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HDAC2 inhibits EMT-mediated cancer metastasis by downregulating the long noncoding RNA H19 in colorectal cancer
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HDAC2 inhibits EMT-mediated cancer metastasis by downregulating the long noncoding RNA H19 in colorectal cancer
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Journal Article
HDAC2 inhibits EMT-mediated cancer metastasis by downregulating the long noncoding RNA H19 in colorectal cancer
2020
Overview
Background
Emerging evidence suggests that epithelial mesenchymal transition (EMT) and epigenetic mechanisms promote metastasis
.
Histone deacetylases (HDACs) and noncoding RNAs (ncRNAs) are important epigenetic regulators. Here, we elucidated a novel role of histone deacetylase 2 (
HDAC2
) in regulating EMT and CRC metastasis via ncRNA.
Methods
The expression of HDACs in CRC was analyzed using the public databases and matched primary and metastatic tissues, and CRC cells with different metastatic potentials (DLD1, HCT116, SW480 and SW620). Microarray analysis was used to identify differential genes in parental and
HDAC2
knockout CRC cells. EMT and histone modifications were determined using western blot and immunofluorescence. Migration ability was assessed by transwell assay, and metastasis was assessed in vivo using a tail vain injection. Gene expression and regulation was assessed by RT-PCR, chromatin immunoprecipitation and reporter assays. Protein interaction was assessed by immunoprecipitation. Specific siRNAs targeting
H19
,
SP1
and
MMP14
were used to validate their role in
HDAC2
loss induced EMT and metastasis.
Results
Reduced HDAC2 expression was associated with poor prognosis in CRC patients and found in CRC metastasis.
HDAC2
deletion or knockdown induced EMT and metastasis by upregulating the long noncoding RNA
H19
(
LncRNA H19
). HDAC2 inhibited LncRNA H19 expression by histone H3K27 deacetylation in its promoter via binding with SP1. LncRNA H19 functioned as a
miR-22-3P
sponge to increase the expression of MMP14.
HDAC2
loss strongly promoted CRC lung metastasis, which was suppressed
LncRNA H19
knockdown.
Conclusion
Our study supports HDAC2 as a CRC metastasis suppressor through the inhibition of EMT and the expression of H19 and MMP14.
