scholarly journals Antitumor effects of metformin are a result of inhibiting nuclear factor kappa B nuclear translocation in esophageal squamous cell carcinoma

2018 ◽  
Vol 109 (4) ◽  
pp. 1066-1074 ◽  
Author(s):  
Nobufumi Sekino ◽  
Masayuki Kano ◽  
Yasunori Matsumoto ◽  
Haruhito Sakata ◽  
Yasunori Akutsu ◽  
...  
Keyword(s):  
Squamous Cell Carcinoma ◽  
Esophageal Squamous Cell Carcinoma ◽  
Cell Carcinoma ◽  
Squamous Cell ◽  
Nuclear Factor Kappa B ◽  
Nuclear Translocation ◽  
Nuclear Factor ◽  
Antitumor Effects ◽  
Nuclear Factor Kappa

scholarly journals The Effect of Neddylation Inhibition on Inflammation-Induced MMP9 Gene Expression in Esophageal Squamous Cell Carcinoma

2021 ◽  
Vol 22 (4) ◽  
pp. 1716
Author(s):  
Anita Hryniewicz-Jankowska ◽  
Jaroslaw Wierzbicki ◽  
Renata Tabola ◽  
Kamilla Stach ◽  
Khalid Sossey-Alaoui ◽  
...  
Keyword(s):  
Squamous Cell Carcinoma ◽  
Cell Migration ◽  
Esophageal Squamous Cell Carcinoma ◽  
Cell Carcinoma ◽  
Squamous Cell ◽  
Nuclear Factor Kappa B ◽  
Nuclear Factor ◽  
Nuclear Factor Kappa ◽  
Tnf Α ◽  
Mmp9 Gene

Inhibition of the protein neddylation process by the small-molecule inhibitor MLN4924 has been recently indicated as a promising direction for cancer treatment. However, the knowledge of all biological consequences of MLN4924 for cancer cells is still incomplete. Here, we report that MLN4924 inhibits tumor necrosis factor-alpha (TNF-α)-induced matrix metalloproteinase 9 (MMP9)-driven cell migration. Using real-time polymerase chain reaction (PCR) and gelatin zymography, we found that MLN4924 inhibited expression and activity of MMP9 at the messenger RNA (mRNA) and protein levels in both resting cells and cells stimulated with TNF-α, and this inhibition was closely related to impaired cell migration. We also revealed that MLN4924, similar to TNF-α, induced phosphorylation of inhibitor of nuclear factor kappa B-alpha (IκB-α). However, contrary to TNF-α, MLN4924 did not induce IκB-α degradation in treated cells. In coimmunoprecipitation experiments, nuclear IκB-α which formed complexes with nuclear factor kappa B p65 subunit (NFκB/p65) was found to be highly phosphorylated at Ser32 in the cells treated with MLN4924, but not in the cells treated with TNF-α alone. Moreover, in the presence of MLN4924, nuclear NFκB/p65 complexes were found to be enriched in c-Jun and cyclin dependent kinase inhibitor 1 A (CDKN1A/p21) proteins. In these cells, NFκB/p65 was unable to bind to the MMP9 gene promoter, which was confirmed by the chromatin immunoprecipitation (ChIP) assay. Taken together, our findings identified MLN4924 as a suppressor of TNF-α-induced MMP9-driven cell migration in esophageal squamous cell carcinoma (ESCC), likely acting by affecting the nuclear ubiquitin–proteasome system that governs NFκB/p65 complex formation and its DNA binding activity in regard to the MMP9 promoter, suggesting that inhibition of neddylation might be a new therapeutic strategy to prevent invasion/metastasis in ESCC patients.

PTK7 regulates radioresistance through nuclear factor-kappa B in esophageal squamous cell carcinoma

Tumor Biology ◽  
2016 ◽  
Vol 37 (10) ◽  
pp. 14217-14224 ◽  
Author(s):  
Misun Park ◽  
Hyeon-joon Yoon ◽  
Moon Chul Kang ◽  
Junhye Kwon ◽  
Hae Won Lee
Keyword(s):  
Squamous Cell Carcinoma ◽  
Esophageal Squamous Cell Carcinoma ◽  
Cell Carcinoma ◽  
Squamous Cell ◽  
Nuclear Factor Kappa B ◽  
Nuclear Factor ◽  
Nuclear Factor Kappa

scholarly journals Nickel Ion Inhibits Nuclear Factor-Kappa B Activity in Human Oral Squamous Cell Carcinoma

PLoS ONE ◽  
2013 ◽  
Vol 8 (7) ◽  
pp. e68257 ◽  
Author(s):  
Takashi Shionome ◽  
Shigeki Endo ◽  
Daisuke Omagari ◽  
Masatake Asano ◽  
Hitoshi Toyoma ◽  
...  
Keyword(s):  
Squamous Cell Carcinoma ◽  
Oral Squamous Cell Carcinoma ◽  
Cell Carcinoma ◽  
Squamous Cell ◽  
Nuclear Factor Kappa B ◽  
Nuclear Factor ◽  
Nickel Ion ◽  
Nuclear Factor Kappa

scholarly journals The therapeutic activity of curcumin through its anti-cancer potential on oral squamous cell carcinoma: A study on Sprague Dawley rat

2019 ◽  
Vol 7 ◽  
pp. 205031211987598 ◽  
Author(s):  
Tantry Maulina ◽  
Indra Hadikrishna ◽  
Andri Hardianto ◽  
Endang Sjamsudin ◽  
Bambang Pontjo ◽  
...  
Keyword(s):  
Squamous Cell Carcinoma ◽  
Oral Squamous Cell Carcinoma ◽  
Cell Carcinoma ◽  
Squamous Cell ◽  
Nuclear Factor Kappa B ◽  
Cyclooxygenase 2 ◽  
Epithelial Dysplasia ◽  
Nuclear Factor ◽  
Nuclear Factor Kappa ◽  
Anti Cancer

Objectives: Being the most common type of oral malignancies, oral squamous cell carcinoma is initiated by epithelial dysplasia, which can be marked by the expression of nuclear factor kappa B and cyclooxygenase 2. Curcumin has been known for its anti-cancer potential. The objective of this study was to evaluate the anti-cancer potential of curcumin on oral squamous cell carcinoma based on the expression of the nuclear factor kappa B and cyclooxygenase 2 during epithelial dysplasia stage. Methods: This experimental study was performed on 35 Sprague Dawley rats at the Veterinary Medicine Faculty, Bogor Agricultural Institute, Indonesia. At the beginning of the experiments, all rats were induced by 100 µg 0.5% 7,12-dimethylbenz(a)anthracene every 2 days for the duration of 28 days. Once epithelial dysplasia stage was reached, all rats were then randomly divided into control group (that did not receive curcumin) or the experimental group (the group that received curcumin for the next 4 weeks). After 4 weeks, the histopathological examination of haematoxylin and eosin and immunohistochemistry examination were conducted. Data were gathered and analyzed by using the Wilcoxon–Mann–Whitney test. Results: The results of the current study revealed that the experimental group showed significantly less nuclear factor kappa B (p < 0.01) and cyclooxygenase 2 (p = 0.03) expressions compared to the control group. Conclusion: The results of the study suggested that curcumin was effective in suppressing nuclear factor kappa B and cyclooxygenase 2 expression in experimentally induced oral squamous cell carcinoma. Future studies investigating curcumin anti-cancer potential in a further stage of oral squamous cell carcinoma, as well as the involvement of other components that might improve curcumin anti-cancer potential, are of importance.

Corilagin Inhibits Esophageal Squamous Cell Carcinoma by Inducing DNA Damage and Down-Regulation of RNF8

2019 ◽  
Vol 19 (8) ◽  
pp. 1021-1028 ◽  
Author(s):  
Fanghua Qiu ◽  
Lifang Liu ◽  
Yu Lin ◽  
Zetian Yang ◽  
Feng Qiu
Keyword(s):  
Cell Proliferation ◽  
Dna Damage ◽  
Squamous Cell Carcinoma ◽  
Esophageal Squamous Cell Carcinoma ◽  
Cell Carcinoma ◽  
Squamous Cell ◽  
Cell Apoptosis ◽  
Cell Counting ◽  
Antitumor Effects

Background:Esophageal squamous cell carcinoma (ESCC), the most prevalent histologic subtype of esophageal cancer, is an aggressive malignancy with poor prognosis and a high incidence in the East. Corilagin, an active component present in Phyllanthus niruri L., has been shown to suppress tumor growth in various cancers. However, the effects of corilagin on ESCC and the mechanisms for its tumor suppressive function remain unknown.Methods:Cell proliferation was measured by Cell Counting Kit-8 assay and colony formation assays. Annexin V/PI double-staining was performed to assess cell apoptosis. Immunofluorescence staining and western blotting were used to evaluate the protein expression. A xenograft mice model was used to assess the in vivo antitumor effects of corilagin alone or in combination with cisplatin.Results:We for the first time showed that corilagin was effectively able to inhibit ESCC cell proliferation and induce cell apoptosis. Additionally, our results validated its antitumor effects in vivo using a xenograft mouse model. Mechanistically, we found that corilagin caused significant DNA damage in ESCC cells. We found that corilagin could significantly attenuate the expression of the E3 ubiquitin ligase RING finger protein 8 (RNF8) through ubiquitin-proteasome pathway, leading to the inability of DNA damage repair response and eventually causing cell apoptosis. Furthermore, we also showed that corilagin substantially enhanced the antitumor effects of chemotherapy drug cisplatin both in vitro and in vivo.Conclusion:Our results not only provided novel and previously unrecognized evidences for corilagin-induced tumor suppression through inducing DNA damage and targeting RNF8 in ESCC, but also highlighted that corilagin might serve as an adjunctive treatment to conventional chemotherapeutic drugs in ESCC patients.

scholarly journals A COX-2 inhibitor enhances the antitumor effects of chemotherapy and radiotherapy for esophageal squamous cell carcinoma

2014 ◽  
Vol 44 (4) ◽  
pp. 1146-1152 ◽  
Author(s):  
GULBOSTAN YUSUP ◽  
YASUNORI AKUTSU ◽  
MURADIL MUTALLIP ◽  
WEI QIN ◽  
XIN HU ◽  
...  
Keyword(s):  
Squamous Cell Carcinoma ◽  
Esophageal Squamous Cell Carcinoma ◽  
Cell Carcinoma ◽  
Squamous Cell ◽  
Antitumor Effects ◽  
Cox 2
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