We are analyzing https://link.springer.com/article/10.1007/s13277-014-1651-4.

Title:
Hypoxia and hypoxia-inducible factor 1 repress SEMA4B expression to promote non-small cell lung cancer invasion | Tumor Biology
Description:
Sema domain of semaphorin 4B (SEMA4B), which is an interacting protein of LNM35, plays an important role in lung cancer invasion. However, the regulation mechanism of this protein is completely unknown. Here, we report that hypoxia and hypoxia mimic reagent could downregulate the expression of SEMA4B in human non-small cell lung cancer (NSCLC) lines. We provide evidences that SEMA4B is a direct target of hypoxia-inducible factor 1 (HIF-1). Silencing the expression of HIF-1α in cancer cells by RNA interference abolished hypoxia-repressed SEMA4B expression. Using luciferase reporter assay, we showed that HIF-1α recognized a hypoxia-responsive element (HRE) of SEMA4B gene, which is required for HIF-1-repressed SEMA4B expression. Moreover, ectopic expression of SEMA4B abolished invasion of hypoxia-induced NSCLC cells. Taken together, these data would shed novel insights on the mechanisms for invasion of hypoxia-induced NSCLC cells.
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Keywords {🔍}

pubmed, article, google, scholar, cancer, cas, lung, cell, hypoxia, shanghai, semab, expression, central, tumor, hypoxiainducible, invasion, biol, cells, privacy, cookies, content, factor, nonsmall, liu, zhang, semaphorin, role, hif, access, transcription, factors, data, publish, research, search, january, jie, regulation, gene, angiogenesis, information, log, journal, biology, repress, jian, nsclc, hifα, discover, metastasis,

Topics {✒️}

month download article/chapter small-cell lung cancer hif-1alpha promotes metastasis regulating immune-mediated diseases o2-regulated prolyl hydroxylation hif-1-repressed sema4b expression hypoxia-induced nsclc cells hypoxia-inducible factor 1 lung cancer invasion sema4b abolished invasion repress e-cadherin hypoxia-inducible factors vhl gene mutation related subjects full article pdf lung cancer cells lung cancer surgery privacy choices/manage cookies exp cell res nat cell biol mol cell biol hypoxia-responsive element gene transcription article jian hypoxia mimic reagent tumor metastasis ovarian carcinoma cells cancer biol ther tumour biol clin transl oncol shanghai chest hospital european economic area semin radiat oncol /arnt/sim domains lysyl oxidases lox front mol neurosci hif-mediated regulation hypoxia attenuates semaphorin 4b conditions privacy policy e-cadherin lung cancer luciferase reporter assay cellular oxygen sensing article log check access instant access sema4b gene accepting optional cookies invasion assay

Schema {🗺️}

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         description:Sema domain of semaphorin 4B (SEMA4B), which is an interacting protein of LNM35, plays an important role in lung cancer invasion. However, the regulation mechanism of this protein is completely unknown. Here, we report that hypoxia and hypoxia mimic reagent could downregulate the expression of SEMA4B in human non-small cell lung cancer (NSCLC) lines. We provide evidences that SEMA4B is a direct target of hypoxia-inducible factor 1 (HIF-1). Silencing the expression of HIF-1α in cancer cells by RNA interference abolished hypoxia-repressed SEMA4B expression. Using luciferase reporter assay, we showed that HIF-1α recognized a hypoxia-responsive element (HRE) of SEMA4B gene, which is required for HIF-1-repressed SEMA4B expression. Moreover, ectopic expression of SEMA4B abolished invasion of hypoxia-induced NSCLC cells. Taken together, these data would shed novel insights on the mechanisms for invasion of hypoxia-induced NSCLC cells.
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            Hypoxia-inducible factor 1
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            Cancer Research
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      headline:Hypoxia and hypoxia-inducible factor 1 repress SEMA4B expression to promote non-small cell lung cancer invasion
      description:Sema domain of semaphorin 4B (SEMA4B), which is an interacting protein of LNM35, plays an important role in lung cancer invasion. However, the regulation mechanism of this protein is completely unknown. Here, we report that hypoxia and hypoxia mimic reagent could downregulate the expression of SEMA4B in human non-small cell lung cancer (NSCLC) lines. We provide evidences that SEMA4B is a direct target of hypoxia-inducible factor 1 (HIF-1). Silencing the expression of HIF-1α in cancer cells by RNA interference abolished hypoxia-repressed SEMA4B expression. Using luciferase reporter assay, we showed that HIF-1α recognized a hypoxia-responsive element (HRE) of SEMA4B gene, which is required for HIF-1-repressed SEMA4B expression. Moreover, ectopic expression of SEMA4B abolished invasion of hypoxia-induced NSCLC cells. Taken together, these data would shed novel insights on the mechanisms for invasion of hypoxia-induced NSCLC cells.
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         Hypoxia-inducible factor 1
         Invasion
         Lung cancer
         Cancer Research
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