IL-1? induces stabilization of IL-8 mRNA in malignant breast cancer cellsvia the 3? untranslated region: Involvement of divergent RNA-binding factors HuR, KSRP and TIAR

Suswam, Esther A.; Nabors, L. Burt; Huang, Yuanyuan; Yang, Xiuhua; King, Peter H.

doi:10.1002/ijc.20675

Cited by 97 publications

(88 citation statements)

References 51 publications

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“…TNF-α upregulated CXCL-8 drastically in de novo pathway. In contrast, IL-1ß induces stabilization of CXCL-8 mRNA in malignant breast cancer cells via the 3' untranslated region: involvement of divergent RNA-binding factors HuR, KSRP and TIAR (15). Nitric oxide also upregulated the expression of CXCL-8 by an increase in CXCL-8 gene transcription and mRNA stability in pancreatic cancer (16).…”

Section: Discussionmentioning

confidence: 95%

Induction of interleukin-8 (CXCL-8) by tumor necrosis factor-α and leukemia inhibitory factor in pancreatic carcinoma cells: Impact of CXCL-8 as an autocrine growth factor

Kamohara

Takahashi²,

Ishiko³

et al. 2007

Int J Oncol

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Abstract. Pancreatic carcinoma is one of the most lethal of the gastrointestinal malignant tumors. Chronic inflammation leads to cancer development and progression. Interleukin-8 (CXCL-8) is a CXC chemokine, which plays an important role in neutrophil chemotaxis and activation. We previously reported that CXCL-8 was produced by a variety of human carcinoma cells and tissues, and that CXCL-8 promoted proliferation in pancreatic carcinoma cells (SUIT-2). In the present study, we analyzed whether various cytokines affect cell proliferation by CXCL-8 expression in pancreas carcinoma cells. All examined pancreatic carcinoma cells expressed CXCL-8 and TNFRII mRNA constitutively in RPMI-1640 medium without FBS. TNF-α, LIF, IL-1ß, IL-6, IL-8, or IFN-ß enhanced the expression of CXCL-8 mRNA, but IL-10 did not in Hs-700T cells. Actinomycin D suppressed and cycloheximide augmented CXCL-8 mRNA which was induced by TNF-α or not. The half-life of CXCL-8 mRNA was 36.5 min by TNF-α and 35.2 min by no stimulation. In our previous study, LIF promoted cell growth in Hs-700T cells. LIF induced CXCL-8 mRNA in a dose-and time-dependent manner. Addition of recombinant CXCL-8 did not induce cell growth of Hs-700T. Anti-CXCL-8 IgG significantly suppressed cell growth. CXCL-8 would act as an autocrine growth factor in Hs-700T cells, which expressed CXCL-8 mRNA highly without stimulation. Curcumin (diferuloylmethane), NF-κB inhibitor, suppressed cell proliferation in Hs-700T cells. These results suggest that CXCL-8 plays a pivotal role in progression of pancreatic cancer, and its expression is influenced by inflammatory cytokines in pancreatic tumor microenvironment.

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Section: Discussionmentioning

confidence: 95%

Induction of interleukin-8 (CXCL-8) by tumor necrosis factor-α and leukemia inhibitory factor in pancreatic carcinoma cells: Impact of CXCL-8 as an autocrine growth factor

Kamohara

Takahashi²,

Ishiko³

et al. 2007

Int J Oncol

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“…17 Several previous studies have characterized HuR as a nuclear shuttling protein involved in cytoplasmic export and stabilization of mRNA and have shown in different cell culture models that HuR and COX-2 are causally related in vitro. In addition to COX-2, other mRNAs such as the mRNA of the angiogenic factor VEGF, 18,19 the protein kinase C substrate Marcks 20 and various cytokines 21 are regulated by HuR. These target proteins are products of immediate early genes that are involved in inflammation and stress response.…”

Section: Discussionmentioning

confidence: 99%

Expression of the ELAV-like protein HuR in human colon cancer: association with tumor stage and cyclooxygenase-2

et al. 2006

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There is growing body of evidence that post-translational events contribute-in addition to genetic changes-to the progression of malignant tumors. These post-translational alterations may provide targets for new therapeutic approaches. The ELAV-like protein HuR stabilizes a group of cellular mRNAs which contain AU-rich elements in their 3 0 untranslated region. To investigate a possible contribution of post-translational changes to the progression of colon cancer and to overexpression of COX-2, we studied expression of HuR and COX-2 a cohort of colorectal adenocarcinomas and in colon cancer cell lines. All cell lines showed an expression of HuR mRNA and protein. In tumor tissue of colon carcinomas we observed two different staining patterns of HuR: A nuclear expression in 98% as well as an additional cytoplasmic expression in 53% of cases. COX-2 was expressed in 63% of carcinomas. Cytoplasmic expression of HuR was significantly associated with increased COX-2 expression as well as with high tumor stage. In univariate Kaplan-Meier analysis, grading, tumor stage and nodal status but not HuR or COX-2 expression were prognostic factors for overall survival. Our results suggest that the overexpression of HuR in colon cancer may be part of a regulatory pathway that controls the mRNA stability of cyclooxygenase-2 and provides an interesting example for a contribution of a dysregulation of mRNA stability to the progression of colorectal cancer. Based on our results, further studies are necessary to investigate whether HuR might be a potential target for a molecular tumor therapy.

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“…The list has considerably increased thanks to genomesequencing programs (Bakheet et al 2001). Many RBPs have been described, which selectively recognize these sequences and modulate their translation and/or stability (Ross 1995, Lal et al 2004, including Hu proteins (HuB, HuC, HuD, and HuR), BRF1, TIAR, TIA-1, KSRP, TTP, and AUF1 (Zhang et al 1993, Park-Lee et al 2003, Gherzi et al 2004, Fenger-Gron et al 2005, Lopez de Silanes et al 2005, Suswam et al 2005. Two AREs have been studied most extensively: AUF1, which is related to degradation of target mRNAs and HuR, which promotes stabilization of several transcripts by enhancing their stability, altering their translation, or performing both functions (Loflin et al 1999, Brennan & Steitz 2001.…”

Section: Introductionmentioning

confidence: 99%

The role of AUF1 in thyroid carcinoma progression

Trojanowicz¹,

Brodauf²,

Sekulla³

et al. 2009

Endocrine-Related Cancer

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AUF1/heterogeneous nuclear ribonucleoprotein D is an adenylate-uridylate-rich elements (AREs) -binding protein, which regulates the mRNA stability of many genes related to growth regulation, such as proto-oncogenes, growth factors, cytokines, and cell cycle-regulatory genes. Several studies demonstrated AUF1 involvement in the processes of apoptosis, tumorigenesis, and development by its interactions with ARE-bearing mRNAs. We report here that AUF1 may be involved in thyroid carcinoma progression. Investigations on thyroid tissues revealed that cytoplasmic expression of AUF1 in malignant tissues was increased when compared with benign thyroid tissues. In thyroid carcinoma cell lines, AUF1 was mostly detectable in the nucleus; however, in dividing cells, its increased production was also observed in the cytoplasm. We found AUF1 in complexes with ARE-bearing mRNAs, previously described to be crucial for proliferation and cell cycle of thyroid carcinoma. Total or exon-selective knockdown of AUF1 led to growth inhibition accompanied by induction of cell cycle inhibitors and decreased levels of cell cycle promoters. Our data demonstrate the existence of a complex network between AUF1 and mRNAs encoding proteins related to cell proliferation. AUF1 may control the balance between stabilizing and destabilizing effects, both of which are exerted on cell cycle machinery in thyroid carcinoma. Although we cannot exclude participation of other factors, thyroid carcinoma may recruit cytoplasmic AUF1 to disturb the stability of mRNAs encoding cyclin-dependent kinase inhibitors, leading to uncontrolled growth and progression of tumor cells. Thus, AUF1 may be considered as a new, additional marker for thyroid carcinoma.

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IL-1? induces stabilization of IL-8 mRNA in malignant breast cancer cellsvia the 3? untranslated region: Involvement of divergent RNA-binding factors HuR, KSRP and TIAR

Cited by 97 publications

References 51 publications

Induction of interleukin-8 (CXCL-8) by tumor necrosis factor-α and leukemia inhibitory factor in pancreatic carcinoma cells: Impact of CXCL-8 as an autocrine growth factor

Induction of interleukin-8 (CXCL-8) by tumor necrosis factor-α and leukemia inhibitory factor in pancreatic carcinoma cells: Impact of CXCL-8 as an autocrine growth factor

Expression of the ELAV-like protein HuR in human colon cancer: association with tumor stage and cyclooxygenase-2

The role of AUF1 in thyroid carcinoma progression

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