HIF-1α promotes the migration and invasion of hepatocellular carcinoma cells via the IL-8–NF-κB axis

Feng, Wei; Xue, Ting; Huang, Sanxiong; Shi, Qilin; Tang, Chengwu; Cui, Ge; Yang, Guanghui; Gong, Hui; Guo, Huihui

doi:10.1186/s11658-018-0077-1

Cited by 38 publications

(31 citation statements)

References 40 publications

(32 reference statements)

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“…However, it has not been clarified whether these two pathways are activated by related regulatory mechanisms in HCC. Interestingly, consistent with our previous findings on Nogo‐B, knockdown of HIF‐1 or AP‐1 was also reported to attenuate proliferation, migration, and invasion of HCC cells 53,54 . As most of the angiogenic factors, including VEGF, are induced by a hypoxic TME, we first examined the association between Nogo‐B expression and hypoxic conditions.…”

Section: Discussionsupporting

confidence: 72%

Upregulation of Nogo‐B by hypoxia inducible factor‐1 and activator protein‐1 in hepatocellular carcinoma

et al. 2021

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Nogo‐B is an important regulator of tumor angiogenesis. Expression of Nogo‐B is remarkably upregulated in multiple tumor types, especially hepatocellular carcinoma (HCC). Here, we show the transcriptional regulation mechanisms of Nogo‐B in liver cancer. In response to hypoxia, expression of Nogo‐B significantly increased in HCC tissues and cells. The distal hypoxia‐responsive element in the promoter was essential for transcriptional activation of Nogo‐B under hypoxic conditions, which is the specific site for hypoxia inducible factor‐1α (HIF‐1α) binding. In addition, Nogo‐B expression was associated with c‐Fos expression in HCC tissues. Nogo‐B expression was induced by c‐Fos, yet inhibited by a dominant negative mutant A‐Fos. Deletion and mutation analysis of the predicted activator protein‐1 binding sites revealed that functional element mediated the induction of Nogo‐B promoter activity, which was confirmed by ChIP. These results indicate that HIF‐1α and c‐Fos induce the expression of Nogo‐B depending on tumor microenvironments, such as hypoxia and low levels of nutrients, and play a role in upregulation of Nogo‐B in tumor angiogenesis.

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Section: Discussionsupporting

confidence: 72%

Upregulation of Nogo‐B by hypoxia inducible factor‐1 and activator protein‐1 in hepatocellular carcinoma

et al. 2021

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“…In contrast, in some bladder cancer lines, it is associated with the activation of NF-κB but not AP-1 [ 185 ]. In turn, in hepatocellular carcinoma cells, an increase in the expression of CXCL8 in chronic hypoxia is dependent on the activation of HIF-1 and the effect of this transcription factor on NF-κB [ 186 , 187 ]. In other types of cancer, the effect of HIF-1 may differ—for example, in colon cancer cells, chronic hypoxia increases the expression of CXCL8 via NF-κB [ 188 ].…”

Section: Ligands Of Receptors Cxcr1 and Cxcr2mentioning

confidence: 99%

The Effect of Hypoxia on the Expression of CXC Chemokines and CXC Chemokine Receptors—A Review of Literature

Korbecki

Kojder

Kapczuk

et al. 2021

IJMS

145

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Hypoxia is an integral component of the tumor microenvironment. Either as chronic or cycling hypoxia, it exerts a similar effect on cancer processes by activating hypoxia-inducible factor-1 (HIF-1) and nuclear factor (NF-κB), with cycling hypoxia showing a stronger proinflammatory influence. One of the systems affected by hypoxia is the CXC chemokine system. This paper reviews all available information on hypoxia-induced changes in the expression of all CXC chemokines (CXCL1, CXCL2, CXCL3, CXCL4, CXCL5, CXCL6, CXCL7, CXCL8 (IL-8), CXCL9, CXCL10, CXCL11, CXCL12 (SDF-1), CXCL13, CXCL14, CXCL15, CXCL16, CXCL17) as well as CXC chemokine receptors—CXCR1, CXCR2, CXCR3, CXCR4, CXCR5, CXCR6, CXCR7 and CXCR8. First, we present basic information on the effect of these chemoattractant cytokines on cancer processes. We then discuss the effect of hypoxia-induced changes on CXC chemokine expression on the angiogenesis, lymphangiogenesis and recruitment of various cells to the tumor niche, including myeloid-derived suppressor cells (MDSCs), tumor-associated macrophages (TAMs), tumor-associated neutrophils (TANs), regulatory T cells (Tregs) and tumor-infiltrating lymphocytes (TILs). Finally, the review summarizes data on the use of drugs targeting the CXC chemokine system in cancer therapies.

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“…Tumor hypoxia is one of the main reasons for chemoradiotherapeutic resistance, which affects tumor invasiveness and poor prognosis [162]. HIF1A is a transcription factor with critical functions in the hypoxia response by induction of metastasis and angiogenesis [163][164][165]. It was reported that there was miR-338-3p downregulation in BC tissue and cells.…”

Section: Transcription Factors and Regulatorsmentioning

confidence: 99%

Molecular interactions of miR-338 during tumor progression and metastasis

Moghbeli

2021

Cell Mol Biol Lett

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Background Cancer, as one of the main causes of human deaths, is currently a significant global health challenge. Since the majority of cancer-related deaths are associated with late diagnosis, it is necessary to develop minimally invasive early detection markers to manage and reduce mortality rates. MicroRNAs (miRNAs), as highly conserved non-coding RNAs, target the specific mRNAs which are involved in regulation of various fundamental cellular processes such as cell proliferation, death, and signaling pathways. MiRNAs can also be regulated by long non-coding RNAs (lncRNAs) and circular RNAs (circRNAs). They are highly stable in body fluids and have tumor-specific expression profiles, which suggest their suitability as efficient non-invasive diagnostic and prognostic tumor markers. Aberrant expression of miR-338 has been widely reported in different cancers. It regulates cell proliferation, migration, angiogenesis, and apoptosis in tumor cells. Main body In the present review, we have summarized all miR-338 interactions with other non-coding RNAs (ncRNAs) and associated signaling pathways to clarify the role of miR-338 during tumor progression. Conclusions It was concluded that miR-338 mainly functions as a tumor suppressor in different cancers. There were also significant associations between miR-338 and other ncRNAs in tumor cells. Moreover, miR-338 has a pivotal role during tumor progression using the regulation of WNT, MAPK, and PI3K/AKT signaling pathways. This review highlights miR-338 as a pivotal ncRNA in biology of tumor cells.

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HIF-1α promotes the migration and invasion of hepatocellular carcinoma cells via the IL-8–NF-κB axis

Cited by 38 publications

References 40 publications

Upregulation of Nogo‐B by hypoxia inducible factor‐1 and activator protein‐1 in hepatocellular carcinoma

Upregulation of Nogo‐B by hypoxia inducible factor‐1 and activator protein‐1 in hepatocellular carcinoma

The Effect of Hypoxia on the Expression of CXC Chemokines and CXC Chemokine Receptors—A Review of Literature

Molecular interactions of miR-338 during tumor progression and metastasis

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