2015
DOI: 10.1172/jci77976
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Increased H3K9me3 drives dedifferentiated phenotype via KLF6 repression in liposarcoma

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Cited by 31 publications
(32 citation statements)
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“…Similarly, several previous studies found that WDL had a lower MDM2 /CEP12 ratio than DDL . These findings suggest that increased amplification of the 12q amplicon may also be related to the progression to higher‐grade tumours, although amplification and overexpression of ASK1 , JUN and increased H3K9me3 by silencing KLF6 have been reported to be involved in the progression from ALT/WDL to DDL …”
Section: Discussionsupporting
confidence: 64%
“…Similarly, several previous studies found that WDL had a lower MDM2 /CEP12 ratio than DDL . These findings suggest that increased amplification of the 12q amplicon may also be related to the progression to higher‐grade tumours, although amplification and overexpression of ASK1 , JUN and increased H3K9me3 by silencing KLF6 have been reported to be involved in the progression from ALT/WDL to DDL …”
Section: Discussionsupporting
confidence: 64%
“…3, I and J ). In addition, we analyzed a published microarray dataset of human LPS cell lines ( Keung et al, 2015 ) and found that Notch ligands and target genes were expressed at significantly higher levels in human DDLPS (LPS224a and LPS224b) compared with WDLPS cell lines (LPS247b and LPS029b; Fig. 3 K ).…”
Section: Resultsmentioning
confidence: 99%
“…Another equally important yet largely unknown aspect is the molecular regulation of the initiation, development, and metastasis of LPS. Although several players, including Pten, p53, miR-155, and epigenetic modification, were shown to regulate LPS malignancy ( Zhang et al, 2012 ; Keung et al, 2015 ; Ou et al, 2015 ; Puzio-Kuter et al, 2015 ), it’s unknown whether one single gene mutation event is sufficient to cause the development of malignant LPS in vivo. Certainly, gaining more insights on these aspects is essential to designing specific and effective therapeutic interventions to treat human LPS.…”
Section: Introductionmentioning
confidence: 99%
“…This suggests that the Klf6-related super enhancer can be formed in the posterior and posterior processes of tumor formation in normal cells. Some researchers [Emily et al, 2015] have found evidence of an epigenetic basis for the transition between WDLPS (well differentiated LPS) and DDLPS (dedifferentiated LPS) in Liposarcoma (LPS). They observed elevated H3K9me3 levels in DDLPS tumours and found that increased H3K9me3 may mediate through Klf6 and these increased H3K9me3 sites are associated with super enhancers as the upstream region of Klf6.…”
Section: Discussionmentioning
confidence: 99%