Gene/Protein Disease Symptom Drug Enzyme Compound
Pivot Concepts:   Target Concepts:
Query: UNIPROT:P17931 (galectin-3)
 2,860 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Lymph node metastasis is recognized as an important mode of liver cancer metastasis. Our previous study has built two hepatocarcinoma cell lines, Hca-F with high (75%) and Hca-P with low (25%) incidences of lymph node metastasis, and has indicated that annexin A7 is an important factor in the lymphatic metastasis of tumors. There is evidence that galectin-3 is the binding protein of annexin A7 and works in protein complexes. Our current study shows that both annexin A7 and galectin-3 express higher in Hca-F than Hca-P. Annexin A7 was successfully down-regulated in Hca-P by RNA interference, and this resulted in concomitant reduction of galactin 3 expression in annexin A7 down regulated compared to the control and N-control cells. Using CCK-8 assay, the expression level of annexin A7 and galectin-3 were found to have correlation with the proliferation ability; Transwell assay showed annexin A7 and galectin-3 are involved in cell migration and invasion regulation in mouse hepatocellular carcinoma cell lines, immunofluorescence assay indicate annexin A7 and galectin-3 were co-located annexin A7 and galectin-3 played roles in DNA damage and cell proliferation cycle checkpoint arrest pathway. Those phenomena indicated that annexin A7 influences lymphatic metastasis of tumors by interacting with galectin-3 through the regulation of tumor cell proliferation, attachment, migration and invasion.
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PMID:Annexin A7 and its binding protein galectin-3 influence mouse hepatocellular carcinoma cell line in vitro. 2437 98

Galectin-3 (Gal-3) is a multifunctional carbohydrate-binding protein associated with cell migration, cell proliferation, cell adhesion, and cell-cell interaction in tumor cells. It has been implied to be involved in the tumor progression and chemoresistance of epithelial ovarian cancer (EOC). However, it is unclear whether the Gal-3-mediated regulation on the EOC chemosensitivity is associated with hypoxia or mitochondrial dysfunction. In the present study, we examined the regulation by Gal-3 overexpression on cisplatin-sensitivity or cisplatin-resistance in EOC cells in vitro. We manipulated Gal-3 via plasmid transfection and RNA interference in the cisplatin-resistant EOC cells, and re-evaluated the sensitivity of the cisplatin-resistant EOC cells to cisplatin, with CCK-8 assay, colony forming assay, apoptosis analysis and mitochondrial function examination. Results demonstrated that galectin-3 overexpression downregulated the cisplatin sensitivity in EOC OVCAR-3 cell clone, resulting in an upregulated growth and a reduced apoptosis in the cisplatin-treated OVCAR-3 cells. On the other hand, the Gal-3 knockdown with Gal-3-specific siRNA transfection aggravated cisplatin-induced apoptosis in OVCAR-3 cells. In conclusion, Galectin-3 reduces the sensitivity of ovarian cancer cells to cisplatin via regulating cisplatin-induced mitochondrial dysfunction. Galectin-3 knockdown inhibits the chemo-resistance of EOC cells. It implies that Galectin-3 might be a potential target to overcome the chemo-resistance in EOC cells.
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PMID:Galectin-3 regulates chemotherapy sensitivity in epithelial ovarian carcinoma via regulating mitochondrial function. 3062 79

Ovarian cancer (OC) is one of the most common gynaecologic malignancies. Deleted in malignant brain tumors 1 (DMBT1) was considered as a tumour suppressor in multiple cancers, but there have been no systemic profiling studies of DMBT1 in OC until now. The aim of this study is to explore the role and the potential mechanism of DMBT1 in OC. mRNA levels and protein expressions of corresponding genes were detected by quantitative real-time polymerase chain reaction and western blot. Cell proliferation was detected by CCK-8 assay and cell colony formation. Cell migration and invasion were detected by wound healing and transwell assay. The combination between DMBT1 and galectin-3 was demonstrated by immunoprecipitation. We demonstrated that DMBT1 was downregulated in OC cell lines, especially SKOV3 cells. Overexpression of DMBT1 significantly inhibited cell proliferation, colony formation, migration and invasion, as well as decreased Matrix Metalloproteinase-2 (MMP-2) and MMP-7. DMBT1 caused a reduction of cell viability by treatment with cisplatin. Immunoprecipitation assay revealed a combination between DMBT1 and galectin-3. DMBT1 could decrease the expression of galectin-3 and inhibit the phosphorylation of PI3K and AKT, while overexpression of galectin-3 reversed this effect. In summary, DMBT1 might inhibit the progression of OC and improve the sensitivity of SKOV3 cells to cisplatin through galectin-3/PI3K/AKT pathway, giving a new insight into the role of DMBT1 in OC and enriching the potential strategies for OC treatment. SIGNIFICANCE OF THE STUDY: The present study focus on the role and the potential mechanism of DMBT1 in ovarian cancer (OC). We demonstrated that DMBT1 might inhibit the progression of ovarian by inhibiting cell proliferation, migration and invasion and increased the sensitivity to cisplatin through galectin-3/PI3K/AKT pathway. The findings ensure the interaction relation between DMBT1 and galectin-3 in OC, providing a novel biological marker for OC and enriching the potential strategies for OC treatment.
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PMID:DMBT1 suppresses cell proliferation, migration and invasion in ovarian cancer and enhances sensitivity to cisplatin through galectin-3/PI3k/Akt pathway. 3242 18