Gene/Protein
Disease
Symptom
Drug
Enzyme
Compound
Pivot Concepts:
Gene/Protein
Disease
Symptom
Drug
Enzyme
Compound
Target Concepts:
Gene/Protein
Disease
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Enzyme
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Query: UMLS:C0598934 (
tumor growth
)
58,965
document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)
PRR11
is a newly identified oncogene in lung cancer, yet its role in others tumors remains unclear. Gastrointestinal tissue microarrays were used to evaluate
PRR11
expression and its association with clinical outcome was analyzed in patients with hilar cholangiocarcinoma. Overexpression of
PRR11
was observed in esophageal, gastric, pancreatic, colorectal, and hilar cholangiocarcinoma. Expression of
PRR11
correlated with lymph node metastasis and CA199 level in two HC patient cohorts. After an R0 resection, a high level of
PRR11
expression was found to be an independent indicator of recurrence (P = 0.001). In cell culture,
PRR11
silencing resulted in decreased cellular proliferation, cell migration,
tumor growth
of QBC939 cells. Microarray analysis revealed that several genes involved in cell proliferation, cell adhesion, and cell migration were altered in
PRR11
-knockout cells, including: vimentin (VIM), Ubiquitin carboxyl-terminal hydrolase 1 (UCHL1), early growth response protein (EGR1), and System A amino acid transporter1 (SNAT1). Silencing
PRR11
inhibited the expression of UCHL1, EGR1, and SNAT1 proteins, with immunoassays revealing a significant correlation among the levels of these four proteins. These results indicate that
PRR11
is an independent prognostic indicator for patients with HC.
...
PMID:The prognostic potential and oncogenic effects of PRR11 expression in hilar cholangiocarcinoma. 2597 32
Background
: We previously demonstrated that
Proline rich 11
(
PRR11
) gene is associated with the development and progression of tongue squamous cell carcinoma (TSCC), but the underlying mechanism is unknown. This study aimed to investigate the molecular mechanism underlying oncogenic potential of
PRR11
in TSCC cells.
Methods
: Overexpression and knockdown of
PRR11
were performed by plasmid transfection into SCC15 and HSC3 human TSCC cells. Expressions of mRNA and protein were assessed by qRT-PCR and Western blot, respectively. Cell proliferation and invasion were determined by CCK-8 and Transwell assay, respectively.
In vivo
tumor growth
and cell cycle were determined by a nude mice model of subcutaneous tumorigenesis and flow cytometry, respectively.
Results
: Overexpression of
PRR11
significantly enhanced TSCC cells proliferation and the invasive ability of TSCC cells, whereas
PRR11
knockdown in TSCC cells exhibited a reverse trend. In addition, the
in vivo
subcutaneous tumorigenicity assay showed that
PRR11
knockdown significantly reduced tumor size and the Ki67 (a proliferation marker)expression in the tumor tissue. Flow cytometry analysis revealed that
PRR11
overexpression significantly decreased the proportion of cells in S phase, whereas
PRR11
knockdown in TSCC cells exhibited a reverse trend. Furthermore,
PRR11
overexpression simultaneously down-regulated two cyclin-dependent kinase inhibitors (CKIs), p21 and p27 and up-regulated CDK2 and Cyclin A2 in TSCC cells.
PRR11
knockdown again exhibited reverse trends of expressions of the above proteins.
Conclusion
: These results suggested that
PRR11
promoted cell proliferation by regulating the expressions of p21, p27, CDK2 and Cyclin A to facilitate S/G phase transition in TSCC cells.
...
PMID:The oncogenic potential of PRR11 gene in Tongue Squamous Cell Carcinoma cells. 3125 60
