scholarly journals Epidermal Growth Factor Receptor-targeted 131I-therapy of Liver Cancer Following Systemic Delivery of the Sodium Iodide Symporter Gene

2011 ◽  
Vol 19 (4) ◽  
pp. 676-685 ◽  
Author(s):  
Kathrin Klutz ◽  
David Schaffert ◽  
Michael J Willhauck ◽  
Geoffrey K Grünwald ◽  
Rudolf Haase ◽  
...  
Keyword(s):  
Epidermal Growth Factor Receptor ◽  
Growth Factor ◽  
Epidermal Growth Factor ◽  
Liver Cancer ◽  
Sodium Iodide ◽  
Growth Factor Receptor ◽  
131I Therapy ◽  
Sodium Iodide Symporter ◽  
Systemic Delivery ◽  
Epidermal Growth

SERUM LEVEL OF EPIDERMAL GROWTH FACTOR RECEPTOR AS A BIOMARKER OF LIVER CANCER

Epidemiology ◽  
2004 ◽  
Vol 15 (4) ◽  
pp. S71
Author(s):  
How-Ran Guo ◽  
Tzu-I Sung ◽  
Ying-Jan Wang ◽  
Tsui-Lien Hung ◽  
Chi-Yi Chen
Keyword(s):  
Epidermal Growth Factor Receptor ◽  
Growth Factor ◽  
Epidermal Growth Factor ◽  
Serum Level ◽  
Liver Cancer ◽  
Growth Factor Receptor ◽  
Epidermal Growth

scholarly journals Efficient Epidermal Growth Factor Receptor Targeting Oligonucleotide as a Potential Molecule for Targeted Cancer Therapy

2019 ◽  
Vol 20 (19) ◽  
pp. 4700 ◽  
Author(s):  
Tao Wang ◽  
Svetlana Philippovich ◽  
Jun Mao ◽  
Rakesh N. Veedu
Keyword(s):  
Breast Cancer ◽  
Epidermal Growth Factor Receptor ◽  
Growth Factor ◽  
Epidermal Growth Factor ◽  
Liver Cancer ◽  
Growth Factor Receptor ◽  
Egfr Inhibitors ◽  
Egfr Inhibition ◽  
Wide Range ◽  
Epidermal Growth

Epidermal growth factor receptor (EGFR) is associated with the progression of a wide range of cancers including breast, glioma, lung, and liver cancer. The observation that EGFR inhibition can limit the growth of EGFR positive cancers has led to the development of various EGFR inhibitors including monoclonal antibodies and small-molecule inhibitors. However, the reported toxicity and drug resistance greatly compromised the clinical outcome of such inhibitors. As a type of chemical antibodies, nucleic acid aptamer provides an opportunity to overcome the obstacles faced by current EGFR inhibitors. In this study, we have developed and investigated the therapeutic potential of a 27mer aptamer CL-4RNV616 containing 2′-O-Methyl RNA and DNA nucleotides. Our results showed that CL-4RNV616 not only displayed enhanced stability in human serum, but also effectively recognized and inhibited the proliferation of EGFR positive Huh-7 liver cancer, MDA-MB-231 breast cancer, and U87MG glioblastoma cells, with an IC50 value of 258.9 nM, 413.7 nM, and 567.9 nM, respectively. Furthermore, TUNEL apoptosis assay revealed that CL-4RNV616 efficiently induced apoptosis of cancer cells. In addition, clinical breast cancer biopsy-based immunostaining assay demonstrated that CL-4RNV616 had a comparable detection efficacy for EGFR positive breast cancer with commonly used commercial antibodies. Based on the results, we firmly believe that CL-4RNV616 could be useful in the development of targeted cancer therapeutics and diagnostics.

scholarly journals Epidermal Growth Factor Receptor (EGFR) Crosstalks in Liver Cancer

Cancers ◽  
2011 ◽  
Vol 3 (2) ◽  
pp. 2444-2461 ◽  
Author(s):  
Carmen Berasain ◽  
María Ujue Latasa ◽  
Raquel Urtasun ◽  
Saioa Goñi ◽  
María Elizalde ◽  
...  
Keyword(s):  
Epidermal Growth Factor Receptor ◽  
Growth Factor ◽  
Epidermal Growth Factor ◽  
Liver Cancer ◽  
Growth Factor Receptor ◽  
Epidermal Growth

The Epidermal Growth Factor Receptor: A Link Between Inflammation and Liver Cancer

2009 ◽  
Vol 234 (7) ◽  
pp. 713-725 ◽  
Author(s):  
Carmen Berasain ◽  
Maria J. Perugorria ◽  
Maria Ujue Latasa ◽  
Josefa Castillo ◽  
Saioa Goñi ◽  
...  
Keyword(s):  
Epidermal Growth Factor Receptor ◽  
Growth Factor ◽  
Epidermal Growth Factor ◽  
Liver Cancer ◽  
Growth Factor Receptor ◽  
Epidermal Growth

scholarly journals The Effect of and Mechanism Underlying Autophagy in Hepatocellular Carcinoma Induced by CH12, a Monoclonal Antibody Directed Against Epidermal Growth Factor Receptor Variant III

2018 ◽  
Vol 46 (1) ◽  
pp. 226-237 ◽  
Author(s):  
Wen Xu ◽  
Fei Song ◽  
Biao Wang ◽  
Kesang Li ◽  
Mi Tian ◽  
...  
Keyword(s):  
Monoclonal Antibody ◽  
Cell Proliferation ◽  
Epidermal Growth Factor Receptor ◽  
Growth Factor ◽  
Epidermal Growth Factor ◽  
Liver Cancer ◽  
Growth Factor Receptor ◽  
Beclin 1 ◽  
Epidermal Growth ◽  
Autophagy Pathway

Background/Aims: Epidermal growth factor receptor variant III (EGFRvIII), the most frequent EGFR variant, is constitutively activated without binding to EGF and is correlated with a poor prognosis. CH12, a human-mouse chimeric monoclonal antibody, has been developed in our laboratory and selectively binds to overexpressed EGFR and EGFRvIII. A previous study had reported that EGFR could influence autophagic activity, and autophagy is closely related to tumor development and the response to drug therapy. In this study, we aimed to elucidate the effect of CH12 on autophagy and efficacy of combining CH12 with an autophagy inhibitor against EGFRvIII-positive tumors. Methods: EGFRvIII was overexpressed in liver cancer, glioblastoma and breast cancer, and the change in the autophagy-relevant protein levels was analyzed by western blot assays, LC3 punctate aggregation was analyzed by immunofluorescence. The interaction of Beclin-1 and Rubicon was assessed by co-immunoprecipitation (Co-IP) after CH12 treatment. The efficacy of ATG7 or Beclin-1 siRNA in combination with CH12 in Huh-7-EGFRvIII cells was assessed by CCK-8 assays. The autophagy and apoptosis signaling events in Huh-7-EGFRvIII cells upon treatment with control, CH12, siRNA or combination for 48 h were assessed by western blot assays. Results: Our results showed that, in cancer cell lines overexpressing EGFRvIII, only the liver cancer cell lines Huh-7 and PLC/PRF/5 suggested autophagy activation. We then investigated the mechanism of autophagy activation after EGFRvIII overexpression. The results showed that EGFRvIII interacted with Rubicon, an autophagy inhibition protein, and released Beclin-1 to form the inducer complex, thus contributing to autophagy. In addition, CH12, via inhibiting the phosphorylation of EGFRvIII, promoted the interaction of EGFRvIII with Rubicon, further inducing autophagy. In vitro assays suggested that knocking down the expression of the key proteins ATG7 or Beclin-1 in the autophagy pathway with siRNA inhibits tumor cell proliferation. Combining autophagy-related proteins 7 (ATG7) or Beclin-1 siRNA with CH12 in Huh-7-EGFRvIII cells showed better inhibition of cell proliferation. Conclusion: EGFRvIII could induce autophagy, and CH12 treatment could improve autophagy activity in EGFRvIII-positive liver cancer cells. The combination of CH12 with an autophagy inhibitor or siRNA against key proteins in the autophagy pathway displayed more significant efficacy on EGFRvIII-positive tumor cells than monotherapy, and induced cell apoptosis.

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