ANLN-induced EZH2 upregulation promotes pancreatic cancer progression by mediating miR-218-5p/LASP1 signaling axis View Full Text


Ontology type: schema:ScholarlyArticle      Open Access: True


Article Info

DATE

2019-08-08

AUTHORS

Anbin Wang, Haisu Dai, Yi Gong, Chengcheng Zhang, Junjie Shu, Yuandeng Luo, Yan Jiang, Wei Liu, Ping Bie

ABSTRACT

BackgroundPancreatic cancer is a highly lethal malignancy with poor prognosis. Anillin (ANLN), an actin binding protein, is upregulated and plays an important role in many malignant tumors. However, the precise role of ANLN in pancreatic cancer remains unclear.MethodsThe expression of ANLN and its association with pancreatic cancer patient survival were analyzed using an online database and confirmed by immunohistochemistry. The ANLN protein expression in pancreatic cancer cell lines was detected by Western blot. Cell proliferation, colony formation and transwell assays in vitro and in vivo tumor growth were used to determine the role of ANLN in pancreatic cancer. Gene expression microarray analysis and a series of in vitro assays were used to elucidate the mechanisms of ANLN regulating pancreatic cancer progression.ResultsWe found that the ANLN expression was significantly upregulated in pancreatic cancer tissues and cell lines. The high expression of ANLN was associated with tumor size, tumor differentiation, TNM stage, lymph node metastasis, distant metastasis and poor prognosis in pancreatic cancer. ANLN downregulation significantly inhibited cell proliferation, colony formation, migration, invasion and tumorigenicity in nude mice. Meanwhile, we found that ANLN knockdown inhibited several cell-cell adhesion related genes, including the gene encoding LIM and SH3 protein 1 (LASP1). LASP1 upregulation partially reversed the tumor-suppressive effect of ANLN downregulation on pancreatic cancer cell progression. Moreover, we found that ANLN downregulation induced the expression of miR-218-5p which inhibited LASP1 expression through binding to its 3’UTR. We also found that ANLN-induced enhancer of zeste homolog 2 (EZH2) upregulation was involved in regulating miR-218-5p/LASP1 signaling axis. EZH2 upregulation or miR-218-5p downregulation partially reversed the tumor-suppressive effect of ANLN downregulation on pancreatic cancer cell progression.ConclusionANLN contributed to pancreatic cancer progression by regulating EZH2/miR-218-5p/LASP1 signaling axis. These findings suggest that ANLN may be a candidate therapeutic target in pancreatic cancer. More... »

PAGES

347

Identifiers

URI

http://scigraph.springernature.com/pub.10.1186/s13046-019-1340-7

DOI

http://dx.doi.org/10.1186/s13046-019-1340-7

DIMENSIONS

https://app.dimensions.ai/details/publication/pub.1120207387

PUBMED

https://www.ncbi.nlm.nih.gov/pubmed/31395079


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44 schema:description BackgroundPancreatic cancer is a highly lethal malignancy with poor prognosis. Anillin (ANLN), an actin binding protein, is upregulated and plays an important role in many malignant tumors. However, the precise role of ANLN in pancreatic cancer remains unclear.MethodsThe expression of ANLN and its association with pancreatic cancer patient survival were analyzed using an online database and confirmed by immunohistochemistry. The ANLN protein expression in pancreatic cancer cell lines was detected by Western blot. Cell proliferation, colony formation and transwell assays in vitro and in vivo tumor growth were used to determine the role of ANLN in pancreatic cancer. Gene expression microarray analysis and a series of in vitro assays were used to elucidate the mechanisms of ANLN regulating pancreatic cancer progression.ResultsWe found that the ANLN expression was significantly upregulated in pancreatic cancer tissues and cell lines. The high expression of ANLN was associated with tumor size, tumor differentiation, TNM stage, lymph node metastasis, distant metastasis and poor prognosis in pancreatic cancer. ANLN downregulation significantly inhibited cell proliferation, colony formation, migration, invasion and tumorigenicity in nude mice. Meanwhile, we found that ANLN knockdown inhibited several cell-cell adhesion related genes, including the gene encoding LIM and SH3 protein 1 (LASP1). LASP1 upregulation partially reversed the tumor-suppressive effect of ANLN downregulation on pancreatic cancer cell progression. Moreover, we found that ANLN downregulation induced the expression of miR-218-5p which inhibited LASP1 expression through binding to its 3’UTR. We also found that ANLN-induced enhancer of zeste homolog 2 (EZH2) upregulation was involved in regulating miR-218-5p/LASP1 signaling axis. EZH2 upregulation or miR-218-5p downregulation partially reversed the tumor-suppressive effect of ANLN downregulation on pancreatic cancer cell progression.ConclusionANLN contributed to pancreatic cancer progression by regulating EZH2/miR-218-5p/LASP1 signaling axis. These findings suggest that ANLN may be a candidate therapeutic target in pancreatic cancer.
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51 BackgroundPancreatic cancer
52 EZH2 upregulation
53 EZH2/miR
54 LASP1
55 LASP1 expression
56 LIM
57 MethodsThe expression
58 ResultsWe
59 SH3 protein 1
60 TNM stage
61 Western blot
62 actin binding proteins
63 adhesion
64 analysis
65 anillin
66 assays
67 association
68 axis
69 binding protein
70 blot
71 cancer
72 cancer cell lines
73 cancer cell progression
74 cancer patient survival
75 cancer progression
76 cancer tissues
77 candidate therapeutic target
78 cell lines
79 cell progression
80 cell proliferation
81 cell-cell adhesion
82 colony formation
83 database
84 differentiation
85 distant metastasis
86 downregulation
87 effect
88 enhancer
89 expression
90 expression microarray analysis
91 findings
92 formation
93 gene expression microarray analysis
94 genes
95 growth
96 high expression
97 immunohistochemistry
98 important role
99 invasion
100 knockdown
101 lethal malignancy
102 lines
103 lymph node metastasis
104 malignancy
105 malignant tumors
106 mechanism
107 metastasis
108 miR
109 mice
110 microarray analysis
111 migration
112 node metastasis
113 nude mice
114 online databases
115 pancreatic cancer
116 pancreatic cancer cell lines
117 pancreatic cancer cell progression
118 pancreatic cancer patient survival
119 pancreatic cancer progression
120 pancreatic cancer tissues
121 patient survival
122 poor prognosis
123 precise role
124 prognosis
125 progression
126 proliferation
127 protein
128 protein 1
129 protein expression
130 role
131 role of anillin
132 series
133 size
134 stage
135 survival
136 target
137 therapeutic target
138 tissue
139 transwell assays
140 tumor differentiation
141 tumor growth
142 tumor size
143 tumor-suppressive effects
144 tumorigenicity
145 tumors
146 upregulation
147 vitro
148 vivo tumor growth
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