Gene/Protein
Disease
Symptom
Drug
Enzyme
Compound
Pivot Concepts:
Gene/Protein
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Target Concepts:
Gene/Protein
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Query: UNIPROT:P04637 (
p53
)
77,613
document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)
S100A16 is a member of S100 protein super family that carries calcium-binding EF-hand motifs. Its expression is ubiquitous and elevated in various types of tumors. The functions of S100 proteins are still being defined, although many members of S100 protein family are traditionally considered as markers of tumor tissues. Using 3T3-L1 preadipocyte model, we investigated the expression and function of S100A16 during differentiation into adipocytes as well as the potential roles of S100A16 in the regulation of insulin sensitivity. We found that the expression of S100A16 was increased during differentiation and that elevation of intracellular Ca(2+) via calcium ionophores led to its nucleus exclusion. Overexpression of S100A16 in 3T3-L1 preadipocytes increased their proliferation and markedly enhanced adipogenesis but resulted in significant reduction of insulin-stimulated glucose uptake and phosphorylation of AKT. In contrast, suppression of S100A16 expression with two different types of RNA interference significantly inhibited adipogenesis and preadipocyte proliferation. Immunoprecipitation analysis revealed that S100A16 could physically interact with
tumor suppressor protein p53
, also a known inhibitor of adipogenesis. Overexpression or RNA interference-initiated reduction of S100A16 led to the inhibition or activation of the expression of
p53
-responsive genes, respectively. Interestingly, Western blot assays showed that
S100A16 protein
levels were markedly higher in the adipose tissues of diet-induced obese mice and the ob/ob mice than that in control lean mice. Thus, we reveal for the first time that
S100A16 protein
is a novel adipogenesis-promoting factor and that increased expression of S100A16 in 3T3-L1 adipocytes can have a negative impact on insulin sensitivity.
...
PMID:Identification of S100A16 as a novel adipogenesis promoting factor in 3T3-L1 cells. 2126 6
Cancer stem-like cells (CSCs), which possess the ability to self-renewal and are multipotent, are regarded as the cause of tumor formation, recurrence, metastasis and drug resistance. It is necessary to understand the properties of CSCs in order to treat them effectively. It has been previously reported that S100 family proteins, which carry calcium-binding EF-hand motifs and are associated with tumorigenic processes, serve crucial roles in maintaining cancer stem-like properties. S100A16 is upregulated in various types of cancer, including bladder, lung and pancreatic. However, the roles of S100A16 in cancer cells, particularly CSCs, are not clear. The present study investigated the roles of S100A16 in CSCs using the sphere formation assay of Yumoto cells, which are a human cervical carcinoma cell line. The mRNA expression levels were evaluated by reverse transcription-polymerase chain reaction and the protein expression levels were detected by western blot analysis. Following the sphere formation of Yumoto cells, the mRNA and protein expression level of Oct4, Nanog and S100A16 were increased compared with the control cells. Following transfection with S100A16 small interfering RNA (siRNA), the mRNA and protein expression of Oct4 and Nanog were decreased and the spheroid size was significantly decreased in the sphere formation of Yumoto cells compared with control siRNA treated cells. There was no change in the
p53
mRNA expression level, whereas the
p53 protein
expression level, which was decreased by the sphere formation, was recovered by S100A16 knockdown. In addition, the protein expression levels of Oct4 and Nanog, which were increased in the sphere formation, were decreased by the proteasome inhibitor lactacystin. No differences were observed in the
S100A16 protein
expression between the presence or absence of lactacystin. These results suggest that S100A16 serves an important role in the CSCs of human cervical carcinoma and is a positive regulator of Oct4 and Nanog.
...
PMID:S100A16 up-regulates Oct4 and Nanog expression in cancer stem-like cells of Yumoto human cervical carcinoma cells. 2992 66