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UseCases_ArguminSci_Discourse  

PubMed:22410125 JSONTXT 11 Projects

Annnotations TAB TSV DIC JSON TextAE Lectin_function IAV-Glycan

Id Subject Object Predicate Lexical cue
T1 0-139 DRI_Background denotes Silencing of HSulf-2 expression in MCF10DCIS.com cells attenuate ductal carcinoma in situ progression to invasive ductal carcinoma in vivo.
T2 145-302 DRI_Background denotes DUCTION: Ductal carcinoma in situ (DCIS) of the breast is a heterogeneous group of proliferative cellular lesions that have the potential to become invasive.
T3 303-429 DRI_Background denotes Very little is known about the molecular alterations involved in the progression from DCIS to invasive ductal carcinoma (IDC).
T4 430-636 DRI_Background denotes Heparan endosulfatase (HSulf-2) edits sulfate moieties on heparan sulfate proteoglycans (HSPGs) and has been implicated in modulating heparin binding growth factor signaling, angiogenesis and tumorigenesis.
T5 637-716 DRI_Background denotes However, the role of HSulf-2 in breast cancer progression is poorly understood.
T6 717-935 DRI_Background denotes MCF10DCIS.com cells (referred as MCF10DCIS) express HSulf-2 and form comedo type DCIS and progress to IDC when transplanted in immune-deficient mice and, therefore, is an ideal model to study breast cancer progression.
T7 936-1040 DRI_Approach denotes We evaluated the role of HSulf-2 in progression from DCIS to IDC using mouse fat pad mammary xenografts.
T8 1050-1174 DRI_Background denotes Non-target control (NTC) and HSulf-2 knockdown in MCF10DCIS breast cancer cells were achieved by NTC shRNA and two different
T9 1175-1191 Token_Label.OUTSIDE denotes lentiviral shRNA
T10 1192-1221 DRI_Background denotes against HSulf-2 respectively.
T11 1222-1331 DRI_Background denotes Xenografts were established by injecting NTC and HSulf-2 deficient MCF10DCIS cells in mouse mammary fat pads.
T12 1332-1515 DRI_Background denotes Xenografts were subjected to H&E staining for morphological analysis, TUNEL and Propidium iodide staining (to determine the extent of apoptosis), Western blot analysis and zymography.
T13 1525-1740 DRI_Approach denotes Using a mouse mammary fat pad derived xenograft model, we observed that compared to control treated xenografts, down-regulation of HSulf-2 was associated with significant delays in growth at Week 7 (P-value < 0.05).
T14 1741-1977 DRI_Background denotes Histological examination of the tumors demonstrated substantial differences in comedo necrosis, with marked luminal apoptosis and up-regulation of apoptotic markers Bim, cleaved PARP and cleaved caspase 3 in HSulf-2 depleted xenografts.
T15 1978-2229 DRI_Outcome denotes Furthermore, HSulf-2 depleted xenografts retained the basement membrane integrity with decreased activity and expression of matrix metalloproteinase 9 (MMP-9), an enzyme critical for degradation of extracellular matrix compared to nontargeted control.
T16 2242-2335 DRI_Outcome denotes Our data suggest that HSulf-2 expression may be critical for human breast cancer progression.
T17 2336-2444 DRI_Background denotes Down-regulation of HSulf-2 leads to retention of comedo type DCIS and delays the progression of DCIS to IDC.
T18 2445-2578 DRI_Approach denotes Further studies are necessary to determine if therapeutic targeting of HSulf-2 expression might delay the progression of DCIS to IDC.