CDK11p58 inhibits ERα-positive breast cancer invasion by targeting integrin β3 via the repression of ERα signaling View Full Text


Ontology type: schema:ScholarlyArticle      Open Access: True


Article Info

DATE

2014-08-08

AUTHORS

Yayun Chi, Sheng Huang, Lei Wang, Ruoji Zhou, Lisha Wang, Xiuying Xiao, Dali Li, Ying Cai, Xiaoyan Zhou, Jiong Wu

ABSTRACT

BACKGROUND: CDK11(p58), a Ser/Thr kinase that belongs to the cell division cycle 2-like 1 (CDC2L1) subfamily, is associated with cell cycle progression, tumorigenesis and apoptotic signaling. CDK11(p58) is also involved in the regulation of steroid receptors, such as androgen and estrogen receptors. We previously found that CDK11(p58) was abnormally expressed in prostate cancer. However, its role in breast cancer remains unclear. METHODS: CDK11(p58) expression was evaluated by immunohistochemical staining in a tissue array. A Transwell assay was used to detect invasion and metastasis in breast cancer cells. The TaqMan® Metastasis Gene Expression Assay was used to search for potential downstream factors in the CDK11(p58) signaling pathway. qRT-PCR was used to evaluate mRNA levels, and the dual luciferase array was used to analyze promoter activity. Western blotting was used to detect the protein level. RESULTS: CDK11(p58) expression was negatively correlated with node status (P = 0.012), relapse status (P = 0.002) and metastasis status (P = 0.023). Kaplan-Meier survival curves indicated that the disease-free survival (DFS) was significantly poor in breast cancer patients with low CDK11 expression. Interestingly, using the breast cancer cell lines ZR-75-30 and MDA-MB-231, we found that CDK11(p58) was capable of repressing the migration and invasion of ERα-positive breast cancer cells, but not ERα-negative breast cancer cells, in a kinase-dependent manner. Gene expression assays demonstrated that integrin β3 mRNA was dramatically repressed by CDK11(p58), and luciferase results confirmed that the integrin β3 promoter was inhibited by CDK11(p58) through ERα repression. The expression of integrin β3 was highly related to ERα signaling; ERα overexpression stimulated integrin β3 expression, whereas siRNA-mediated knockdown of ERα attenuated integrin β3 expression. CONCLUSIONS: These data indicate that CDK11(p58) is an anti-metastatic gene in ERα-positive breast cancer and that the regulation of integrin β3 by CDK11(p58) via the repression of ERα signaling may constitute part of a signaling pathway underlying breast cancer invasion. More... »

PAGES

577

Identifiers

URI

http://scigraph.springernature.com/pub.10.1186/1471-2407-14-577

DOI

http://dx.doi.org/10.1186/1471-2407-14-577

DIMENSIONS

https://app.dimensions.ai/details/publication/pub.1041115626

PUBMED

https://www.ncbi.nlm.nih.gov/pubmed/25106495


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32 schema:description BACKGROUND: CDK11(p58), a Ser/Thr kinase that belongs to the cell division cycle 2-like 1 (CDC2L1) subfamily, is associated with cell cycle progression, tumorigenesis and apoptotic signaling. CDK11(p58) is also involved in the regulation of steroid receptors, such as androgen and estrogen receptors. We previously found that CDK11(p58) was abnormally expressed in prostate cancer. However, its role in breast cancer remains unclear. METHODS: CDK11(p58) expression was evaluated by immunohistochemical staining in a tissue array. A Transwell assay was used to detect invasion and metastasis in breast cancer cells. The TaqMan® Metastasis Gene Expression Assay was used to search for potential downstream factors in the CDK11(p58) signaling pathway. qRT-PCR was used to evaluate mRNA levels, and the dual luciferase array was used to analyze promoter activity. Western blotting was used to detect the protein level. RESULTS: CDK11(p58) expression was negatively correlated with node status (P = 0.012), relapse status (P = 0.002) and metastasis status (P = 0.023). Kaplan-Meier survival curves indicated that the disease-free survival (DFS) was significantly poor in breast cancer patients with low CDK11 expression. Interestingly, using the breast cancer cell lines ZR-75-30 and MDA-MB-231, we found that CDK11(p58) was capable of repressing the migration and invasion of ERα-positive breast cancer cells, but not ERα-negative breast cancer cells, in a kinase-dependent manner. Gene expression assays demonstrated that integrin β3 mRNA was dramatically repressed by CDK11(p58), and luciferase results confirmed that the integrin β3 promoter was inhibited by CDK11(p58) through ERα repression. The expression of integrin β3 was highly related to ERα signaling; ERα overexpression stimulated integrin β3 expression, whereas siRNA-mediated knockdown of ERα attenuated integrin β3 expression. CONCLUSIONS: These data indicate that CDK11(p58) is an anti-metastatic gene in ERα-positive breast cancer and that the regulation of integrin β3 by CDK11(p58) via the repression of ERα signaling may constitute part of a signaling pathway underlying breast cancer invasion.
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39 schema:keywords CDK11 expression
40 CDK11p58
41 ERα
42 ERα overexpression
43 ERα repression
44 ERα-negative breast cancer cells
45 ERα-positive breast cancer
46 ERα-positive breast cancer cells
47 ERα-positive breast cancer invasion
48 Kaplan-Meier survival curves
49 MDA-MB-231
50 Metastasis Gene Expression Assay
51 Ser/Thr
52 TaqMan
53 Thr
54 Transwell
55 Western blotting
56 ZR-75
57 activity
58 androgens
59 anti-metastatic gene
60 apoptotic signaling
61 array
62 assays
63 blotting
64 breast cancer
65 breast cancer cell line ZR-75
66 breast cancer cells
67 breast cancer invasion
68 breast cancer patients
69 cancer
70 cancer cell lines ZR-75
71 cancer cells
72 cancer invasion
73 cancer patients
74 cell cycle progression
75 cell division cycle 2
76 cell lines ZR-75
77 cells
78 curves
79 cycle 2
80 cycle progression
81 data
82 disease-free survival
83 division cycle 2
84 downstream factors
85 dual luciferase array
86 estrogen receptor
87 expression
88 expression assays
89 factors
90 gene expression assays
91 genes
92 immunohistochemical staining
93 integrin β3
94 integrin β3 expression
95 integrin β3 mRNA
96 integrin β3 promoter
97 invasion
98 kinase-dependent manner
99 knockdown
100 knockdown of ERα
101 levels
102 lines ZR-75
103 low CDK11 expression
104 luciferase array
105 luciferase results
106 mRNA
107 mRNA levels
108 manner
109 metastasis
110 metastasis status
111 migration
112 node status
113 overexpression
114 part
115 pathway
116 patients
117 potential downstream factors
118 progression
119 promoter
120 promoter activity
121 prostate cancer
122 protein levels
123 qRT-PCR
124 receptors
125 regulation
126 relapse status
127 repression
128 repression of ERα
129 results
130 role
131 siRNA
132 signaling
133 staining
134 status
135 steroid receptors
136 survival
137 survival curves
138 tissue arrays
139 tumorigenesis
140 β3
141 β3 expression
142 β3 mRNA
143 β3 promoter
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