The Transcription Factor Nuclear Factor-kappa B and Cancer

Escárcega, Ricardo O.; Fuentes-Alexandro, Salvador; Garcı́a-Carrasco, Mario; Gatica, Arnaldo; Zamora, A.

doi:10.1016/j.clon.2006.11.013

Cited by 218 publications

(161 citation statements)

References 79 publications

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“…Our results show that NFκB immunoexpression in the carcinoma infiltration can be a marker of an invasive behavior of the neoplastic cells. This is in line with data of other reports introducing the important role of NFκB in the development of cancer [36][37][38][39][40]. In the literature, many researchers confirm a high transcription activity of NFκB in neoplastic cells and a high proportion with positive reaction in advanced tumors tissue (36)(37)(38)(39)(40).…”

Section: Discussionsupporting

confidence: 79%

“…In the literature, many researchers confirm a high transcription activity of NFκB in neoplastic cells and a high proportion with positive reaction in advanced tumors tissue (36)(37)(38)(39)(40). According to recent reports, the activation of NF-κB determined by the different methods used in respective studies, emerge as an independent prognostic marker connected with clinical and pathological characteristic of the various types of neoplasms [36][37][38][39][40].…”

Section: Discussionmentioning

confidence: 99%

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The expression of SOCS1 and TLR4-NFkappaB pathway molecules in neoplastic cells as potential biomarker for the aggressive tumor phenotype in laryngeal carcinoma.

Starska

Forma²,

Lewy-Trenda³

et al. 2010

Folia Histochem Cytobiol.

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Suppressor of cytokine signaling 1 (SOCS1) is the key regulator of cytokine-mediated innate and adaptive immunity. One of the molecular mechanisms of SOCS1 is connected with inhibition of TLR4-NFκB pathway. The relationships among these molecules in laryngeal carcinoma are not exactly known. In this preliminary study we focused on their special activity and role in regulation of development and progression of laryngeal carcinoma. To investigate NFκB (p65 subunit) nuclear and cytoplasmic expression in 45 tumor samples of advanced laryngeal carcinoma IHC staining was performed. To determine the mRNA expression levels of TLR4, IRAK1, TRAF6 and SOCS1 in isolated neoplasm cells and non-cancerous adjacent mucosa epithelial cells RT-PCR was used. The invasiveness of laryngeal carcinomas was evaluated according to tumor front grading, TFG, which included tumor-related features (cytoplasmic differentiation, nuclear polymorphism, number of mitoses) and adjacent stroma-related characteristics of the peripheral edge of tumor infiltration (mode of infiltration, depth of invasion and plasmalymphocytic infiltration). The relationships between pT, pN status, the histological G grade, certain clinicopathological characteristics as well as postoperative observation time and the mRNA expression of the molecules mentioned earlier were investigated. Significant differences of TLR4-NFκB pathway molecules and SOCS1 mRNA expression in laryngeal tumor cells and normal adjacent mucosa cells as well as significant interconnections of TLR4, SOCS1 and NFκB(p65) in isolated tumor cells were obtained. This preliminary study demonstrated that the expression of SOCS1 and TLR4-NFκB pathway molecules had a strong association with the aggressiveness of laryngeal carcinoma. Positive relationships of TRAF6 in tumor margin cells with the histological grade and the mode of tumor invasion as well as the TFG total score were highlighted. Significant positive correlations were found between the TLR4 in tumor central cells and the TFG total score. Negative relationships of SOCS1 in tumor central cells with the histological grade were also noted. Significant positive correlations were found between the cytoplasmic NFκB(p65) and the mode of invasion as well as TFG total score. Our findings confirmed the importance of SOCS1 and TLR4-NFκB pathway molecules as potential biomarkers for assessment of the aggressive tumor phenotype in laryngeal carcinoma.Key words: laryngeal carcinoma, SOCS1 (suppressor of cytokine signaling 1), TLR4 (toll-like receptor 4), IRAK1 (interleukin -1 receptor -associated kinase), TRAF6 (TNF receptor-associated factor 6), NFκB (nuclear factor kappa B, p65 subunit), TFG (tumor front grading)

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Section: Discussionsupporting

confidence: 79%

Section: Discussionmentioning

confidence: 99%

The expression of SOCS1 and TLR4-NFkappaB pathway molecules in neoplastic cells as potential biomarker for the aggressive tumor phenotype in laryngeal carcinoma.

Starska

Forma²,

Lewy-Trenda³

et al. 2010

Folia Histochem Cytobiol.

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“…However, substantial evidence also indicates that NF-κB plays a pivotal role in the onset and development of malignancies. Recent observations have shown that there is a close relationship between NF-κB and hematopoietic malignancies such as leukemia, lymphoma and multiple myeloma (6,7), as aberrant activation of the NF-κB pathway is involved in the pathogenesis of these diseases. Moreover, some studies have suggested that blocking the NF-κB signaling pathway can cause tumor cells to cease proliferation, die, or become more sensitive to the action of antitumor agents (7).…”

Section: Introductionmentioning

confidence: 99%

Scorpion venom component III inhibits cell proliferation by modulating NF-κB activation in human leukemia cells

Song

Zhang

Sun

et al. 2012

Experimental and Therapeutic Medicine

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Abstract. Scorpion venom contains various groups of compounds that exhibit anticancer activity against a variety of malignancies through a poorly understood mechanism. While the aberrant activation of nuclear factor κB (NF-κB) has been linked with hematopoietic malignancies, we hypothesized that scorpion venom mediates its effects by modulating the NF-κB signaling pathway. In the present study, we examined the effects of scorpion venom component III (SVCIII) on the human leukemia cell lines THP-1 and Jurkat and focused on the NF-κB signaling pathway. Our results showed that SVCIII inhibited cell proliferation, caused cell cycle arrest at G1 phase and inhibited the expression of cell cycle regulatory protein cyclin D1 in a dose-dependent manner in THP-1 and Jurkat cells. SVCIII also suppressed the constitutive NF-κB activation through inhibition of the phosphorylation and degradation of IκBα. NF-κB luciferase reporter activity was also inhibited by SVCIII. Our data suggest that SVCIII, a natural compound, may exert its antiproliferative effects by inhibiting the activation of NF-κB and, thus, has potential use in the treatment of hematopoietic malignancies, alone or in combination with other agents.

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“…Moreover, the same authors used an inhibitor of NF-κB and predicted that its combination with 5-FU and CPT-11 may be a more effective treatment option instead of chemotherapy alone for gastric cancer (Camp et al, 2004). Since the discovery that blocking NF-κB can cause tumor cells to stop proliferating, to die, or enhance their sensitivity to the action of anti-tumor agents NF-κB has been widely used as a target for anti-cancer therapy (Escarcega et al, 2007). HIF-1 , one of the components of hypoxia-inducible factor 1 (HIF-1), has been directly implicated in tumorigenesis including angiogenesis, tumor cell proliferation, metastasis, as well as chemo-and radiotherapy response, particularly in gastric cancer ( Liu et al, 2008;Weidemann & Johnson, 2008).…”

Section: Nf-k B Pathwaymentioning

confidence: 99%

Oncogenic Signaling in Gastric Carcinoma

Santos-Silva¹

2011

Gastric Carcinoma - Molecular Aspects and Current Advances

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The Transcription Factor Nuclear Factor-kappa B and Cancer

Cited by 218 publications

References 79 publications

The expression of SOCS1 and TLR4-NFkappaB pathway molecules in neoplastic cells as potential biomarker for the aggressive tumor phenotype in laryngeal carcinoma.

The expression of SOCS1 and TLR4-NFkappaB pathway molecules in neoplastic cells as potential biomarker for the aggressive tumor phenotype in laryngeal carcinoma.

Scorpion venom component III inhibits cell proliferation by modulating NF-κB activation in human leukemia cells

Oncogenic Signaling in Gastric Carcinoma

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