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The clinical significance of γ-catenin in acute myeloid leukemia.

Xu J, Wu W, Shen W, Liu P - Onco Targets Ther (2016)

Bottom Line: The expression levels of γ-catenin in AML patients with mutated CEBPα were significantly higher than those with unmutated CEBPα.AML patients with lower γ-catenin levels were more likely to achieve complete remission compared with patients who have higher γ-catenin levels.Moreover, knocking down of γ-catenin enhanced the cytotoxicity of decitabine in K562 cells.

View Article: PubMed Central - PubMed

Affiliation: Department of Hematology, The First Affiliated Hospital of Nanjing Medical University, Nanjing.

ABSTRACT
Dysregulation of γ-catenin may function as an oncogenic factor in various malignancies. We investigated γ-catenin expression in acute myeloid leukemia (AML) and explored its role in the pathogenesis of AML. γ-Catenin was significantly overexpressed in AML patients compared to healthy donors. The γ-catenin expression in AML patients with lower white blood cells (<30×10(9)/L) was significantly higher than those with higher white blood cells (≥30×10(9)/L). The expression levels of γ-catenin in AML patients with mutated CEBPα were significantly higher than those with unmutated CEBPα. AML patients with lower γ-catenin levels were more likely to achieve complete remission compared with patients who have higher γ-catenin levels. In K562 cells, γ-catenin knockdown suppressed cellular proliferation, while the cellular migration was greatly enhanced. Moreover, knocking down of γ-catenin enhanced the cytotoxicity of decitabine in K562 cells. Our investigation has indicated a potential role of γ-catenin in the pathogenesis of AML.

No MeSH data available.


Related in: MedlinePlus

The effect of decitabine.Notes: (A) The sensitivity of K562 cell line to decitabine therapy after the suppression of γ-catenin protein expression. (B) The cell viability of K562 cell line after treatment separately with 1) growth media, 2) decitabine, 3) zVAD (20 µM) + decitabine, and 4) Nec-1 (30 µM) + decitabine.Abbreviations: KD, knockdown; Nec-1, Necrostatin-1; NC, negative control; WT, wild type; zVAD, Benzyloxycarbonyl-Val-Ala-Asp.
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f7-ott-9-3861: The effect of decitabine.Notes: (A) The sensitivity of K562 cell line to decitabine therapy after the suppression of γ-catenin protein expression. (B) The cell viability of K562 cell line after treatment separately with 1) growth media, 2) decitabine, 3) zVAD (20 µM) + decitabine, and 4) Nec-1 (30 µM) + decitabine.Abbreviations: KD, knockdown; Nec-1, Necrostatin-1; NC, negative control; WT, wild type; zVAD, Benzyloxycarbonyl-Val-Ala-Asp.

Mentions: To understand how the knockdown of γ-catenin affects K562 cells, we treated K562/KD, K562/NC, and K562/WT cells with decitabine (4.4, 8.8, and 17.6 µM) and examined the inhibitory effects of this agent using CCK-8 assay kit, and then the inhibitory rate and half maximal inhibitory concentration (IC50) were calculated. The results showed that the inhibitory rate of decitabine in K562/KD cells (IC50 =6.24±0.77 µM) was significantly higher than that in K562/NC cells (IC50 =12.14±1.38 µM) or K562/WT cells (IC50 =22.51±3.83 µM), indicating that the downregulation of γ-catenin could sensitize K562 cells to decitabine (P<0.05, Figure 7A).


The clinical significance of γ-catenin in acute myeloid leukemia.

Xu J, Wu W, Shen W, Liu P - Onco Targets Ther (2016)

The effect of decitabine.Notes: (A) The sensitivity of K562 cell line to decitabine therapy after the suppression of γ-catenin protein expression. (B) The cell viability of K562 cell line after treatment separately with 1) growth media, 2) decitabine, 3) zVAD (20 µM) + decitabine, and 4) Nec-1 (30 µM) + decitabine.Abbreviations: KD, knockdown; Nec-1, Necrostatin-1; NC, negative control; WT, wild type; zVAD, Benzyloxycarbonyl-Val-Ala-Asp.
© Copyright Policy
Related In: Results  -  Collection

License 1 - License 2
Show All Figures
getmorefigures.php?uid=PMC4930232&req=5

f7-ott-9-3861: The effect of decitabine.Notes: (A) The sensitivity of K562 cell line to decitabine therapy after the suppression of γ-catenin protein expression. (B) The cell viability of K562 cell line after treatment separately with 1) growth media, 2) decitabine, 3) zVAD (20 µM) + decitabine, and 4) Nec-1 (30 µM) + decitabine.Abbreviations: KD, knockdown; Nec-1, Necrostatin-1; NC, negative control; WT, wild type; zVAD, Benzyloxycarbonyl-Val-Ala-Asp.
Mentions: To understand how the knockdown of γ-catenin affects K562 cells, we treated K562/KD, K562/NC, and K562/WT cells with decitabine (4.4, 8.8, and 17.6 µM) and examined the inhibitory effects of this agent using CCK-8 assay kit, and then the inhibitory rate and half maximal inhibitory concentration (IC50) were calculated. The results showed that the inhibitory rate of decitabine in K562/KD cells (IC50 =6.24±0.77 µM) was significantly higher than that in K562/NC cells (IC50 =12.14±1.38 µM) or K562/WT cells (IC50 =22.51±3.83 µM), indicating that the downregulation of γ-catenin could sensitize K562 cells to decitabine (P<0.05, Figure 7A).

Bottom Line: The expression levels of γ-catenin in AML patients with mutated CEBPα were significantly higher than those with unmutated CEBPα.AML patients with lower γ-catenin levels were more likely to achieve complete remission compared with patients who have higher γ-catenin levels.Moreover, knocking down of γ-catenin enhanced the cytotoxicity of decitabine in K562 cells.

View Article: PubMed Central - PubMed

Affiliation: Department of Hematology, The First Affiliated Hospital of Nanjing Medical University, Nanjing.

ABSTRACT
Dysregulation of γ-catenin may function as an oncogenic factor in various malignancies. We investigated γ-catenin expression in acute myeloid leukemia (AML) and explored its role in the pathogenesis of AML. γ-Catenin was significantly overexpressed in AML patients compared to healthy donors. The γ-catenin expression in AML patients with lower white blood cells (<30×10(9)/L) was significantly higher than those with higher white blood cells (≥30×10(9)/L). The expression levels of γ-catenin in AML patients with mutated CEBPα were significantly higher than those with unmutated CEBPα. AML patients with lower γ-catenin levels were more likely to achieve complete remission compared with patients who have higher γ-catenin levels. In K562 cells, γ-catenin knockdown suppressed cellular proliferation, while the cellular migration was greatly enhanced. Moreover, knocking down of γ-catenin enhanced the cytotoxicity of decitabine in K562 cells. Our investigation has indicated a potential role of γ-catenin in the pathogenesis of AML.

No MeSH data available.


Related in: MedlinePlus