Introduction
The hypoxia-inducible factors (HIF) are
alpha/beta heterodimeric transcription factors of the basic
helix-loop-helix-Per-Arnt-Sim (bHLH-PAS) superfamily and are
chiefly responsible for cellular adaptation to oxygen
deprivation. HIF function relies on the stabilization of the
alpha subunit. When oxygen tension falls, HIF-alpha subunits
translocate to the nucleus and, upon dimerization with HIF-beta,
activate transcription of target genes, including vascular
endothelial growth factor, vascular endothelial growth factor
receptor-1 and -2, and WT-1, which are vital for kidney
development. HIF-beta subunits are stable regardless of oxygen
concentration and constitutively translocate to the nucleus. It
was shown previously that HIF-1beta protein expression is nearly
ubiquitous in newborn kidney and that HIF-1beta dimerizes with
either HIF-1alpha or -2alpha.
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an endogenous hypoxia marker and associated
radioresistance..
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the oxygen-regulated subunit of HIF-1, which
regulates the transcription of genes involved in oxygen
homeostasis in response to hypoxia.
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a key element in allowing cells to adapt and
survive in a hostile hypoxic environment via a variety of
pathways.
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plays a key role in responses to hypoxia and
expression of HIF-1alpha downstream genes leads to both an
adapted metabolism and increased oxygen supply.
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a protein of cellular response to hypoxia.
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a central component of the oxygen sensing
system that coordinates cellular responses to conditions of
decreased oxygen availability.
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regulates vascular endothelial growth factor
(VEGF), the presumed principal mediator of angiogenesis in
malignant gliomas, under normal physiologic conditions.
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an oxygen-dependent transcriptional
activator, plays a major role in tumor angiogenesis and in the
response of tumors to hypoxia, and it is mainly responsible for
the "angiogenic switch".
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a potential endogenous marker of tumor
hypoxia and therapeutic target.
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a transcription factor that is involved in
tumour growth and metastasis by regulating genes involved in
response to hypoxia.
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a transcription factor that plays a
regulatory role in the expression of VEGF.
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HIF-1 complex is composed of two b-HLH
proteins: HIF-1beta that is constitutively expressed, and
HIF-1alpha, that is present only in hypoxic cells.
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Normal Expression
HIF-1alpha immunoreaction was recognized
through nuclear staining of positive cells.
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Normally, HIF-1alpha protein, the dominant
subunit of HIF-1, is accumulated in nuclei when cells are
exposed to hypoxia (1% O2) and rapidly degraded when cells are
re-oxygenated. Here, we found that constitutive nuclear
expression of HIF-1alpha protein was a general phenomenon in
vitro under normoxic conditions in human malignant cells
including those derived from the hematopoietic system, such as
lymphoma and leukemia cells.
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HIF-1alpha expression was liver and blood
specific.
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in normal tissue neither HIF-1alpha nor
HIF-2alpha molecule was detectable except within subsets of bone
marrow macrophages, where HIF-2alpha was strongly expressed.
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expression pattern of HIF1alpha in both
epithelial and mesenchymal structures of the chicken embryo
through the first 7 days of development is reported here.
HIF1alpha transcript is expressed diffusely throughout the
neuroepithelium, limb, mesonephritic and cephalic mesenchyme,
progressively becoming restricted to known proliferative zones
of the central nervous system. Specific, strong expression is
unexpectedly found in the endoderm of Sessel's pouch and in the
ectoderm of both Rathke's pouch and the first branchial arch
before the disappearance of the buccopharyngeal membrane.
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aHIF is widely expressed in normal foetal and
adult human tissues as in tumour tissues. Foetal aHIF expression
level is higher than adult one and high enough to affect the
HIF-1alpha mRNA/aHIF transcripts ratio.
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Abnormal Expresion
Nuclear HIF-1alpha expression in tumor cells
was detected in 57.1% of 144 bladder cancer cases. A trend of
correlation of this expression with poorly differentiated tumors
was observed.
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HIF-1alpha expression in colorectal carcinoma
was significantly higher than in non-neoplasm colorectal mucosa.
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HIF-1alpha was detected only in astrocytic
gliomas grades III and IV, both in the nucleus and in the
cytoplasm.
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Overexpression of HIF-1alpha in gastric
carcinomas may upregulate its downstream gene products leading
to VEGF-mediated angiogenesis, and resulting in a poor prognosis
for patients.
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HIF-1alpha staining was found mainly in the
cytoplasm. The tumours were subdivided into HIF-1alpha(LOW) and
HIF-1alpha(HIGH) on the basis of staining intensity.
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It is concluded that in normal cardiac
fibers, basal expression of HIF-1alpha is not appreciable, but
it steadily increases after ischemia.
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HIF-1alpha is commonly expressed in Malignant
pleural mesothelioma (MPM) but not in normal mesothelium,
consistent with the presence of hypoxia.
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we report that in old rat cerebral cortex
exposed to hypoxia, the accumulation in the cytoplasm of hypoxic
inducible factor 1alpha (HIF-1alpha)--the master regulator of
oxygen homeostasis--concomitant with p66(Shc) activation and
reduced IkBalpha phosphorylation is associated with tissue
apoptosis or necrosis.
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Under hypoxic conditions, HIF-1alpha is
stabilized and enters the nucleus, to form a dimer with
HIF-1beta, where it induces the expression of its target genes.
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HIF-1alpha immunoreactivity, confined to the
nucleoplasm, was present in both tumor and vascular endothelial
cells.
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Thirty-two of the 82 (39%) tumour specimens
showed high levels of HIF-1alpha immunoreactivity in the nuclei
and/or cytoplasm of cancer cells.
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VEGF expression correlated with HIF-1alpha
expression, suggesting that HIF-1alpha may contribute to the
overexpression of VEGF observed in epithelial ovarian cancer.
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immunoreactivity (IR) of HIF-1alpha was
distributed numerously in the nuclei of glomus (type-I) and
other cells since hypoxia for 1 day, but was faint and scattered
in the normoxic CBs.
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Focal adhesion kinase (FAK) and
hypoxia-inducible factor (HIF-1alpha) are both up-regulated in
glioblastoma multiforme (GBMs), particularly in invasive zones.
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HIF-1alpha immunoreactivity was confined to
the nucleoplasm whereas the nucleoli were unconspicuous. The
distribution of HIF-1alpha was evident in the tumours whereas
normal adenohypophysial cells showed no HIF-1alpha staining.
HIF-1alpha expression was detected not only in the tumour cells
but also in endothelial cells lining the blood vessels within
the tumour.
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In the majority of solid tumors examined,
including bladder, brain, breast, colon, ovarian, pancreatic,
prostate, and renal carcinomas, nuclear expression of HIF-1alpha
and -2alpha was observed in varying subsets of the tumor cells.
HIF-2alpha was also strongly expressed by subsets of
tumor-associated macrophages, sometimes in the absence of any
tumor cell expression. Less frequently staining was observed in
other stromal cells within the tumors and in normal tissue
adjacent to tumor margins.
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normal prostates (NP) manifested no
immunoreactivity, whereas prostate adenocarcinoma (Pca) and
benign prostatic glandular hyperplasia (BPH) showed
significantly increased HIF-1alpha protein expression.
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HIF-1alpha was expressed abundantly by
macrophages in most rheumatoid synovia, predominantly close to
the intimal layer but also in the subintimal zone. There was
markedly lower expression of HIF-1alpha in OA synovia, and it
was absent from all of the healthy synovia.
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transplanted islets strongly express
HIF-1alpha in association with beta-cell death and decreased
insulin production until adequate revascularization is
established and (2) early suppression of HIF-1alpha results in
less beta-cell death thereby minimizing early graft failure.
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Expression Alteration
Aluminum toxicity creates hypoxic environment
that promotes the translocation of HIF-1alpha to the nucleus and
stimulates the anaerobic metabolism of D-glucose.
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UV radiation induced HIF-1alpha and VEGF
protein expression in a dose- and time-dependent manner in
cultured human keratinocytes.
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Our results showed that green tea extract and
EGCG significantly inhibited hypoxia- and serum-induced
HIF-1alpha protein accumulation in these cancer cells but had no
effects on HIF-1alpha mRNA expression.
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Hyperbaric oxygen reduced early APAP-induced
hepatocellular injury. APAP poisoning increases HIF-1alpha
protein levels and functional activity. HBO2 increases
HIF-1alpha protein levels and DNA binding without a
corresponding increase in transcriptional activity.
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We demonstrate that noscapine treatment of
human glioma U87MG and T98G cell lines exposed to the hypoxic
mimetic agent, CoCl2, inhibits hypoxia-mediated HIF-1alpha
expression and transcriptional activity as measured by decreased
secretion of VEGF, a HIF-1 target gene.
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HIF-1alpha concentrations increase during
breast carcinogenesis, and are associated with poor prognosis.
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both normal and malignant chondrocytes
increased HIF-1alpha protein expression in an oxygen
concentration dependent manner and also increased VEGF mRNA
expression in response to hypoxia.
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HIF-1alpha protein was detectable in wound
cells 1 and 5 days after injury.
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NO does not only modulate the HIF-1 response
under hypoxic conditions, but it also functions as a HIF-1
inducer. We conclude that accumulation of HIF-1 occurs during
hypoxia but also under inflammatory conditions that are
characterized by sustained NO formation.
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significant evaluation in HIF-1alpha
expression was revealed in regenerating rat livers. HIF-1alpha
expression was preceded by VEGF and flt-1 expression and thus
may be related to sinusoidal endothelial reconstruction.
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Function
under hypoxia, hypoxia-inducible factor
1alpha has a significantly prolonged half-life and up-regulates
a number of hypoxia genes.
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HIF-1alpha polymorphisms may have an
important impact on HIF-protein stability and, eventually,
function.
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HIF-1alpha are critical regulators of
endochondral bone development.
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HIF-1alpha alone was associated with a worse
disease-specific survival (DSS) (P =.05) and disease-free
survival (DFS) (P = .03) in multivariate analyses.
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HIF-1alpha upgrades many gene products which
include the glucose transporter protein 1 (Glut-1).
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the use of HIF-1alpha as an indicator of
tumor hypoxia and aggressiveness as well as development of
hypoxia-directed antitumor therapies based on the expression of
HIF-1alpha.
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HIF-1alpha is associated with a worse
prognosis in patients with invasive breast carcinoma.
Furthermore HIF-1alpha immunodetection may be considered as a
potential indicator for selecting patients who could benefit
from specific therapies interfering with HIF-1alpha pathway.
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HIF-1alpha can prompt apoptotic cell death
after experimental traumatic brain injury.
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HIF-1 may be the major hypoxia-inducible
transcription factor in macrophages and that HIF-1-regulated
constructs are likely to be effective in macrophage delivery of
hypoxia-regulated gene therapy to human tumours.
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HIF-1alpha is considered to be a useful
independent prognostic factor in gastric cancer, and the
combination of a HIF-1alpha protein overexpression with
nonfunctional p53 tends to indicate a dismal prognosis.
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HIF-1alpha as regulator of tumor-associated
lymphangiogenesis in human breast cancer and emphasizes the
promising status of HIF-1alpha as a therapeutical target against
tumor progression and metastasis.
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HIF-1alpha may play a role in angiogenesis
and tumor progression via regulation of VEGF in human colorectal
carcinoma.
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Applications
ELISA
We developed and validated an enzyme-linked
immunosorbent assay (ELISA) approach to measure HIF-1alpha
levels in cultured tumor cell lines in vitro.
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HIF-1alpha expression and VEGF secretion in
glioma cell lines under normoxia and hypoxia were examined using
ELISA and Western blot.
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Flow Cytometry (FC)
HIF-1alpha expression following in vitro
hypoxia was measured in U87 MG glioblastoma cells by Western
blot and flow cytometry.
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Gel Shift Assay (Gel)
Expression and function of HIF-1alpha were
assessed by immunofluorescence microscopy, Western blot
analysis, gel shift assays, and luciferase reporter assays.
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Immunofluorescence (IF)
Expression and function of HIF-1alpha were
assessed by immunofluorescence microscopy, Western blot
analysis, gel shift assays, and luciferase reporter assays.
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indirect immunofluorescence and confocal
microscopy were used for subcellular localization of HIF-1alpha
and 2alpha in clear cell renal carcinoma cells.
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Immunocytochemistry (ICC)
regional localization of HIF-1alpha mRNA and
protein was determined by in situ hybridization and
immunocytochemistry in adult male rats exposed to moderate
hypoxia (10% O2) for 1-6 h. HIF-1alpha protein was found in cell
types identified by immunocytochemistry as catecholaminergic
neurons.
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Immunohistochemistry (IHC)
expression of HIF-1alpha was assessed by
immunohistochemistry in 187 patients with T(2-4) N(0-1) breast
cancer enrolled in a randomized trial comparing four cycles of
single agent epirubicin versus epirubicin + tamoxifen as primary
systemic treatment.
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HIF-1alpha expression using
immunohistochemistry and related the results to RCC type and
clinicopathologic variables.
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Sixty-three human astrocytic gliomas were
analyzed by immunohistochemistry for HIF-1alpha and iNOS using
formalin-fixed paraffin-embedded material.
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HIF-1alpha expression in human ischemic
hearts with the ABC-inmunohistochemistry technique and
amplification by biotinylated tyramide.
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The immunohistochemical expression of
HIF-1alpha and VEGF was evaluated in 30 formalin-fixed,
paraffin-embedded postoperative rectal adenocarcinoma tissue
samples.
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Immunohistochemical studies using a
monoclonal antibody specific for HIF-1alpha indicate that the
overexpression of HIF-1alpha occurs in the most common forms of
human cancer, including bladder cancer.
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HIF-1alpha expression was investigated using
immunohistochemical assays on frozen sections, and correlated
with patients' outcome (median follow-up = 13.5 years).
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HIF-1alpha protein expression was determined
by immunohistochemistry in formalin-fixed and paraffin-embedded
specimens obtained from 13 cases of NP, 28 cases of BPH, and 34
cases of Pca.
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We investigated HIF-1alpha expression
immunohistochemically in pancreatic carcinoma tissues and
regional lymph node metastasis.
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HIF-1alpha, CA IX, and GLUT-1 expression was
studied by immunohistochemistry, including double staining for
CA IX and HIF-1alpha.
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Using immunohistochemistry, we have now
analyzed the spatial distribution of HIF-1alpha and its target
genes in normal cartilage and in cartilage from knee joints with
osteoarthritis.
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Accumulation of HIF1alpha and HIF2alpha was
detected immunohistochemically in a series of 46 nodular
malignant melanomas of the skin (epithelioid cell variant),
treated with wide local excision.
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expression of HIF-1alpha and apoptosis in 37
samples of tissues around cerebral bleeding loci and 9 samples
of normal cerebral tissues was assessed by immunohistochemical
straining and terminal deoxynucleotidyl transferase-mediated
dUTP nick end labeling methods.
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Western Blot (WB)
Western blotting studies demonstrate a
significant increase in the expression of PHD-2 ( approximately
1.8-2-fold increase, at 0.5, 16 and 24 h after reoxygenation; p
< 0.01) and HIF-1alpha (approximately 1.7-fold increase
immediately after hypoxia; p < 0.05) proteins following hypoxic
preconditioning relative to normoxic control tissue.
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Using a left inguinal surgical incision, a 1
cm section of ISV was resected from each patient in both groups
as specimens for immunoblotting and immunohistochemical staining
of HIF-1alpha.
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Western blot was used to examine the
expression of HIF-1alpha in prostate cancer cell line (PC-3M)
induced by different oxygen tension.
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Two physiological situations were studied
using HIF-1alpha-specific Western blotting and semiquantitative
RT-PCR.
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Northern and Western blot analysis were used
to assess VEGF and HIF-1alpha expression in the different
culture conditions.
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Western blot analyses indicated that HIF-1alpha rapidly accumulated during the onset of hypoxia and did not fall for 14 days but fell to normal by 21 days despite the continuous low arterial oxygen tension. PMID: 11053346