Growth Inhibition and Induction of Apoptosis in NB4 Promyelocytic Leukemia Cells by Trypsin Inhibitor from Sweet Potato Storage Roots

2007 ◽  
Vol 55 (7) ◽  
pp. 2548-2553 ◽  
Author(s):  
Guan-Jhong Huang ◽  
Ming-Jyh Sheu ◽  
Hsien-Jung Chen ◽  
Yuan-Shiun Chang ◽  
Yaw-Huei Lin
Keyword(s):  
Growth Inhibition ◽  
Sweet Potato ◽  
Trypsin Inhibitor ◽  
Promyelocytic Leukemia ◽  
Leukemia Cells ◽  
Potato Storage ◽  
Storage Roots ◽  
Induction Of Apoptosis

Isolation and characterisation of invertase inhibitor from sweet potato storage roots

2008 ◽  
Vol 88 (15) ◽  
pp. 2615-2621 ◽  
Author(s):  
Guan-Jhong Huang ◽  
Ming-Jyh Sheu ◽  
Yuan-Shiun Chang ◽  
Te-Ling Lu ◽  
Heng-Yuan Chang ◽  
...  
Keyword(s):  
Sweet Potato ◽  
Potato Storage ◽  
Storage Roots ◽  
Invertase Inhibitor

Inhibition of Reactive Nitrogen Species in Vitro and ex Vivo by Trypsin Inhibitor from Sweet Potato ‘Tainong 57' Storage Roots

2007 ◽  
Vol 55 (15) ◽  
pp. 6000-6006 ◽  
Author(s):  
Guan-Jhong Huang ◽  
Ming-Jyh Sheu ◽  
Hsien-Jung Chen ◽  
Yuan-Shiun Chang ◽  
Yaw-Huei Lin
Keyword(s):  
Sweet Potato ◽  
Trypsin Inhibitor ◽  
Reactive Nitrogen Species ◽  
Ex Vivo ◽  
Reactive Nitrogen ◽  
Nitrogen Species ◽  
Storage Roots

All-trans-Retinoic acid (ATRA) and Arsenic Trioxide-Induced Expression and Regulation of Programmed Cell Death 4 (PDCD4) in Acute Promyelocytic Leukemia.

Blood ◽  
2004 ◽  
Vol 104 (11) ◽  
pp. 886-886
Author(s):  
Bulent Ozpolat ◽  
Maribel Tirado-Gomez ◽  
Nancy H. Colburn ◽  
Gabriel Lopez-Berestein
Keyword(s):  
Growth Inhibition ◽  
Translational Control ◽  
Molecular Mechanisms ◽  
Promyelocytic Leukemia ◽  
Leukemia Cells ◽  
Control Of Gene Expression ◽  
Trans Retinoic Acid ◽  
All Trans Retinoic Acid ◽  
Programmed Cell Death 4 ◽  
Translational Suppression

Abstract All-trans-retinoic acid (ATRA) induces growth inhibition, differentiation and apoptosis in acute promyelocytic leukemia (APL) characterized by t(15;17), which leads to expression of PML-RARa and differentiation arrest. ATRA treatment alone results in complete remission (CR) about 90% of APL patients. However these remissions are transient and APL patients commonly become resistant to ATRA therapy. Recently, arsenic trioxide, As(2)O(3), was proven to be highly effective in inducing CRs not only in relapsed after ATRA and primary APL patients. Despite the well documented clinical efficacy ATRA and As(2)O(3) in APL, precise downstream molecular mechanisms of action of these agents and the molecular mechanisms responsible for the resistance largely remain unknown. Recently, employing comprehensive proteomics methods we studied molecular mechanisms of ATRA-induced growth inhibition in APL cells. We reported that ATRA induces translational suppression through multiple posttranscriptional mechanisms involved in translation initiation and elongation phases (Harris &Ozpolat et al, Blood, 104 (5) 2004). We also demonstrated that ATRA inhibits expression translation initiation factors including IF2, eIF4AI, eIF4G, eIF5, eIF6 but upregulates expression of translation inhibitor DAP5/p97/NAT1 in APL cells. Translational control of gene expression has been identified as an important regulatory mechanism for gene products involved in regulation of cell proliferation, differentiation and apoptosis. Programmed cell death 4(PDCD4) inhibits cap-dependent translation and exerts transformation-suppressing activity by inhibiting the helicase activity of eIF4A. . Here we investigated whether PDCD4 plays a role in ATRA-induced growth inhibition and terminal differentiation by mediating translational suppression. We found for the first time that ATRA (1 mM) and As(2)O(3) ( 0.4 mM and 2 mM) induced PDCD4 expression at mRNA and protein level detected by RT-PCR and western blotting analyses, respectively, after 24 h of treatment in NB4 cells. As(2)O(3) induced maximum PDCD4 protein expression at 72 h of treatment in NB4 cells ATRA induced PDCD4 mRNA expression in ATRA responsive human acute myeloid leukemia cells (HL-60) but not in ATRA-resistant HL60 cells (HL-60R), which express a point mutation in ATRA binding domain of RARa, suggesting PDCD4 expression is mediated through retinoid receptor alpha in HL-60 leukemia cells. Overall data suggest that translational control may play a role in ATRA-induced differentiation and As(2)O(3)-induced effects. We are currently determining whether other retinoid receptors are involved in ATRA-induced expression of PDCD4 and testing the hypothesis that whether PDCD4-mediated translational suppression is critical to ATRA-induced APL cell differentiation. Activation of these pathways that lead to translational suppression reveals a novel mechanism of ATRA action and provide novel insights into ATRA-induced differentiation program in APL cells.Better understanding of posttranscriptional control of gene expression may offer targets for the differentiation therapy and chemo preventive strategies.

All-Trans Retinoic Acid and Induction of Apoptosis in Acute Promyelocytic Leukemia Cells

1994 ◽  
Vol 14 (5-6) ◽  
pp. 503-507 ◽  
Author(s):  
Patrizia Tosi ◽  
Giuseppe Visani ◽  
Davide Gibellini ◽  
Giorgio Zauli ◽  
Emanuela Ottaviani ◽  
...  
Keyword(s):  
Retinoic Acid ◽  
Acute Promyelocytic Leukemia ◽  
Promyelocytic Leukemia ◽  
Leukemia Cells ◽  
Trans Retinoic Acid ◽  
All Trans Retinoic Acid ◽  
Induction Of Apoptosis

scholarly journals Induction of Apoptosis in HL-60 Human Promyelocytic Leukemia Cells by Adenosine A3Receptor Agonists

1996 ◽  
Vol 219 (3) ◽  
pp. 904-910 ◽  
Author(s):  
Yutaka Kohno ◽  
Yoshitatsu Sei ◽  
Masahiro Koshiba ◽  
Hea O. Kim ◽  
Kenneth A. Jacobson
Keyword(s):  
Promyelocytic Leukemia ◽  
Leukemia Cells ◽  
Induction Of Apoptosis

scholarly journals Guanine analog-induced differentiation of human promyelocytic leukemia cells and changes in queuine modification of tRNA.

1987 ◽  
Vol 7 (10) ◽  
pp. 3613-3619 ◽  
Author(s):  
K A Kretz ◽  
J R Katze ◽  
R W Trewyn
Keyword(s):  
Structural Change ◽  
Cell Differentiation ◽  
Growth Inhibition ◽  
Aspartic Acid ◽  
Promyelocytic Leukemia ◽  
Leukemia Cells ◽  
Primary Role ◽  
Trna Modification ◽  
Hypoxanthine Guanine Phosphoribosyltransferase ◽  
Modification Enzyme

Treatment of hypoxanthine-guanine phosphoribosyltransferase (HGPRT)-deficient human promyelocytic leukemia (HL-60) cells with 6-thioguanine results in growth inhibition and cell differentiation. 6-Thioguanine is a substrate for the tRNA modification enzyme tRNA-guanine ribosyltransferase, which normally catalyzes the exchange of queuine for guanine in position 1 of the anticodon of tRNAs for asparagine, aspartic acid, histidine, and tyrosine. During the early stages of HGPRT-deficient HL-60 cell differentiation induced by 6-thioguanine, there was a transient decrease in the queuine content of tRNA, and changes in the isoacceptor profiles of tRNA(His) indicate that 6-thioguanine was incorporated into the tRNA in place of queuine. Reversing this structural change in the tRNA anticodon by addition of excess exogenous queuine reversed the 6-thioguanine-induced growth inhibition and differentiation. Similar results were obtained when 8-azaguanine (another inhibitor of queuine modification of tRNA that can be incorporated into the anticodon) replaced 6-thioguanine as the inducing agent. The data suggest a primary role for the change in queuine modification of tRNA in mediating the differentiation of HGPRT-deficient HL-60 cells induced by guanine analogs.

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