Expression of SDF-1α and nuclear CXCR4 predicts lymph node metastasis in colorectal cancer

Yoshitake, Naoto; Fukui, Hirokazu; Yamagishi, Hidetsugu; Fujii, Shigehiko; Tomita, Shigeki; Ichikawa, Kazuhito; Imura, Johji; Hiraishi, Hideyuki; Fujimori, Takahiro

doi:10.1038/sj.bjc.6604363

Cited by 131 publications

(114 citation statements)

References 29 publications

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“…A second mechanism that links visfatin to increased cancer risk is its role in enhancing cancer cell survival. Specifically, CRC cells express chemokine receptors, CXCR4 and CXCR7, both of which can bind SDF-1 that promotes survival and migration of the cancerous cells [101,102]. Wen-Shih Huang et al [96] demonstrated that increased production of visfatin leads to increased expression of SDF-1.…”

Section: Visfatinmentioning

confidence: 99%

Adipose tissue, obesity and adipokines: role in cancer promotion

Booth

Magnuson

Fouts

et al. 2015

Hormone Molecular Biology and Clinical Investigation

239

235

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Adipose tissue is a complex organ with endocrine, metabolic and immune regulatory roles. Adipose depots have been characterized to release several adipocytokines that work locally in an autocrine and paracrine fashion or peripherally in an endocrine fashion. Adipocyte hypertrophy and excessive adipose tissue accumulation, as occurs during obesity, dysregulates the microenvironment within adipose depots and systemically alters peripheral tissue metabolism. The term "adiposopathy" is used to describe this promotion of pathogenic adipocytes and associated adipose -elated disorders. Numerous epidemiological studies confirm an association between obesity and various cancer forms. Proposed mechanisms that link obesity/adiposity to high cancer risk and mortality include, but are not limited to, obesity-related insulin resistance, hyperinsulinemia, sustained hyperglycemia, glucose intolerance, oxidative stress, inflammation and/or adipocktokine production. Several epidemiological studies have demonstrated a relationship between specific circulating adipocytokines and cancer risk. The aim of this review is to define the function, in normal weight and obesity states, of wellcharacterized and novel adipokines including leptin, adiponectin, apelin, visfatin, resistin, chemerin, omentin, nesfatin and vaspin and summarize the data that relates their dysfunction, whether associated or direct effects, to specific cancer outcomes. Overall research suggests most adipokines promote cancer cell progression via enhancement of cell proliferation and migration, inflammation and anti-apoptosis pathways, which subsequently can prompt cancer metastasis. Further research and longitudinal studies are needed to define the specific independent and additive roles of adipokines in cancer progression and reoccurrence.

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Section: Visfatinmentioning

confidence: 99%

Adipose tissue, obesity and adipokines: role in cancer promotion

Booth

Magnuson

Fouts

et al. 2015

Hormone Molecular Biology and Clinical Investigation

239

235

View full text Add to dashboard Cite

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“…SW403 cells were pretreated with or without STAT3-siRNA or 20 mM PD 98059, followed by stimulation with IL-22 (10 ng/ml) for 30 min, and nuclear protein was extracted as previously described. 28 EMSA was carried out with a Gel Shift Assay System (Promega) in accordance with the manufacturer's recommendation. Briefly, the probes were generated by 5 0 -end labeling with [g-32 P]ATP (Amersham Biosciences) and T4 polynucleotide kinase (Promega).…”

Section: Promoter Assaymentioning

confidence: 99%

Involvement of the IL-22/REG Iα axis in ulcerative colitis

Sekikawa

Fukui

Suzuki

et al. 2010

Laboratory Investigation

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The Regenerating gene (REG) Ia protein, a trophic and/or anti-apoptotic factor, is important in the pathophysiology of gastrointestinal inflammation. Interleukin (IL)-22 is a recently identified cytokine that is suggested to have pivotal roles in inflammatory bowel diseases. We therefore investigated the involvement of the IL-22/REG Ia axis and examined the mechanism of regulation of REG Ia expression by IL-22 stimulation in ulcerative colitis (UC) mucosa. Expression of IL-22, IL-22 receptor 1 (IL-22R1), and REG Ia in UC mucosa was analyzed by real-time RT-PCR and immunohistochemistry. The effects of IL-22 on REG Ia protein expression were examined using a small-interfering RNA for STAT3, an MAPK inhibitor or a PI3K inhibitor. The element responsible for IL-22-induced REG Ia promoter activation was determined by a promoter deletion and electrophoretic mobility shift assay. The expression of IL-22 was enhanced in infiltrating inflammatory cells, and that of IL-22R1 and REG Ia was concurrently enhanced in the inflamed epithelium in UC mucosa. The levels of REG Ia and IL-22 mRNA expression were strongly correlated, and the distributions of REG Ia-and IL-22R1-positive epithelial cells were very similar. IL-22 simulation enhanced the expression of REG Ia protein through STAT3 tyrosine phosphorylation in colon cancer cells. The IL-22-responsive element was located between À142 and À134 in the REG Ia promoter region. REG Ia protein may have a pathophysiological role as a biological mediator for immune cell-derived IL-22 in the UC mucosa.

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“…HGF/Met couple is important for the cross-talk between metastasis and microenvironment [2], and its activation by hypoxia might be hypothesized based on data from normal and neoplastic cell types [19,20]. CXCR4 may drive tumor cells to the secondary sites (lymph nodes, bones) where CXCL12 specific ligand is produced [21], but the experimental data on human metastases are still preliminary [22,23]. Moreover, HIF-1α correlates with Met and metastasis in node-negative breast cancer [24,25].…”

mentioning

confidence: 99%

Nuclear co-localization and functional interaction of COX-2 and HIF-1α characterize bone metastasis of human breast carcinoma

Maroni

Matteucci²,

Luzzati³

et al. 2010

Breast Cancer Res Treat

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The aim of the present paper was to identify nuclear co-localization of COX-2 and HIF-1α in human-bone metastasis of breast cancer, index of transcriptionally-activated cells and functional for gene expression. In particular, we verified whether hypoxia exerted a direct role on metastasis-gene expression or through COX-2 signaling, due to the relevance for clinical implications to individuate molecular targets for diagnosis and therapy. The experiments were performed in vitro with two autoregulatory loops triggered a specific array of transcription factors responsible for COX-2 transactivation. The novelty was that HGF and TGF-β1 biological signals were produced by hypoxic metastatic cells and, therefore, the microenvironment seemed to be modified by metastaticcell engraftment in the bone. In agreement, HIF-1α expression in bone-marrow supportive cells occurred in metastasis-bearing animals. Altogether, the data supported the pre-metastatic-niche theory. Our observations might be useful to design therapies against bone metastasis, by affecting the phenotype changes of metastatic cells occurring at the secondary growth site through COX-2-HIF-1 interaction.Keywords bone microenvironment · bone metastasis · breast cancer · COX-2 · HIF-1 3

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Expression of SDF-1α and nuclear CXCR4 predicts lymph node metastasis in colorectal cancer

Cited by 131 publications

References 29 publications

Adipose tissue, obesity and adipokines: role in cancer promotion

Adipose tissue, obesity and adipokines: role in cancer promotion

Involvement of the IL-22/REG Iα axis in ulcerative colitis

Nuclear co-localization and functional interaction of COX-2 and HIF-1α characterize bone metastasis of human breast carcinoma

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