Abstract:The proliferation-specific Forkhead box M1 (FoxM1) transcription factor is overexpressed in cancer cells and acts as an important regulator of cancer cell growth and survival. Here, we show the molecular mechanisms by which hypoxia regulate FoxM1 expression in cancer cells. When cells were subjected to hypoxia (1% O2), the mRNA and protein levels of FoxM1 had a significant increase in cancer cells (HepG2, MCF-7, and HeLa). Such increase was due to the direct binding of hypoxia-inducible factor 1 (HIF-1) to the… Show more
“…It has been reported that ROS induced FoxM1 overexpression [11] and ERK/ GLI1 signaling activated FoxM1 expression [19]. In a previous study, we had found that hypoxia induced FoxM1 overexpression through the binding of HIF-1 to the FoxM1 promoter [12]. Our unpublished data also revealed that TNF-a could induce FoxM1 expression through the ROS/HIF-1 pathway.…”
Section: Discussionmentioning
confidence: 72%
“…FoxM1 levels were dramatically decreased in adult tissues, but FoxM1 expression was reactivated by oncogenic signaling pathways and reactive oxygen species, resulting in the malignant progression of numerous cancers [10,11]. We had previously reported that hypoxia induced FoxM1 expression and FoxM1 overexpression accelerated the growth and survival of cancer cells under hypoxic stress [12]. Interestingly, several recent studies reported that FoxM1 was a master regulator of tumor metastasis [13].…”
“…It has been reported that ROS induced FoxM1 overexpression [11] and ERK/ GLI1 signaling activated FoxM1 expression [19]. In a previous study, we had found that hypoxia induced FoxM1 overexpression through the binding of HIF-1 to the FoxM1 promoter [12]. Our unpublished data also revealed that TNF-a could induce FoxM1 expression through the ROS/HIF-1 pathway.…”
Section: Discussionmentioning
confidence: 72%
“…FoxM1 levels were dramatically decreased in adult tissues, but FoxM1 expression was reactivated by oncogenic signaling pathways and reactive oxygen species, resulting in the malignant progression of numerous cancers [10,11]. We had previously reported that hypoxia induced FoxM1 expression and FoxM1 overexpression accelerated the growth and survival of cancer cells under hypoxic stress [12]. Interestingly, several recent studies reported that FoxM1 was a master regulator of tumor metastasis [13].…”
“…More importantly, the cross talks between HIF-1 and p53 (Fels and Koumenis 2005;Obacz et al 2013), HIF-1 and FOXM1 (Xia et al 2009), or even FOXO3a and c-Myc (Ferber et al 2012) added weights to the complex associations among these genes. It might be the complex associations among these genes that caused divergent expression patterns of PRX3 in different cancer types or in the different areas of the same sample, depending on the redox status or/and the contexts of cancer cells.…”
Since most of chemotherapy or radiotherapy for cancers is through ROS increase and apoptotic induction, PRX3 might be involved in the chemotherapeutic resistance of cancers.
“…Levels of mRNA were quantified by one-step real-time RT-PCR in accordance with the SYBR-Green PCR Master Mix manual (Applied Biosystems, Foster City, CA, USA). Primers of HIF1 were 5′-CTAACGTGTT ATCTGTCGCT-3′ and 5′-GGTTTCTGCTGCCTTGT AT-3′, as reported elsewhere [21].…”
Section: Tissue Specimens and Rna Extractionmentioning
HIF1 was identified as an independent prognostic biomarker in osteosarcoma. It can promote osteosarcoma cell invasion by inducing VEGF-A expression, indicating that HIF1 is a potential drug target in osteosarcoma.
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