Abstract 965: Mechanistic studies of a dietary combination in cancer prevention: The effects of manganese superoxide dismutase on tumor suppressor gene activation

2010 ◽  
Author(s):  
Delira F. Robbins ◽  
Kerri Morris ◽  
Yunfeng Zhao
Keyword(s):  
Superoxide Dismutase ◽  
Tumor Suppressor ◽  
Cancer Prevention ◽  
Tumor Suppressor Gene ◽  
Manganese Superoxide Dismutase ◽  
Gene Activation ◽  
Suppressor Gene ◽  
Mechanistic Studies ◽  
Manganese Superoxide

scholarly journals Natural products targeting the p53 tumor suppressor-A novel approach for future cancer therapy- A review

2021 ◽  
Vol 1 (2) ◽  
pp. 167-176
Author(s):  
Ali Esmail Al-Snafi
Keyword(s):  
Natural Products ◽  
Cancer Therapy ◽  
Tumor Suppressor ◽  
Medicinal Plants ◽  
Cancer Prevention ◽  
Tumor Suppressor Gene ◽  
Suppressor Gene ◽  
Novel Approach ◽  
Prevention And Treatment ◽  
Expression And Activity

Mutations of p53, a tumor suppressor gene, are known to be involved in multiplication and metastasis of tumors. A number of natural products targeted the p53-MDM2 pathway. This review is an attempt to highlight the medicinal plants that can modulate the expression and activity ofp53tumor suppression, for cancer prevention and treatment.

scholarly journals Pengaruh P53 Dan YY1 Terhadap Terjadinya Kanker Serviks

Medicinus ◽  
2018 ◽  
Vol 5 (1) ◽  
Author(s):  
Jacobus Jeno Wibisono
Keyword(s):  
Cervical Cancer ◽  
Tumor Suppressor ◽  
Tumor Suppressor Gene ◽  
Gene Activation ◽  
P53 Gene ◽  
Suppressor Gene ◽  
E6 Oncoprotein ◽  
P53 Activation ◽  
Ubiquitination Pathway ◽  
E6 And E7

<p><em>Cervical cancer is one of the most prevalent cancer in the world and caused by Human Papilloma Virus (HPV). The pathogenesis of cancer as whole (50%) is caused by gene mutation. HPV stimulates carcinogenesis on cervix epitel cells by HPV-Encoded viral oncoproteins, E6 and E7, which will inhibit tumor suppressor gene activation, such as p53 gene. HPV-encoded E6 oncoprotein  is able to directly attached on p53 causing degeneration via E6-AP-mediated ubiquitination pathway. Moreover, overexpression on YY1 gene has significant role on the progression of HPV on cervical cancer. YY1 inhibits p53 activation dan inhibits apoptosis on cells infected by HPV. Overexpression of YY1 induces reduction of endogenous p53, which will inhibit p53 function as tumor suppressor gene.</em></p><p><strong><em>Keywords: cervical cancer, HPV, P53, YY1</em></strong></p>

scholarly journals The tumor suppressor gene WWOX links the canonical and noncanonical NF-κB pathways in HTLV-I Tax-mediated tumorigenesis

Blood ◽  
2011 ◽  
Vol 117 (5) ◽  
pp. 1652-1661 ◽  
Author(s):  
Jing Fu ◽  
Zhaoxia Qu ◽  
Pengrong Yan ◽  
Chie Ishikawa ◽  
Rami I. Aqeilan ◽  
...  
Keyword(s):  
Tumor Suppressor ◽  
Signaling Pathways ◽  
Tumor Suppressor Gene ◽  
Nuclear Factor Κb ◽  
Suppressor Gene ◽  
Nuclear Factor ◽  
Mechanistic Studies ◽  
Viral Oncoprotein

Abstract Both the canonical and noncanonical nuclear factor κB (NF-κB) pathways have been linked to tumorigenesis. However, it remains unknown whether and how the 2 signaling pathways cooperate during tumorigenesis. We report that inhibition of the noncanonical NF-κB pathway significantly delays tumorigenesis mediated by the viral oncoprotein Tax. One function of noncanonical NF-κB activation was to repress expression of the WWOX tumor suppressor gene. Notably, WWOX specifically inhibited Tax-induced activation of the canonical, but not the noncanonical NF-κB pathway. Mechanistic studies indicated that WWOX blocked Tax-induced inhibitors of κB kinaseα (IKKα) recruitment to RelA and subsequent RelA phosphorylation at S536. In contrast, WWOX Y33R, a mutant unable to block the IKKα recruitment and RelA phosphorylation, lost the ability to inhibit Tax-mediated tumorigenesis. These data provide one important mechanism by which Tax coordinates the 2 NF-κB pathways for tumorigenesis. These data also suggest a novel role of WWOX in NF-κB regulation and viral tumorigenesis.

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