Imbalance between MMP-2, 9 and TIMP-1 promote the invasion and metastasis of renal cell carcinoma via SKP2 signaling pathways

Abstract S-phase kinase-associated protein-2 (Skp2) is overexpressed in human cancers and acted as an oncogenic protein associated with poor prognosis by enhancing tumor metastasis. The present study has demonstrated that Skp2 overexpresses stable transfectants from 786-0 human renal cancer cells. W...
Ausführliche Beschreibung

Gespeichert in:

Autor*in:	Lu, Hongsheng [verfasserIn] Cao, Xuequan Zhang, Hui Sun, Gang Fan, Guangmin Chen, Lili Wang, Siling

Format:	E-Artikel
Sprache:	Englisch

Erschienen:	2014

Schlagwörter:	SKP2 Invasion MMP-2 MMP-9 TIMP-1

Anmerkung:	© International Society of Oncology and BioMarkers (ISOBM) 2014

Übergeordnetes Werk:	Enthalten in: Tumor biology - Amsterdam : IOS Press, 1987, 35(2014), 10 vom: 02. Juli, Seite 9807-9813
Übergeordnetes Werk:	volume:35 ; year:2014 ; number:10 ; day:02 ; month:07 ; pages:9807-9813

Links:	Volltext

DOI / URN:	10.1007/s13277-014-2256-7

Katalog-ID:	SPR031133460

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520			\|a Abstract S-phase kinase-associated protein-2 (Skp2) is overexpressed in human cancers and acted as an oncogenic protein associated with poor prognosis by enhancing tumor metastasis. The present study has demonstrated that Skp2 overexpresses stable transfectants from 786-0 human renal cancer cells. We found that these stable transfectants exhibited increased migratory and invasive abilities. In addition, expression of matrix metalloproteinase-2 (MMP-2) and MMP-9 was upregulated and tissue inhibitor of matrix metalloproteinase-1 (TIMP-1) was downregulated. In contrast, RNA interference-mediated knockdown Skp2 expression suppressed the ability of ACHN cells to migratory and invasive. Skp2 depletion increased P27 and decreased cyclin E activity, and then induced cell cycle arrest in the G0/G1 phase. Skp2 depletion also downregulated MMP-2 and MMP-9, while upregulated the TIMP-1 activity and expression. The results suggest that Skp2 signaling pathways promoted the ability to metastasize, by stimulating cell proliferation and increasing the ratio of MMP-2 and MMP-9/TIMP-1. So, in conclusion, we provide the first evidence that the imbalance of MMP/TIMP, including upregulation of MMP-2 and MMP-9 and downregulation of TIMP-1, is one of the mechanisms by which Skp2 promotes cell invasion.
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allfields	10.1007/s13277-014-2256-7 doi (DE-627)SPR031133460 (SPR)s13277-014-2256-7-e DE-627 ger DE-627 rakwb eng Lu, Hongsheng verfasserin aut Imbalance between MMP-2, 9 and TIMP-1 promote the invasion and metastasis of renal cell carcinoma via SKP2 signaling pathways 2014 Text txt rdacontent Computermedien c rdamedia Online-Ressource cr rdacarrier © International Society of Oncology and BioMarkers (ISOBM) 2014 Abstract S-phase kinase-associated protein-2 (Skp2) is overexpressed in human cancers and acted as an oncogenic protein associated with poor prognosis by enhancing tumor metastasis. The present study has demonstrated that Skp2 overexpresses stable transfectants from 786-0 human renal cancer cells. We found that these stable transfectants exhibited increased migratory and invasive abilities. In addition, expression of matrix metalloproteinase-2 (MMP-2) and MMP-9 was upregulated and tissue inhibitor of matrix metalloproteinase-1 (TIMP-1) was downregulated. In contrast, RNA interference-mediated knockdown Skp2 expression suppressed the ability of ACHN cells to migratory and invasive. Skp2 depletion increased P27 and decreased cyclin E activity, and then induced cell cycle arrest in the G0/G1 phase. Skp2 depletion also downregulated MMP-2 and MMP-9, while upregulated the TIMP-1 activity and expression. The results suggest that Skp2 signaling pathways promoted the ability to metastasize, by stimulating cell proliferation and increasing the ratio of MMP-2 and MMP-9/TIMP-1. So, in conclusion, we provide the first evidence that the imbalance of MMP/TIMP, including upregulation of MMP-2 and MMP-9 and downregulation of TIMP-1, is one of the mechanisms by which Skp2 promotes cell invasion. SKP2 (dpeaa)DE-He213 Invasion (dpeaa)DE-He213 MMP-2 (dpeaa)DE-He213 MMP-9 (dpeaa)DE-He213 TIMP-1 (dpeaa)DE-He213 Cao, Xuequan aut Zhang, Hui aut Sun, Gang aut Fan, Guangmin aut Chen, Lili aut Wang, Siling aut Enthalten in Tumor biology Amsterdam : IOS Press, 1987 35(2014), 10 vom: 02. Juli, Seite 9807-9813 (DE-627)300897855 (DE-600)1483579-4 1423-0380 nnns volume:35 year:2014 number:10 day:02 month:07 pages:9807-9813 https://dx.doi.org/10.1007/s13277-014-2256-7 lizenzpflichtig Volltext GBV_USEFLAG_A SYSFLAG_A GBV_SPRINGER SSG-OLC-PHA GBV_ILN_22 GBV_ILN_31 GBV_ILN_32 GBV_ILN_39 GBV_ILN_63 GBV_ILN_95 GBV_ILN_138 GBV_ILN_150 GBV_ILN_151 GBV_ILN_152 GBV_ILN_187 GBV_ILN_213 GBV_ILN_230 GBV_ILN_285 GBV_ILN_370 GBV_ILN_702 GBV_ILN_2001 GBV_ILN_2003 GBV_ILN_2005 GBV_ILN_2007 GBV_ILN_2009 GBV_ILN_2011 GBV_ILN_2014 GBV_ILN_2015 GBV_ILN_2021 GBV_ILN_2025 GBV_ILN_2026 GBV_ILN_2031 GBV_ILN_2034 GBV_ILN_2037 GBV_ILN_2038 GBV_ILN_2039 GBV_ILN_2044 GBV_ILN_2055 GBV_ILN_2059 GBV_ILN_2064 GBV_ILN_2065 GBV_ILN_2068 GBV_ILN_2070 GBV_ILN_2086 GBV_ILN_2106 GBV_ILN_2108 GBV_ILN_2111 GBV_ILN_2112 GBV_ILN_2113 GBV_ILN_2116 GBV_ILN_2118 GBV_ILN_2119 GBV_ILN_2122 GBV_ILN_2129 GBV_ILN_2143 GBV_ILN_2144 GBV_ILN_2147 GBV_ILN_2148 GBV_ILN_2152 GBV_ILN_2153 GBV_ILN_2188 GBV_ILN_2190 GBV_ILN_2232 GBV_ILN_4012 GBV_ILN_4035 GBV_ILN_4037 GBV_ILN_4112 GBV_ILN_4125 GBV_ILN_4126 GBV_ILN_4242 GBV_ILN_4246 GBV_ILN_4249 GBV_ILN_4251 GBV_ILN_4305 GBV_ILN_4307 GBV_ILN_4313 GBV_ILN_4322 GBV_ILN_4323 GBV_ILN_4324 GBV_ILN_4328 GBV_ILN_4333 GBV_ILN_4338 AR 35 2014 10 02 07 9807-9813
spelling	10.1007/s13277-014-2256-7 doi (DE-627)SPR031133460 (SPR)s13277-014-2256-7-e DE-627 ger DE-627 rakwb eng Lu, Hongsheng verfasserin aut Imbalance between MMP-2, 9 and TIMP-1 promote the invasion and metastasis of renal cell carcinoma via SKP2 signaling pathways 2014 Text txt rdacontent Computermedien c rdamedia Online-Ressource cr rdacarrier © International Society of Oncology and BioMarkers (ISOBM) 2014 Abstract S-phase kinase-associated protein-2 (Skp2) is overexpressed in human cancers and acted as an oncogenic protein associated with poor prognosis by enhancing tumor metastasis. The present study has demonstrated that Skp2 overexpresses stable transfectants from 786-0 human renal cancer cells. We found that these stable transfectants exhibited increased migratory and invasive abilities. In addition, expression of matrix metalloproteinase-2 (MMP-2) and MMP-9 was upregulated and tissue inhibitor of matrix metalloproteinase-1 (TIMP-1) was downregulated. In contrast, RNA interference-mediated knockdown Skp2 expression suppressed the ability of ACHN cells to migratory and invasive. Skp2 depletion increased P27 and decreased cyclin E activity, and then induced cell cycle arrest in the G0/G1 phase. Skp2 depletion also downregulated MMP-2 and MMP-9, while upregulated the TIMP-1 activity and expression. The results suggest that Skp2 signaling pathways promoted the ability to metastasize, by stimulating cell proliferation and increasing the ratio of MMP-2 and MMP-9/TIMP-1. So, in conclusion, we provide the first evidence that the imbalance of MMP/TIMP, including upregulation of MMP-2 and MMP-9 and downregulation of TIMP-1, is one of the mechanisms by which Skp2 promotes cell invasion. SKP2 (dpeaa)DE-He213 Invasion (dpeaa)DE-He213 MMP-2 (dpeaa)DE-He213 MMP-9 (dpeaa)DE-He213 TIMP-1 (dpeaa)DE-He213 Cao, Xuequan aut Zhang, Hui aut Sun, Gang aut Fan, Guangmin aut Chen, Lili aut Wang, Siling aut Enthalten in Tumor biology Amsterdam : IOS Press, 1987 35(2014), 10 vom: 02. Juli, Seite 9807-9813 (DE-627)300897855 (DE-600)1483579-4 1423-0380 nnns volume:35 year:2014 number:10 day:02 month:07 pages:9807-9813 https://dx.doi.org/10.1007/s13277-014-2256-7 lizenzpflichtig Volltext GBV_USEFLAG_A SYSFLAG_A GBV_SPRINGER SSG-OLC-PHA GBV_ILN_22 GBV_ILN_31 GBV_ILN_32 GBV_ILN_39 GBV_ILN_63 GBV_ILN_95 GBV_ILN_138 GBV_ILN_150 GBV_ILN_151 GBV_ILN_152 GBV_ILN_187 GBV_ILN_213 GBV_ILN_230 GBV_ILN_285 GBV_ILN_370 GBV_ILN_702 GBV_ILN_2001 GBV_ILN_2003 GBV_ILN_2005 GBV_ILN_2007 GBV_ILN_2009 GBV_ILN_2011 GBV_ILN_2014 GBV_ILN_2015 GBV_ILN_2021 GBV_ILN_2025 GBV_ILN_2026 GBV_ILN_2031 GBV_ILN_2034 GBV_ILN_2037 GBV_ILN_2038 GBV_ILN_2039 GBV_ILN_2044 GBV_ILN_2055 GBV_ILN_2059 GBV_ILN_2064 GBV_ILN_2065 GBV_ILN_2068 GBV_ILN_2070 GBV_ILN_2086 GBV_ILN_2106 GBV_ILN_2108 GBV_ILN_2111 GBV_ILN_2112 GBV_ILN_2113 GBV_ILN_2116 GBV_ILN_2118 GBV_ILN_2119 GBV_ILN_2122 GBV_ILN_2129 GBV_ILN_2143 GBV_ILN_2144 GBV_ILN_2147 GBV_ILN_2148 GBV_ILN_2152 GBV_ILN_2153 GBV_ILN_2188 GBV_ILN_2190 GBV_ILN_2232 GBV_ILN_4012 GBV_ILN_4035 GBV_ILN_4037 GBV_ILN_4112 GBV_ILN_4125 GBV_ILN_4126 GBV_ILN_4242 GBV_ILN_4246 GBV_ILN_4249 GBV_ILN_4251 GBV_ILN_4305 GBV_ILN_4307 GBV_ILN_4313 GBV_ILN_4322 GBV_ILN_4323 GBV_ILN_4324 GBV_ILN_4328 GBV_ILN_4333 GBV_ILN_4338 AR 35 2014 10 02 07 9807-9813
allfields_unstemmed	10.1007/s13277-014-2256-7 doi (DE-627)SPR031133460 (SPR)s13277-014-2256-7-e DE-627 ger DE-627 rakwb eng Lu, Hongsheng verfasserin aut Imbalance between MMP-2, 9 and TIMP-1 promote the invasion and metastasis of renal cell carcinoma via SKP2 signaling pathways 2014 Text txt rdacontent Computermedien c rdamedia Online-Ressource cr rdacarrier © International Society of Oncology and BioMarkers (ISOBM) 2014 Abstract S-phase kinase-associated protein-2 (Skp2) is overexpressed in human cancers and acted as an oncogenic protein associated with poor prognosis by enhancing tumor metastasis. The present study has demonstrated that Skp2 overexpresses stable transfectants from 786-0 human renal cancer cells. We found that these stable transfectants exhibited increased migratory and invasive abilities. In addition, expression of matrix metalloproteinase-2 (MMP-2) and MMP-9 was upregulated and tissue inhibitor of matrix metalloproteinase-1 (TIMP-1) was downregulated. In contrast, RNA interference-mediated knockdown Skp2 expression suppressed the ability of ACHN cells to migratory and invasive. Skp2 depletion increased P27 and decreased cyclin E activity, and then induced cell cycle arrest in the G0/G1 phase. Skp2 depletion also downregulated MMP-2 and MMP-9, while upregulated the TIMP-1 activity and expression. The results suggest that Skp2 signaling pathways promoted the ability to metastasize, by stimulating cell proliferation and increasing the ratio of MMP-2 and MMP-9/TIMP-1. So, in conclusion, we provide the first evidence that the imbalance of MMP/TIMP, including upregulation of MMP-2 and MMP-9 and downregulation of TIMP-1, is one of the mechanisms by which Skp2 promotes cell invasion. SKP2 (dpeaa)DE-He213 Invasion (dpeaa)DE-He213 MMP-2 (dpeaa)DE-He213 MMP-9 (dpeaa)DE-He213 TIMP-1 (dpeaa)DE-He213 Cao, Xuequan aut Zhang, Hui aut Sun, Gang aut Fan, Guangmin aut Chen, Lili aut Wang, Siling aut Enthalten in Tumor biology Amsterdam : IOS Press, 1987 35(2014), 10 vom: 02. Juli, Seite 9807-9813 (DE-627)300897855 (DE-600)1483579-4 1423-0380 nnns volume:35 year:2014 number:10 day:02 month:07 pages:9807-9813 https://dx.doi.org/10.1007/s13277-014-2256-7 lizenzpflichtig Volltext GBV_USEFLAG_A SYSFLAG_A GBV_SPRINGER SSG-OLC-PHA GBV_ILN_22 GBV_ILN_31 GBV_ILN_32 GBV_ILN_39 GBV_ILN_63 GBV_ILN_95 GBV_ILN_138 GBV_ILN_150 GBV_ILN_151 GBV_ILN_152 GBV_ILN_187 GBV_ILN_213 GBV_ILN_230 GBV_ILN_285 GBV_ILN_370 GBV_ILN_702 GBV_ILN_2001 GBV_ILN_2003 GBV_ILN_2005 GBV_ILN_2007 GBV_ILN_2009 GBV_ILN_2011 GBV_ILN_2014 GBV_ILN_2015 GBV_ILN_2021 GBV_ILN_2025 GBV_ILN_2026 GBV_ILN_2031 GBV_ILN_2034 GBV_ILN_2037 GBV_ILN_2038 GBV_ILN_2039 GBV_ILN_2044 GBV_ILN_2055 GBV_ILN_2059 GBV_ILN_2064 GBV_ILN_2065 GBV_ILN_2068 GBV_ILN_2070 GBV_ILN_2086 GBV_ILN_2106 GBV_ILN_2108 GBV_ILN_2111 GBV_ILN_2112 GBV_ILN_2113 GBV_ILN_2116 GBV_ILN_2118 GBV_ILN_2119 GBV_ILN_2122 GBV_ILN_2129 GBV_ILN_2143 GBV_ILN_2144 GBV_ILN_2147 GBV_ILN_2148 GBV_ILN_2152 GBV_ILN_2153 GBV_ILN_2188 GBV_ILN_2190 GBV_ILN_2232 GBV_ILN_4012 GBV_ILN_4035 GBV_ILN_4037 GBV_ILN_4112 GBV_ILN_4125 GBV_ILN_4126 GBV_ILN_4242 GBV_ILN_4246 GBV_ILN_4249 GBV_ILN_4251 GBV_ILN_4305 GBV_ILN_4307 GBV_ILN_4313 GBV_ILN_4322 GBV_ILN_4323 GBV_ILN_4324 GBV_ILN_4328 GBV_ILN_4333 GBV_ILN_4338 AR 35 2014 10 02 07 9807-9813
allfieldsGer	10.1007/s13277-014-2256-7 doi (DE-627)SPR031133460 (SPR)s13277-014-2256-7-e DE-627 ger DE-627 rakwb eng Lu, Hongsheng verfasserin aut Imbalance between MMP-2, 9 and TIMP-1 promote the invasion and metastasis of renal cell carcinoma via SKP2 signaling pathways 2014 Text txt rdacontent Computermedien c rdamedia Online-Ressource cr rdacarrier © International Society of Oncology and BioMarkers (ISOBM) 2014 Abstract S-phase kinase-associated protein-2 (Skp2) is overexpressed in human cancers and acted as an oncogenic protein associated with poor prognosis by enhancing tumor metastasis. The present study has demonstrated that Skp2 overexpresses stable transfectants from 786-0 human renal cancer cells. We found that these stable transfectants exhibited increased migratory and invasive abilities. In addition, expression of matrix metalloproteinase-2 (MMP-2) and MMP-9 was upregulated and tissue inhibitor of matrix metalloproteinase-1 (TIMP-1) was downregulated. In contrast, RNA interference-mediated knockdown Skp2 expression suppressed the ability of ACHN cells to migratory and invasive. Skp2 depletion increased P27 and decreased cyclin E activity, and then induced cell cycle arrest in the G0/G1 phase. Skp2 depletion also downregulated MMP-2 and MMP-9, while upregulated the TIMP-1 activity and expression. The results suggest that Skp2 signaling pathways promoted the ability to metastasize, by stimulating cell proliferation and increasing the ratio of MMP-2 and MMP-9/TIMP-1. So, in conclusion, we provide the first evidence that the imbalance of MMP/TIMP, including upregulation of MMP-2 and MMP-9 and downregulation of TIMP-1, is one of the mechanisms by which Skp2 promotes cell invasion. SKP2 (dpeaa)DE-He213 Invasion (dpeaa)DE-He213 MMP-2 (dpeaa)DE-He213 MMP-9 (dpeaa)DE-He213 TIMP-1 (dpeaa)DE-He213 Cao, Xuequan aut Zhang, Hui aut Sun, Gang aut Fan, Guangmin aut Chen, Lili aut Wang, Siling aut Enthalten in Tumor biology Amsterdam : IOS Press, 1987 35(2014), 10 vom: 02. Juli, Seite 9807-9813 (DE-627)300897855 (DE-600)1483579-4 1423-0380 nnns volume:35 year:2014 number:10 day:02 month:07 pages:9807-9813 https://dx.doi.org/10.1007/s13277-014-2256-7 lizenzpflichtig Volltext GBV_USEFLAG_A SYSFLAG_A GBV_SPRINGER SSG-OLC-PHA GBV_ILN_22 GBV_ILN_31 GBV_ILN_32 GBV_ILN_39 GBV_ILN_63 GBV_ILN_95 GBV_ILN_138 GBV_ILN_150 GBV_ILN_151 GBV_ILN_152 GBV_ILN_187 GBV_ILN_213 GBV_ILN_230 GBV_ILN_285 GBV_ILN_370 GBV_ILN_702 GBV_ILN_2001 GBV_ILN_2003 GBV_ILN_2005 GBV_ILN_2007 GBV_ILN_2009 GBV_ILN_2011 GBV_ILN_2014 GBV_ILN_2015 GBV_ILN_2021 GBV_ILN_2025 GBV_ILN_2026 GBV_ILN_2031 GBV_ILN_2034 GBV_ILN_2037 GBV_ILN_2038 GBV_ILN_2039 GBV_ILN_2044 GBV_ILN_2055 GBV_ILN_2059 GBV_ILN_2064 GBV_ILN_2065 GBV_ILN_2068 GBV_ILN_2070 GBV_ILN_2086 GBV_ILN_2106 GBV_ILN_2108 GBV_ILN_2111 GBV_ILN_2112 GBV_ILN_2113 GBV_ILN_2116 GBV_ILN_2118 GBV_ILN_2119 GBV_ILN_2122 GBV_ILN_2129 GBV_ILN_2143 GBV_ILN_2144 GBV_ILN_2147 GBV_ILN_2148 GBV_ILN_2152 GBV_ILN_2153 GBV_ILN_2188 GBV_ILN_2190 GBV_ILN_2232 GBV_ILN_4012 GBV_ILN_4035 GBV_ILN_4037 GBV_ILN_4112 GBV_ILN_4125 GBV_ILN_4126 GBV_ILN_4242 GBV_ILN_4246 GBV_ILN_4249 GBV_ILN_4251 GBV_ILN_4305 GBV_ILN_4307 GBV_ILN_4313 GBV_ILN_4322 GBV_ILN_4323 GBV_ILN_4324 GBV_ILN_4328 GBV_ILN_4333 GBV_ILN_4338 AR 35 2014 10 02 07 9807-9813
allfieldsSound	10.1007/s13277-014-2256-7 doi (DE-627)SPR031133460 (SPR)s13277-014-2256-7-e DE-627 ger DE-627 rakwb eng Lu, Hongsheng verfasserin aut Imbalance between MMP-2, 9 and TIMP-1 promote the invasion and metastasis of renal cell carcinoma via SKP2 signaling pathways 2014 Text txt rdacontent Computermedien c rdamedia Online-Ressource cr rdacarrier © International Society of Oncology and BioMarkers (ISOBM) 2014 Abstract S-phase kinase-associated protein-2 (Skp2) is overexpressed in human cancers and acted as an oncogenic protein associated with poor prognosis by enhancing tumor metastasis. The present study has demonstrated that Skp2 overexpresses stable transfectants from 786-0 human renal cancer cells. We found that these stable transfectants exhibited increased migratory and invasive abilities. In addition, expression of matrix metalloproteinase-2 (MMP-2) and MMP-9 was upregulated and tissue inhibitor of matrix metalloproteinase-1 (TIMP-1) was downregulated. In contrast, RNA interference-mediated knockdown Skp2 expression suppressed the ability of ACHN cells to migratory and invasive. Skp2 depletion increased P27 and decreased cyclin E activity, and then induced cell cycle arrest in the G0/G1 phase. Skp2 depletion also downregulated MMP-2 and MMP-9, while upregulated the TIMP-1 activity and expression. The results suggest that Skp2 signaling pathways promoted the ability to metastasize, by stimulating cell proliferation and increasing the ratio of MMP-2 and MMP-9/TIMP-1. So, in conclusion, we provide the first evidence that the imbalance of MMP/TIMP, including upregulation of MMP-2 and MMP-9 and downregulation of TIMP-1, is one of the mechanisms by which Skp2 promotes cell invasion. SKP2 (dpeaa)DE-He213 Invasion (dpeaa)DE-He213 MMP-2 (dpeaa)DE-He213 MMP-9 (dpeaa)DE-He213 TIMP-1 (dpeaa)DE-He213 Cao, Xuequan aut Zhang, Hui aut Sun, Gang aut Fan, Guangmin aut Chen, Lili aut Wang, Siling aut Enthalten in Tumor biology Amsterdam : IOS Press, 1987 35(2014), 10 vom: 02. Juli, Seite 9807-9813 (DE-627)300897855 (DE-600)1483579-4 1423-0380 nnns volume:35 year:2014 number:10 day:02 month:07 pages:9807-9813 https://dx.doi.org/10.1007/s13277-014-2256-7 lizenzpflichtig Volltext GBV_USEFLAG_A SYSFLAG_A GBV_SPRINGER SSG-OLC-PHA GBV_ILN_22 GBV_ILN_31 GBV_ILN_32 GBV_ILN_39 GBV_ILN_63 GBV_ILN_95 GBV_ILN_138 GBV_ILN_150 GBV_ILN_151 GBV_ILN_152 GBV_ILN_187 GBV_ILN_213 GBV_ILN_230 GBV_ILN_285 GBV_ILN_370 GBV_ILN_702 GBV_ILN_2001 GBV_ILN_2003 GBV_ILN_2005 GBV_ILN_2007 GBV_ILN_2009 GBV_ILN_2011 GBV_ILN_2014 GBV_ILN_2015 GBV_ILN_2021 GBV_ILN_2025 GBV_ILN_2026 GBV_ILN_2031 GBV_ILN_2034 GBV_ILN_2037 GBV_ILN_2038 GBV_ILN_2039 GBV_ILN_2044 GBV_ILN_2055 GBV_ILN_2059 GBV_ILN_2064 GBV_ILN_2065 GBV_ILN_2068 GBV_ILN_2070 GBV_ILN_2086 GBV_ILN_2106 GBV_ILN_2108 GBV_ILN_2111 GBV_ILN_2112 GBV_ILN_2113 GBV_ILN_2116 GBV_ILN_2118 GBV_ILN_2119 GBV_ILN_2122 GBV_ILN_2129 GBV_ILN_2143 GBV_ILN_2144 GBV_ILN_2147 GBV_ILN_2148 GBV_ILN_2152 GBV_ILN_2153 GBV_ILN_2188 GBV_ILN_2190 GBV_ILN_2232 GBV_ILN_4012 GBV_ILN_4035 GBV_ILN_4037 GBV_ILN_4112 GBV_ILN_4125 GBV_ILN_4126 GBV_ILN_4242 GBV_ILN_4246 GBV_ILN_4249 GBV_ILN_4251 GBV_ILN_4305 GBV_ILN_4307 GBV_ILN_4313 GBV_ILN_4322 GBV_ILN_4323 GBV_ILN_4324 GBV_ILN_4328 GBV_ILN_4333 GBV_ILN_4338 AR 35 2014 10 02 07 9807-9813
language	English
source	Enthalten in Tumor biology 35(2014), 10 vom: 02. Juli, Seite 9807-9813 volume:35 year:2014 number:10 day:02 month:07 pages:9807-9813
sourceStr	Enthalten in Tumor biology 35(2014), 10 vom: 02. Juli, Seite 9807-9813 volume:35 year:2014 number:10 day:02 month:07 pages:9807-9813
format_phy_str_mv	Article
institution	findex.gbv.de
topic_facet	SKP2 Invasion MMP-2 MMP-9 TIMP-1
isfreeaccess_bool	false
container_title	Tumor biology
authorswithroles_txt_mv	Lu, Hongsheng @@aut@@ Cao, Xuequan @@aut@@ Zhang, Hui @@aut@@ Sun, Gang @@aut@@ Fan, Guangmin @@aut@@ Chen, Lili @@aut@@ Wang, Siling @@aut@@
publishDateDaySort_date	2014-07-02T00:00:00Z
hierarchy_top_id	300897855
id	SPR031133460
language_de	englisch
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author	Lu, Hongsheng
spellingShingle	Lu, Hongsheng misc SKP2 misc Invasion misc MMP-2 misc MMP-9 misc TIMP-1 Imbalance between MMP-2, 9 and TIMP-1 promote the invasion and metastasis of renal cell carcinoma via SKP2 signaling pathways
authorStr	Lu, Hongsheng
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topic_title	Imbalance between MMP-2, 9 and TIMP-1 promote the invasion and metastasis of renal cell carcinoma via SKP2 signaling pathways SKP2 (dpeaa)DE-He213 Invasion (dpeaa)DE-He213 MMP-2 (dpeaa)DE-He213 MMP-9 (dpeaa)DE-He213 TIMP-1 (dpeaa)DE-He213
topic	misc SKP2 misc Invasion misc MMP-2 misc MMP-9 misc TIMP-1
topic_unstemmed	misc SKP2 misc Invasion misc MMP-2 misc MMP-9 misc TIMP-1
topic_browse	misc SKP2 misc Invasion misc MMP-2 misc MMP-9 misc TIMP-1
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title	Imbalance between MMP-2, 9 and TIMP-1 promote the invasion and metastasis of renal cell carcinoma via SKP2 signaling pathways
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title_full	Imbalance between MMP-2, 9 and TIMP-1 promote the invasion and metastasis of renal cell carcinoma via SKP2 signaling pathways
author_sort	Lu, Hongsheng
journal	Tumor biology
journalStr	Tumor biology
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author_browse	Lu, Hongsheng Cao, Xuequan Zhang, Hui Sun, Gang Fan, Guangmin Chen, Lili Wang, Siling
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author-letter	Lu, Hongsheng
doi_str_mv	10.1007/s13277-014-2256-7
title_sort	imbalance between mmp-2, 9 and timp-1 promote the invasion and metastasis of renal cell carcinoma via skp2 signaling pathways
title_auth	Imbalance between MMP-2, 9 and TIMP-1 promote the invasion and metastasis of renal cell carcinoma via SKP2 signaling pathways
abstract	Abstract S-phase kinase-associated protein-2 (Skp2) is overexpressed in human cancers and acted as an oncogenic protein associated with poor prognosis by enhancing tumor metastasis. The present study has demonstrated that Skp2 overexpresses stable transfectants from 786-0 human renal cancer cells. We found that these stable transfectants exhibited increased migratory and invasive abilities. In addition, expression of matrix metalloproteinase-2 (MMP-2) and MMP-9 was upregulated and tissue inhibitor of matrix metalloproteinase-1 (TIMP-1) was downregulated. In contrast, RNA interference-mediated knockdown Skp2 expression suppressed the ability of ACHN cells to migratory and invasive. Skp2 depletion increased P27 and decreased cyclin E activity, and then induced cell cycle arrest in the G0/G1 phase. Skp2 depletion also downregulated MMP-2 and MMP-9, while upregulated the TIMP-1 activity and expression. The results suggest that Skp2 signaling pathways promoted the ability to metastasize, by stimulating cell proliferation and increasing the ratio of MMP-2 and MMP-9/TIMP-1. So, in conclusion, we provide the first evidence that the imbalance of MMP/TIMP, including upregulation of MMP-2 and MMP-9 and downregulation of TIMP-1, is one of the mechanisms by which Skp2 promotes cell invasion. © International Society of Oncology and BioMarkers (ISOBM) 2014
abstractGer	Abstract S-phase kinase-associated protein-2 (Skp2) is overexpressed in human cancers and acted as an oncogenic protein associated with poor prognosis by enhancing tumor metastasis. The present study has demonstrated that Skp2 overexpresses stable transfectants from 786-0 human renal cancer cells. We found that these stable transfectants exhibited increased migratory and invasive abilities. In addition, expression of matrix metalloproteinase-2 (MMP-2) and MMP-9 was upregulated and tissue inhibitor of matrix metalloproteinase-1 (TIMP-1) was downregulated. In contrast, RNA interference-mediated knockdown Skp2 expression suppressed the ability of ACHN cells to migratory and invasive. Skp2 depletion increased P27 and decreased cyclin E activity, and then induced cell cycle arrest in the G0/G1 phase. Skp2 depletion also downregulated MMP-2 and MMP-9, while upregulated the TIMP-1 activity and expression. The results suggest that Skp2 signaling pathways promoted the ability to metastasize, by stimulating cell proliferation and increasing the ratio of MMP-2 and MMP-9/TIMP-1. So, in conclusion, we provide the first evidence that the imbalance of MMP/TIMP, including upregulation of MMP-2 and MMP-9 and downregulation of TIMP-1, is one of the mechanisms by which Skp2 promotes cell invasion. © International Society of Oncology and BioMarkers (ISOBM) 2014
abstract_unstemmed	Abstract S-phase kinase-associated protein-2 (Skp2) is overexpressed in human cancers and acted as an oncogenic protein associated with poor prognosis by enhancing tumor metastasis. The present study has demonstrated that Skp2 overexpresses stable transfectants from 786-0 human renal cancer cells. We found that these stable transfectants exhibited increased migratory and invasive abilities. In addition, expression of matrix metalloproteinase-2 (MMP-2) and MMP-9 was upregulated and tissue inhibitor of matrix metalloproteinase-1 (TIMP-1) was downregulated. In contrast, RNA interference-mediated knockdown Skp2 expression suppressed the ability of ACHN cells to migratory and invasive. Skp2 depletion increased P27 and decreased cyclin E activity, and then induced cell cycle arrest in the G0/G1 phase. Skp2 depletion also downregulated MMP-2 and MMP-9, while upregulated the TIMP-1 activity and expression. The results suggest that Skp2 signaling pathways promoted the ability to metastasize, by stimulating cell proliferation and increasing the ratio of MMP-2 and MMP-9/TIMP-1. So, in conclusion, we provide the first evidence that the imbalance of MMP/TIMP, including upregulation of MMP-2 and MMP-9 and downregulation of TIMP-1, is one of the mechanisms by which Skp2 promotes cell invasion. © International Society of Oncology and BioMarkers (ISOBM) 2014
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title_short	Imbalance between MMP-2, 9 and TIMP-1 promote the invasion and metastasis of renal cell carcinoma via SKP2 signaling pathways
url	https://dx.doi.org/10.1007/s13277-014-2256-7
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author2	Cao, Xuequan Zhang, Hui Sun, Gang Fan, Guangmin Chen, Lili Wang, Siling
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Imbalance between MMP-2, 9 and TIMP-1 promote the invasion and metastasis of renal cell carcinoma via SKP2 signaling pathways

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