Blood.
2007 Apr 1;109(7):3015-23.
Links
Comprehensive analysis of homeobox
genes in Hodgkin lymphoma cell lines identifies dysregulated
expression of HOXB9 mediated via ERK5 signaling and BMI1.
Nagel
S, Burek C, Venturini L, Scherr M, Quentmeier H, Meyer
C, Rosenwald A, Drexler HG, MacLeod
RA.
Human and
Animal Cell Cultures, Deutsche Sammlung von Mikroorganismen und Zellkulturen
(DSMZ), Braunschweig, Germany. sna@dsmz.de
Many members of the nearly
200-strong homeobox gene family have been
implicated in cancer, mostly following ectopic
expression. In this study we analyzed homeobox
gene expression in Hodgkin lymphoma (HL) cell lines. Both reverse
transcription-polymerase chain reaction (RT-PCR) using degenerate primers
and microarray profiling identified consistently
up-regulated HOXB9 expression. Analysis of HOXB9 regulation in HL cells
revealed E2F3A and BMI1 as activator and repressor, respectively.
Furthermore, a constitutively active ERK5 pathway was identified in all HL
cell lines analyzed as well as primary HL cells. Our data show that ERK5
probably mediates HOXB9 expression by repressing BMI1. In addition,
expression analysis of the neighboring microRNA
gene mir-196a1 revealed coregulation with HOXB9.
Functional analysis of HOXB9 by knockdown and overexpression
assays indicated their influence on both proliferation and apoptosis in HL
cells. In summary, we identified up-regulation of HOXB9 in HL mediated by
constitutively active ERK5 signaling which may represent novel therapeutic
targets in HL.
PMID: 17148583 [PubMed
- indexed for MEDLINE]
Zhonghua Wei Chang Wai Ke Za
Zhi. 2007 Jul;10(4):365-7. Links
[Expression of 39 HOX genes in esophageal
cancer cell lines]
[Article in Chinese]
Gu ZD, Chen
XM, Zhang
W, Gu J, Chen
KN.
Department of Thoracic
Surgery, Peking University School of Oncology, Beijing Cancer Hospital,
Beijing Institute for Cancer Research, Beijing 100036, China.
OBJECTIVE: To identify whether
HOX genes can be used as markers of esophageal cancer. METHODS: The
expression of 39 HOX genes in esophageal cancer cell lines was examined.
Specific primers were designed and RT- PCR was performed for each HOX gene
members in above esophageal cancer cell lines, EC109 and CAES. RESULTS:
Fifteen out of 39 HOX genes were expressed in esophageal cancer cell lines.
They were HOXA2, HOXA7, HOXA9, HOXA10, HOXA13, HOXB7, HOXB9, HOXC4, HOXC5,
HOXC6, HOXC8, HOXC9, HOXD9, HOXD10, and HOXD13 respectively. Of them. Eleven genes were overlapped with the ones
detected in human esophageal squamous cell carcinoma(ESCC) in our former study. CONCLUSION: This
study reconfirms our former that some HOX genes are deregulated expressed
in ESCC, which provides more positive evidence for their roles in ESCC.
PMID: 17659465 [PubMed
- in process]
Development. 2004 Jun;131(11):2653-67.
Epub 2004 May 5.
Links
Multiple points of
interaction between retinoic acid and FGF signaling during embryonic axis
formation.
Shiotsugu J, Katsuyama Y, Arima K, Baxter
A, Koide
T, Song
J, Chandraratna RA, Blumberg
B.
Department
of Developmental and Cell Biology, University of California, Irvine, CA 92697-2300, USA.
Anteroposterior
(AP) patterning of the developing CNS is crucial for both regional
specification and the timing of neurogenesis.
Several important factors are involved in AP patterning, including members
of the WNT and FGF growth factor families, retinoic acid receptors, and HOX
genes. We have examined the interactions between FGF and retinoic signaling
pathways. Blockade of FGF signaling downregulates
the expression of members of the RAR signaling pathway, RARalpha,
RALDH2 and CYP26. Overexpression of a
constitutively active RARalpha2 rescues the effects of FGF blockade on the
expression of XCAD3 and HOXB9. This suggests that RARalpha2 is required as
a downstream target of FGF signaling for the posterior expression of XCAD3
and HOXB9. Surprisingly, we found that posterior expression of FGFR1 and
FGFR4 was dependent on the expression of RARalpha2. Anterior expression was
also altered with FGFR1 expression being lost, whereas FGFR4 expression was
expanded beyond its normal expression domain. RARalpha2 is required for the
expression of XCAD3 and HOXB9, and for the ability of XCAD3 to induce HOXB9
expression. We conclude that RARalpha2 is required at multiple points in
the posteriorization pathway, suggesting that
correct AP neural patterning depends on a series of mutually interactive
feedback loops among FGFs, RARs
and HOX genes.
Zhonghua Yi Xue Yi Chuan Xue Za Zhi.
2003 Jun;20(3):193-5. Links
[Transmission disequilibrium test for
congenital dislocation of the hip and HOXB9 gene or COL1AI gene]
[Article in Chinese]
Jiang J, Ma
HW, Lu
Y, Wang
YP, Wang
Y, Li
QW, Ji SJ.
Genetic
Laboratory, the Second Clinical College, China Medical University, Shenyang, Liaoning, 110004 PR China. jj816yy@etang.com
OBJECTIVE: To detect the
correlation between the congenital dislocation of the hip (CDH) and HOXB9
gene or COL1AI gene. METHODS: A microsatellite
DNA marker D17S1820 was chosen in the region of chromosome 17q21 where
exists the HOXB9 gene which regulates the embryonic limb development and exists the COL1AI gene. The genotypes of 303 members in
101 CDH nuclear family trios were analyzed by the techniques of polymerase
chain reaction(PCR) and denaturing polyacrylamide gel electrophoresis. Then transmission
disequilibrium test (TDT) was used to test the data of genotypes. RESULTS:
There exist 12 alleles at this polymorphic locus. Transmission
disequilibrium was found between CDH and the fourth allele of D17S1820
(chi-square=6.025,P=0.014). CONCLUSION: CDH is
associated with the region of chromosome 17q21. HOXB9 gene and/or COL1AI
gene may be susceptibility genes of CDH.
PMID: 12778441 [PubMed
- in process]
Esophageal cancer 
