Please use this identifier to cite or link to this item: http://scholarbank.nus.edu.sg/handle/10635/80181
Title: NF-?B-MEDIATED INTEGRIN ?3 EXPRESSION LEADS TO INCREASED LAMELLIPODIA FORMATION AND STAT3 ACTIVITY IN p53-DEPLETED CELLS
Authors: GUO KUNYAO, ALVIN
Keywords: p53, NF-kappaB, STAT3, Integrin, Lamellipodia
Issue Date: 15-Apr-2014
Source: GUO KUNYAO, ALVIN (2014-04-15). NF-?B-MEDIATED INTEGRIN ?3 EXPRESSION LEADS TO INCREASED LAMELLIPODIA FORMATION AND STAT3 ACTIVITY IN p53-DEPLETED CELLS. ScholarBank@NUS Repository.
Abstract: TUMOR SUPPRESSOR P53 PREVENTS CANCER PROGRESSION AND METASTASIS. LOSS OF P53 FUNCTION RESULTS IN BOTH NF-?B AND STAT3 ACTIVATION. CONSTITUTIVE ACTIVATION OF NF-?B OR STAT3 IS ASSOCIATED WITH MALIGNANT PHENOTYPES. HOWEVER, THE LINK BETWEEN NF-?B AND STAT3 IN THE ABSENCE OF P53 REMAINS ELUSIVE. HERE, WE SHOW THAT NF-?B INCREASES STAT3 ACTIVITY IN P53-DEPLETED CELLS. NOTABLY, THE REMODELING OF ACTIN CYTOSKELETON MEDIATED BY NF-?B IS INVOLVE IN STAT3 ACTIVATION. KNOCKDOWN OF P65, A COMPONENT OF NF-?B, ATTENUATES LAMELLIPODIA FORMATION AND STAT3 PHOSPHORYLATION IN THE ABSENCE OF P53. IN CONTRAST, KNOCKDOWN OF STAT3 DOES NOT AFFECT CELL MORPHOLOGY OR P65 PHOSPHORYLATION. STAT3 PHOSPHORYLATION, ENHANCED BY THE LOSS OF P53, IS DIMINISHED WHEN LAMELLIPODIA FORMATION IS DISRUPTED. FURTHERMORE, WE FIND THAT KNOCKDOWN OF P65 DECREASES THE EXPRESSION OF INTEGRIN ?3. THE INHIBITION OF INTEGRIN ?3 FUNCTION ATTENUATES STAT3 PHOSPHORYLATION. COLLECTIVELY, NF-?B ENHANCES STAT3 ACTIVITY VIA INTEGRIN ?3-M
URI: http://scholarbank.nus.edu.sg/handle/10635/80181
Appears in Collections:Ph.D Theses (Open)

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