Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0476089 (endometrial cancer)
 11,379 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

SPARC (a secreted protein acidic and rich in cysteine) has a reputation for being potent anti-cancer and anti-obesity molecule. It is one of the first known matricellular protein that modulates interactions between cells and extracellular matrix (ECM) and is associated with the 'balance' of white adipose tissue (WAT) as well as lipogenesis and lipolysis during adipogenesis. Adipogenesis is an indication for the development of obesity and has been related to a wide variety of cancers including breast cancer, endometrial cancer, esophageal cancer, etc. Adipogenesis mainly involves ECM remodeling, changes in cell-ECM interactions, and cytoskeletal rearrangement. SPARC can also prevent hypertrophy of adipocytes and hyperplasia of adipocyte progenitors. In addition to SPARC's inhibitory role in adipogenesis, it has also been known to be involved in cell cycle, cell proliferation, cell invasion, adhesion, migration, angiogenesis and apoptosis. Molecular cancer biology and clinical biochemistry have significantly enhanced our understanding of the mechanisms that motivate the anti-cancer and anti-obesity action of SPARC. Recent studies elucidating the signaling pathways that are activated by SPARC can help develop the beneficial aspects of SPARC for cancer therapy and obesity prevention. This review focuses on the anti-cancer role of SPARC as it pertains to obesity.
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PMID:Anti-cancer role of SPARC, an inhibitor of adipogenesis. 2123 73

Abnormal expression of SPARC (osteonectin), cwcv and kazal-like domains proteoglycan 2 (SPOCK2) plays a significant role in the development and progression of various human cancers, yet a relationship between SPOCK2 and endometrial cancer (EC) has not been reported. Here, we assessed the potential role and mechanism by which SPOCK2 acts in the pathogenesis and progression of EC. First, protein expression of SPOCK2 in EC tissue from patients was detected by immunohistochemistry and associated clinical data were analyzed. Then, HEC-1A and Ishikawa cells were transfected with an adenoviral vector containing an SPOCK2 recombinant fragment and the biological behavior of transfected cells was observed. Finally, the expression of membrane type 1 matrix metalloproteinase (MT1-MMP) and MMP2 in the transfected cells was detected by Western blot and zymography gel assay to analyze the effect of SPOCK2 on the regulation of the MT1-MMP/MMP2 pathway. We found that there was significantly less SPOCK2 protein expression in the EC tissue than in the normal endometrium tissue, and lack of SPOCK2 protein expression in EC tissue was associated with distant metastasis and myometrial invasion. Upregulation of SPOCK2 in HEC-1A and Ishikawa cells inhibited cell proliferation, invasion, adhesion, and apoptosis. Upregulation of SPOCK2 inhibited the expression of MT1-MMP and MMP2 and activation of MMP2 in HEC-1A and Ishikawa cells. Collectively, our data indicated that SPOCK2 contributed to the progression of EC by regulating the biological behavior of cancer cells, which is achieved partly through regulating protein expression of MT1-MMP and MMP2 and activation of MMP2.
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PMID:SPOCK2 Affects the Biological Behavior of Endometrial Cancer Cells by Regulation of MT1-MMP and MMP2. 3083 59

Abnormal expression of SPARC (osteonectin), cwcv and kazal-like domains proteoglycan 2 (SPOCK2) plays a significant role in the development and progression of various human cancers, yet a relationship between SPOCK2 and endometrial cancer (EC) has not been reported. Here, we assessed the potential role and mechanism by which SPOCK2 acts in the pathogenesis and progression of EC. First, protein expression of SPOCK2 in EC tissue from patients was detected by immunohistochemistry and associated clinical data were analyzed. Then, HEC-1A and Ishikawa cells were transfected with an adenoviral vector containing an SPOCK2 recombinant fragment and the biological behavior of transfected cells was observed. Finally, the expression of membrane type 1 matrix metalloproteinase (MT1-MMP) and MMP2 in the transfected cells was detected by Western blot and zymography gel assay to analyze the effect of SPOCK2 on the regulation of the MT1-MMP/MMP2 pathway. We found that there was significantly less SPOCK2 protein expression in the EC tissue than in the normal endometrium tissue, and lack of SPOCK2 protein expression in EC tissue was associated with distant metastasis and myometrial invasion. Upregulation of SPOCK2 in HEC-1A and Ishikawa cells inhibited cell proliferation, invasion, adhesion, and apoptosis. Upregulation of SPOCK2 inhibited the expression of MT1-MMP and MMP2 and activation of MMP2 in HEC-1A and Ishikawa cells. Collectively, our data indicated that SPOCK2 contributed to the progression of EC by regulating the biological behavior of cancer cells, which is achieved partly through regulating protein expression of MT1-MMP and MMP2 and activation of MMP2.
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PMID:SPOCK2 Affects the Biological Behavior of Endometrial Cancer Cells by Regulation of MT1-MMP and MMP2. 3243 Jul 15