scholarly journals Effects of TACE combined with precise RT on p53 gene expression and prognosis of HCC patients

2018 ◽  
Author(s):  
Yupeng Liu ◽  
Jingchen Yan ◽  
Feng Wang
Keyword(s):  
Gene Expression ◽  
P53 Gene

scholarly journals Inhibition of polyamine synthesis induces p53 gene expression but not apoptosis

1999 ◽  
Vol 276 (4) ◽  
pp. C946-C954 ◽  
Author(s):  
Li Li ◽  
Ji Li ◽  
Jaladanki N. Rao ◽  
Minglin Li ◽  
Barbara L. Bass ◽  
...  
Keyword(s):  
Gene Expression ◽  
Growth Inhibition ◽  
P53 Protein ◽  
Specific Inhibitor ◽  
P53 Gene ◽  
Mrna Levels ◽  
Intestinal Epithelial ◽  
Polyamine Biosynthesis ◽  
Fetal Bovine ◽  
P53 Mrna

The nuclear phosphoprotein p53 acts as a transcription factor and is involved in growth inhibition and apoptosis. The present study was designed to examine the effect of decreasing cellular polyamines on p53 gene expression and apoptosis in small intestinal epithelial (IEC-6) cells. Cells were grown in DMEM containing 5% dialyzed fetal bovine serum in the presence or absence of α-difluoromethylornithine (DFMO), a specific inhibitor of polyamine biosynthesis, for 4, 6, and 12 days. The cellular polyamines putrescine, spermidine, and spermine in DFMO-treated cells decreased dramatically at 4 days and remained depleted thereafter. Polyamine depletion by DFMO was accompanied by a significant increase in expression of the p53 gene. The p53 mRNA levels increased 4 days after exposure to DFMO, and the maximum increases occurred at 6 and 12 days after exposure. Increased levels of p53 mRNA in DFMO-treated cells were paralleled by increases in p53 protein. Polyamines given together with DFMO completely prevented increased expression of the p53 gene. Increased expression of the p53 gene in DFMO-treated cells was associated with a significant increase in G1 phase growth arrest. In contrast, no features of programmmed cell death were identified after polyamine depletion: no internucleosomal DNA fragmentation was observed, and no morphological features of apoptosis were evident in cells exposed to DFMO for 4, 6, and 12 days. These results indicate that 1) decreasing cellular polyamines increases expression of the p53 gene and 2) activation of p53 gene expression after polyamine depletion does not induce apoptosis in intestinal crypt cells. These findings suggest that increased expression of the p53 gene may play an important role in growth inhibition caused by polyamine depletion.

Do wine polyphenols modulate p53 gene expression in human cancer cell lines?

2001 ◽  
Vol 34 (5) ◽  
pp. 415-420 ◽  
Author(s):  
George J Soleas ◽  
David M Goldberg ◽  
Linda Grass ◽  
Michael Levesque ◽  
Eleftherios P Diamandis
Keyword(s):  
Gene Expression ◽  
Cell Lines ◽  
Cancer Cell ◽  
Human Cancer ◽  
P53 Gene ◽  
Cancer Cell Lines ◽  
Human Cancer Cell ◽  
Human Cancer Cell Lines ◽  
Wine Polyphenols

scholarly journals The p53 gene expression and its developmental regulation in schistosomes

1992 ◽  
Vol 87 (suppl 4) ◽  
pp. 71-73 ◽  
Author(s):  
Manami Tanaka ◽  
Tadashi Matsu-Ura ◽  
Hirohisa Hirai
Keyword(s):  
Gene Expression ◽  
Developmental Regulation ◽  
P53 Gene

scholarly journals The clinical impact of miRNA34a and P53 gene expression in colon cancer

2018 ◽  
Vol 16 ◽  
pp. 88-95 ◽  
Author(s):  
Eman A.E. Badr ◽  
Mohamed Farag Ali Assar ◽  
Suzy F. Gohar ◽  
Mohamed Hamdy Badr ◽  
Rawda Magdy Hathout ◽  
...  
Keyword(s):  
Gene Expression ◽  
Colon Cancer ◽  
P53 Gene ◽  
Clinical Impact

scholarly journals HOXA11 Regulates Chemoresistance By Modulating p53 Gene Expression in Acute Myeloid Leukemia

Blood ◽  
2019 ◽  
Vol 134 (Supplement_1) ◽  
pp. 5182-5182
Author(s):  
Xutao Guo ◽  
Bowen Yan ◽  
Yi Qiu
Keyword(s):  
Gene Expression ◽  
Cell Proliferation ◽  
Myeloid Leukemia ◽  
Drug Sensitivity ◽  
P53 Gene ◽  
Resistant Cell ◽  
Wild Type ◽  
P53 Expression ◽  
Acute Myeloid ◽  
Resistant Cells

Acute myeloid leukemia (AML) exhibits large intrinsic variation in drug responsiveness due to its inherent heterogeneity. Therefore, it is important to understand the resistant mechanism in order to improve the treatment. In our previously study, the OCI-AML2-resistant cell lines were established to resist cytarabine (Ara-C) in the concentration of 50 µM (OCI-AML2 R50). The RNA-seq results showed that many genes changed in the resistant cells compared to wild type OCI-AML2 cells. One of the most remarkably decreased gene in resistant cells was HOXA11 (Homeobox A11). It is the part of the A cluster on chromosome 7 and encodes a DNA-binding transcription factor which regulates gene expression, morphogenesis, and differentiation. In this study, we have evaluated the importance of HOXA11 in AML chemoresistance. We found that knockdown of HOXA11 repressed the WT OCI-AML2 cell proliferation and increased the population of cells expressing CD123 and CD47 LSC (Leukemia stem cell) markers and enhanced the resistance to Ara-C in vitro, while overexpression of HOXA11 showed the reverse effect. These results support the idea that HOXA11 promotes drug sensitivity and apoptosis in AML. However, the result also showed that overexpression of HOXA11 repressed the OCI-AML2 R50 cell proliferation and enhanced the resistance. Therefore, HOXA11 plays opposite role in sensitive cells and resistant cells. We further investigated the mechanism for these effects. We found that knockdown of HOXA11 decreased the p53 gene expression and overexpression of HOXA11 increased the expression of p53 in OCI-AML2 and R50 cells. Further, in OCI-AML2 R50 cells p53 has a hotspot mutation in DNA binding site and studies have shown that p53 mutation enhance cancer cell survival and chemoresistance. Therefore, our study shows dual roles for HOXA11 in cell survival. In p53 wild type parental AML2 cells, HOXA11 induces wild type p53 expression to enhance drug sensitivity while in resistant cell, HOXA11 promotes mutant p53 expression and enhances the resistance of chemotherapy. Disclosures No relevant conflicts of interest to declare.

scholarly journals Distinct p53 acetylation cassettes differentially influence gene-expression patterns and cell fate

2006 ◽  
Vol 173 (4) ◽  
pp. 533-544 ◽  
Author(s):  
Chad D. Knights ◽  
Jason Catania ◽  
Simone Di Giovanni ◽  
Selen Muratoglu ◽  
Ricardo Perez ◽  
...  
Keyword(s):  
Gene Expression ◽  
Cell Fate ◽  
Protein Interactions ◽  
Posttranslational Modifications ◽  
Biological Activities ◽  
Expression Profiles ◽  
Expression Patterns ◽  
Gene Expression Profiles ◽  
P53 Gene ◽  
Protein Protein Interactions

The activity of the p53 gene product is regulated by a plethora of posttranslational modifications. An open question is whether such posttranslational changes act redundantly or dependently upon one another. We show that a functional interference between specific acetylated and phosphorylated residues of p53 influences cell fate. Acetylation of lysine 320 (K320) prevents phosphorylation of crucial serines in the NH2-terminal region of p53; only allows activation of genes containing high-affinity p53 binding sites, such as p21/WAF; and promotes cell survival after DNA damage. In contrast, acetylation of K373 leads to hyperphosphorylation of p53 NH2-terminal residues and enhances the interaction with promoters for which p53 possesses low DNA binding affinity, such as those contained in proapoptotic genes, leading to cell death. Further, acetylation of each of these two lysine clusters differentially regulates the interaction of p53 with coactivators and corepressors and produces distinct gene-expression profiles. By analogy with the “histone code” hypothesis, we propose that the multiple biological activities of p53 are orchestrated and deciphered by different “p53 cassettes,” each containing combination patterns of posttranslational modifications and protein–protein interactions.

Sign in / Sign up

Export Citation Format

Share Document