HIF-1alpha and CA IX, but not VEGF or MMP-9, may have a role in progression of surgically resected non-small cell lung cancer

We conclude that HIF-1alpha overexpression enhances lung cancer cell invasion at least through up-regulating the expression and activities of uPAR, MMP1, and MMP2.

DEC1 downregulates hypoxia-inducible factor 1alpha at both mRNA and protein levels at hypoxia in lung adenocarcinoma cells

HIF-1alpha expression has no correlation with GST-pi expression in hypoxic lung adenocarcinoma cells.

mitochondrial abnormalities that disturb the reactive O(2) species HIF-1alpha-Kv1.5 O(2)-sensing pathway contribute to the pathogenesis of pulmonary arterial hypertension and cancer--REVIEW

Under hypoxic conditions an autocrine loop between VEGF-C/VEGFR-3 and HIF-1 alpha is possible in breast carcinoma and lung carcinoma but not in colorectal carcinoma cell lines.

Glut1 and HIF-1 alpha are highly expressed in non-small cell lung carcinoma, and their expressions are associated with tumor differentiation and clinical stage.

HIF-1alpha and VEGF-C were over-expressed in non-small cell lung cancer.

MTA1 may promote lung carcinogenesis by enhancing HIF-1alpha protein activity.

HIF-1alpha expression was was significantly higher in lung cancer than in normal lung tissues.

These findings show that polymorphisms in the HIF-1alphagene do not confer susceptibility to lung cancer.

Suggest that a HIF-1 alpha/VEGF angiogenic pathway may exist in vivo in small cell lung carcinoma.

A region within the 5'-untranslated region of hypoxia-inducible factor-1alpha mRNA mediates its turnover in lung adenocarcinoma cells.

HIF-1alpha expression is positively correlated with VEGF expression in non-small cell lung cancer.

The data suggest that neither HIF1alpha nor CUL2 mutation may play a central role in HIF1alpha activation in gastric, colorectal, breast, lung and hepatocellular carcinomas, and acute leukemias.

high expression in squamous cell lung carcinoma is associated with a poor survival

functional polymorphisms in the HIF-1alpha gene may have an important impact on lung carcinogenesis, especially in adenocarcinomas, possibly by increasing genomic instability

High Coexpression of HIF1alpha and NOTCH1 is associated with Non-Small-Cell lung Carcinoma.

High HIF-1alpha is associated with angiogenic potential in human small cell lung carcinoma.

inhibition of HIF-1 activity in BrCa cells inhibits primary tumor growth and metastasis of BrCa cells to the lungs by blocking expression of angiopoietin-like 4 (ANGPTL4) and L1 cell adhesion molecule (L1CAM);ANGPTL4 inhibits endothelial cell(EC)-EC interaction; L1CAM increases the adherence of BrCa cells to ECs

Angiogenesis and the expressions of CD82 and HIF-1alpha are related to differentiation, lymph node metastasis and clinical staging in non-small cell lung cancer.

In non-smallcell lung cancer higher odds ratios for lung cancer were observed for individuals with HIF-1a-1772 T/T genotype against CC/CT genotypes, and HIF-1a-1790 A/A genotype against GG/GA genotypes.

High HIF1-alpha is associated with small cell lung cancer.

results suggest that exposure to nicotine could mimic effects of hypoxia to stimulate HIF-1alpha accumulation and activity that might underlie the high metastatic potential of lung cancer

studies identify HIF1alpha as a key protein in regulating transcription of XPA in lung cancer cell lines and primary tumors contributing to cisplatin resistance

HIF1A was expressed in NSCLC in lung tissue from uranium miners but less in small cell lung cancer.

High mRNA expression of HIF1-alpha is associated with non-small-cell lung cancer.

pY654-beta-catenin is a critical co-factor in hypoxia-inducible factor-1alpha signaling and tumor responses to hypoxia.pY654-beta-catenin accumulates and associates with HIF1alpha and Src in human lung adenocarcinomas.

Kaplan-Meier survival analysis demonstrated that HIF-1alpha and HIF-2alpha expressions were related to shortened overall survival in small cell lung cancer

HIF-1alpha up-regulates NDRG1 expression through binding to NDRG1 promoter, leading to proliferation of lung cancer A549 cells.

Studies suggest that hypoxia, HIF-1 alpha, PHD3 and pVHL could be considered as potential therapeutic targets for lung cancer pathogenesis and progression.

Elevations of HIF-1alpha expression are associated with non-small cell lung cancer.

High HIF1A expression is associated with non-small cell lung cancer.

Increase of serum HIF-1alpha is associated with response to therapy in non- small cell lung cancer.

HIF1A expresion was greater in small cell and squamous cell lung cancer than in non-small cell lung cancer and lung adenocarcinoma. HIF1A expression was greater in lung neoplasms than in normal lung tissue.[Review and Meta-Analysis]

downregulation of miR-199a is essential for hypoxia-induced proliferation through derepressing the expression of HIF1a expression and affecting HIF1a mediated glycolytic pathway in non-small cell lung cancer progression.

HIF1A single nucleotide polymorphisms may have a role in prognosis of early stage non-small-cell lung cancer patients after surgery

Studied a new therapeutic alternative in the treatment of multiresistant lung adenocarcinoma via siRNA-specific transfection of six crucial molecules involved in lung carcinogenesis: SFR, E2F1, Survivin, HIF1, HIF2 and STAT3.

significant associations were found between the Hif-1/HIF-1 1790G/A polymorphism and lung cancer, pancreatic cancer and oral squamous cell carcinoma

Results suggest that nerve growth factor (NGF) and hypoxia inducible factor-1alpha (HIF-1alpha) are synergically involved in the angiogenesis of non-small cell lung cancer (NSCLC).

Data show that tumor necrosis factor-alpha (TNF-alpha) increased A549 lung adenocarcinoma cell permeability by repressing vasodilator-stimulated phosphoprotein (VASP) expression through the activation of hypoxia inducible factor 1 alpha subunit (HIF-1alpha).

RBP2 promotes HIF-1alpha-VEGF-induced angiogenesis of non-small cell lung cancer via the Akt pathway.

HIF-1alpha and reactive oxygen species mediate radiation-induced invasiveness through the SDF-1alpha/CXCR4 pathway in non-small cell lung carcinoma cells.

Co-expression of HIF-1a and NBS1 in primary tumors of patients with lung adenocarcinoma correlates with a worse prognosis

expression of HIH-1alpha in non-small cell lung cancer patients was related to Treg cell number and immune status.

HIF-1alpha C1772 TT genotype and CC genotype were associated with lung cancer risk, but the T allele was not. Meta-analysis.

expression changes of E6 and E7 significantly promoted the protein expression of HIF-1alpha, the expression of both protein and mRNA of GLUT1, but had no effect on the expression of HIF-1alpha mRNA in lung cancer cells.

miR-622 overexpression mediated by the transcription factor FOXO3a decreased the invasiveness of lung tumor cells by inhibiting HIF-1alpha via inactivation of ERK signaling.

High HIF1A expression is associated with invasion and metastasis of hypoxic non-small cell lung cancer.

MCU downregulation hampered cell motility and invasiveness and reduced tumor growth, lymph node infiltration, and lung metastasis in triple-negative breast cancer xenografts. In MCU-silenced cells, production of mitochondrial reactive oxygen species (mROS) is blunted and expression of the hypoxia-inducible factor-1alpha (HIF-1alpha) is reduced, suggesting a signaling role for mROS and HIF-1alpha, downstream of mitochon...

HIF-1alpha and VEGF expression was significantly related to liver tumor stage and lymph nodes and lung metastases (P < 0.05). HIF-1alpha expression correlated with VEGF expression in PLC (r = 0.665, P < 0.05).

Results provide evidence that following hyperthermia, the proliferation and angiogenesis potential of residual non-small cell lung carcinoma (NSCLC) and small cell lung carcinoma (SCLC) is induced by HIF-1a. However, HIF-1a expression in NSCLCs is regulated by both the AKT and ERK signaling pathway, but HIF-1a expression in SCLCs is regulated only by the AKT signaling pathway.

both FDG uptake and HIF-2alpha expression may represent a more aggressive phenotype and that HIF-2alpha may play a more important role than HIF-1alpha in the uptake of FDG in lung adenocarcinoma

High expression of HIF1A is associated with lung cancer.

Results showed that HIF-1 induced glycolysis and the expression of CAIX, which affected the chemosensitivity and prognosis of lung cancer patients.

We show that the combination of GLDC and HIF-1alpha expression is an independent prognostic factor in early-stage lung non-small cell cancer

Hypoxia-induced expression of GDH relies on the up-regulation of HIF1alpha but not HIF2alpha. HIF1alpha binds the promoter of GDH and promotes the transcription of GDH gene in lung cancer cells.

HIF-1alpha rs2057482 may be associated with lung cancer susceptibility

Data suggest that HIF-1alpha exhibits aberrant high expression in non-small cell lung cancer tissues, which is involved in cancer progression and metastasis, and indicative of a poor prognosis.

Aldolase A promotes lung cancer metastasis via PHD-mediated stabilization of HIF-1alpha and the subsequent activation of MMP9.

we have provided evidence that HIF-1a expression has significant value in predicting survival of patients with small cell lung cancerand is an independent prognostic factor beyond Eastern Cooperative Oncology Group performance and metastasis status.

the findings of the present study demonstrated that MIF is a key component in lung cancer progression through promoting the Warburg effect, and that the novel MIF/NFkappaB/HIF1alpha axis may prove to be useful for the development of new strategies for treating patients with lung cancer

In poorly differentiated lung neuroendocrine carcinomas, RNASET2 expression may be upregulated as a consequence of the activation of the hypoxia-induced HIF-1alpha pathway, thus behaving as an alarmin-like molecule.

these results indicate that miR-18a-5p increases the radiosensitivity in lung cancer cells and CD133(+) stem-like cells via downregulating ATM and HIF-1alpha expressions. Plasma miR-18a-5p would be an available indicator of radiosensitivity in lung cancer patients.

MiR-182 promotes glucose metabolism by upregulating HIF-1alpha in Non-Small Cell lung cancer cells

IDH2 promotes the Warburg effect and lung cancer cell growth, which is mediated through HIF1alpha activation followed by decreased alpha-KG.

These results suggest that MAC induces autophagy via the AMPK/mTOR signalling pathway and by upregulating HIF-1alpha and BNIP3 protein expression in lung cancer cells

Results found that HIF1A overexpression is correlated with worse prognosis for patients with lung adenocarcinomas.

Study confirmed that HIF-1alpha regulates the expression of NDUFA4L2 and facilitates the survival, proliferation, and migration of non-small cell lung cancer (NSCLC) cell lines in a hypoxic environment that is ubiquitous in tumor tissues. Data found that HIF-1alpha induced by hypoxia regulates the phenotype of NSCLC cell lines under hypoxic conditions through mitochondrial NDUFA4L2.

Study results demonstrated that TNFalpha decreased VASP expression by upregulating the expression of HIF1alpha to inhibit A549 cell proliferation and adhesion. Inhibition of transplanted tumor growth was associated with downregulation of VASP expression in nude mice. Bioinformatics analysis indicated that expression levels of VASP or HIF1alpha lead to differential outcomes of overall survival in lung carcinoma.

Circular RNA circPIP5K1A promotes non-small cell lung cancer proliferation and metastasis through miR-600/HIF-1alpha regulation.

The present results indicate that EZH2 regulates the immunosuppressive molecule PD-L1 expression via HIF-1alpha in non-small cell lung cancer cells.

The SRSF1 and RBM4 constitute an antagonistic mechanism on regulating the splicing profiles of HIF-1alpha gene, which is relevant to the oncogenic signatures of lung cancer cells.

hsa-circ-0000211 promoted lung adenocarcinoma cell migration and invasion by modulating the miR-622/HIF1-alpha network.

EtaIotaF1alpha, EGR1 and SP1 co-regulate the erythropoietin receptor expression under hypoxia: an essential role in the growth of non-small cell lung cancer cells.

Influence of miR-199a on rats with non-small cell lung cancer via regulating the HIF-1alpha/VEGF signaling pathway.

Hypoxia-induced lncRNA-AC020978 promotes proliferation and glycolytic metabolism of non-small cell lung cancer by regulating PKM2/HIF-1alpha axis.

Micheliolide Enhances Radiosensitivities of p53-Deficient Non-Small-Cell lung cancer via Promoting HIF-1alpha Degradation.

This meta-analysis was carried out to assess the connection between HIF-1alpha gene polymorphisms (rs11549467, rs11549465, and rs2057482) and lung cancer risk

Study using Runx3 heterozygous mice hindlimb ischemic model and Lewis lung carcinoma cell allograft model revealed that Runx3 inhibits vasculogenesis via the inhibition of endothelial progenitor cells differentiation and function via the suppression of Hif1alpha activity.

Conditional Ror1 knockout reveals crucial involvement in lung adenocarcinoma development and identifies novel HIF-1alpha regulator.