…”

Section: Introductionmentioning

confidence: 99%

Nucleostemin exerts anti-apoptotic function via p53 signaling pathway in cardiomyocytes

Zhang

Shi

Qian

et al. 2015

In Vitro Cell.Dev.Biol.-Animal

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Cardiomyocytes apoptosis following reperfusion injury causes irreversible damage to cardiac function. Understanding the mechanisms underlying cardiomyocytes death under these conditions can be helpful to identify strategies to abrogate such detrimental effects. Stem cell-specific proteins and regulatory pathways become important in understanding reparative processes in the myocardium. One such regulatory protein named nucleostemin (NS) has vital roles in cardiac ischemia. Although the relationship between NS and cell apoptosis has been studied, it is unknown how NS is controlled and how it participates in cardiomyocytes apoptosis induced by ischemia reperfusion (I/R). In the present study, we aimed to investigate the direct role of NS in myocardial I/R. In vivo, NS was highly expressed in cardiac tissues after I/R. Double immunofluorescent staining showed that NS located in the nucleolar of cardiomyocytes and correlated with cardiomyocytes apoptosis. Furthermore, in vitro primary rat cardiomyocytes increased NS expression induced by hypoxia-reoxygenation (H/R) treatment, in line with results in vivo. Suppression of NS expression by siNS promoted the expression of terminal deoxynucleotide transferase-mediated dUTP nick end labeling (TUNEL)-positive cells p53 and cleaved caspase-3, which demonstrates I/R may require increased expression of NS to suppress p53 activation and maintain cardiomyocytes survival.

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In vitro Study of Nucleostemin as a Potential Therapeutic Target in Human Breast Carcinoma SKBR-3 Cells

Cited by 4 publications

References 19 publications

Betaine Effects on Morphology, Proliferation, and p53-induced Apoptosis of HeLa Cervical Carcinoma Cells in Vitro

Betaine Effects on Morphology, Proliferation, and p53-induced Apoptosis of HeLa Cervical Carcinoma Cells in Vitro

Gene expression profiling of NB4 cells following knockdown of nucleostemin using DNA microarrays

Nucleostemin exerts anti-apoptotic function via p53 signaling pathway in cardiomyocytes

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