Gene/Protein
Disease
Symptom
Drug
Enzyme
Compound
Pivot Concepts:
Gene/Protein
Disease
Symptom
Drug
Enzyme
Compound
Target Concepts:
Gene/Protein
Disease
Symptom
Drug
Enzyme
Compound
Query: UMLS:C0029463 (
osteosarcoma
)
16,637
document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)
Monoclonal antibody A2B5 reacts with the cell surface of a series of amine precursor uptake decarboxylation (APUD) cells and their tumors in many vertebrate species including chicken, rat, mouse, and man. We have studied the in vivo and in vitro binding of iodinated monoclonal antibody A2B5 to rat
insulinoma
cells. In vitro, radiolabeled A2B5 binds specifically to RINm5F
insulinoma
cells and the binding of 125I-A2B5 is inhibited by unlabeled A2B5 or a ganglioside extract of RINm5F cells. In vivo, scintigrams taken Day 0 to Day 5 after injection of 131I-labeled A2B5 showed a striking localization of 131I-A2B5 in transplanted RIN tumors grown in syngeneic rats. Other control radiolabeled monoclonal antibodies did not concentrate in the tumors. 131I-labeled A2B5 did not concentrate in other transplantable tumors (colon adenocarcinoma,
osteosarcoma
, renal cell carcinoma, and bladder transitional cell carcinoma) grown in nude mice. The tumor/blood ratio detected 5 days after antibody injection, was approximately two to 12 times higher in the
insulinoma
compared to other organs and only in the
insulinoma
did 131I-A2B5 show a higher concentration than control antibody 125I-P3X63.
...
PMID:In vivo and in vitro binding of iodinated monoclonal antibody A2B5 to RIN insulinoma cells. 608 90
Menin, encoded by MEN1 gene, has been viewed as a tumor suppressor in several types of tumors, such as
insulinoma
, parathyroid tumor, and adrenocortical and lung carcinoma. However, its expression and molecular regulation mechanism in
osteosarcoma
has not been elucidated. Here, our results show menin expression is significantly down-regulated in
osteosarcoma
tissues, compared with adjacent normal tissues. Besides, we report that MicroRNA-142-3p as a novel target of menin. Up-regulation of MicroRNA-142-3p by menin overexpression inhibits cell proliferation in U2OS and MG63 cells. At the molecular level, MicroRNA-142-3p inhibits the protein expression of FASN through binding to its 3'-untranslated region. Therefore, we elucidate a novel regulation pathway in
osteosarcoma
cells and suggest a potential therapeutic approach for the tumor therapy.
...
PMID:MicroRNA-142-3p, a novel target of tumor suppressor menin, inhibits osteosarcoma cell proliferation by down-regulation of FASN. 2879 36
PDZ domain containing 2 (PDZD2) is a multi-PDZ domain protein that promotes the proliferation of
insulinoma
cells, and is upregulated during prostate tumorigenesis. However, the function of PDZD2 in other cancers, including osteosarcoma (OS), remains unclear. Dysregulation of microRNAs (miRNAs) contributes to tumor initiation, proliferation and metastasis, via the regulation of their target genes. The present study investigated the functions of miR-363 and PDZD2 in MG-63 OS cells. The results revealed that MG-63 cells contained low levels of miR-363, and that overexpression of miR-363 in MG-63 cells significantly inhibited the vitality, proliferation, and colony formation ability of the cells, but promoted their apoptosis and G1/S arrest by regulating proliferating cell nuclear antigen (PCNA) and caspase-3 expression. Additionally, miR-363 impaired the migration and invasion of MG-63 cells by regulating the epithelial-mesenchymal transition (EMT) phenotype. Notably, a bioinformatics analysis and luciferase reporter assay indicated that PDZD2 was a direct target of miR-363. miR-363 overexpression reduced PDZD2 protein levels and knockdown of PDZD2 suppressed the colony formation, migration and invasion of MG-63 cells, but promoted their apoptosis by regulating expression of PCNA, caspase-3, and the EMT phenotype. In vivo studies further confirmed that miR-363 functioned as tumor suppressor, by inhibiting tumor growth, promoting cell apoptosis, and reducing PDZD2 and PCNA levels and the prevalence of the EMT phenotype in tumor tissues. The present data demonstrated that downregulation of the tumor suppressor miR-363 may be involved in the development of
osteosarcoma
via regulation of PDZD2.
...
PMID:miR-363 acts as a tumor suppressor in osteosarcoma cells by inhibiting PDZD2. 3089 77