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Expression and distribution of PPP2R5C gene in leukemia.

Zheng H, Chen Y, Chen S, Niu Y, Yang L, Li B, Lu Y, Geng S, Du X, Li Y - J Hematol Oncol (2011)

Bottom Line: Significantly higher expression of PPP2R5C was found in AML, CML, T-ALL, and B-CLL groups in comparison with healthy controls.High expression of PPP2R5C was detected in the B-ALL group; however, no significant difference was found compared with the healthy group.The expression level of PPP2R5C in the CML-CR group decreased significantly compared with that in the de novo CML group and was not significantly different from the level in the healthy group.

View Article: PubMed Central - HTML - PubMed

Affiliation: Institute of Hematology, Medical College, Jinan University, Guangzhou, People's Republic of China.

ABSTRACT

Background: Recently, we clarified at the molecular level novel chromosomal translocation t(14;14)(q11;q32) in a case of Sézary syndrome, which caused a rearrangement from TRAJ7 to the PPP2R5C gene. PPP2R5C is one of the regulatory B subunits of protein phosphatase 2A (PP2A). It plays a crucial role in cell proliferation, differentiation, and transformation. To characterize the expression and distribution of five different transcript variants of the PPP2R5C gene in leukemia, we analyzed the expression level of PPP2R5C in peripheral blood mononuclear cells from 77 patients with de novo leukemia, 26 patients with leukemia in complete remission (CR), and 20 healthy individuals by real-time PCR and identified the different variants of PPP2R5C by RT-PCR.

Findings: Significantly higher expression of PPP2R5C was found in AML, CML, T-ALL, and B-CLL groups in comparison with healthy controls. High expression of PPP2R5C was detected in the B-ALL group; however, no significant difference was found compared with the healthy group. The expression level of PPP2R5C in the CML-CR group decreased significantly compared with that in the de novo CML group and was not significantly different from the level in the healthy group. By using different primer pairs that covered different exons, five transcript variants of PPP2R5C could be identified. All variants could be detected in healthy samples as well as in all the leukemia samples, and similar frequencies and distributions of PPP2R5C were indicated.

Conclusions: Overexpression of PPP2R5C in T-cell malignancy as well as in myeloid leukemia cells might relate to its proliferation and differentiation. Investigation of the effect of target inhibition of this gene might be beneficial to further characterization of molecular mechanisms and targeted therapy in leukemia.

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Expression level of PPP2R5C gene in PBMCs from different leukemia patients and healthy individuals (HI).
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Figure 3: Expression level of PPP2R5C gene in PBMCs from different leukemia patients and healthy individuals (HI).

Mentions: PPP2R5C as a potential tumor suppressor plays a crucial role in cell proliferation and differentiation [4]. Based on our recent finding of a novel gene rearrangement from TRAJ7 to PPP2R5C, it could be interesting to analyze the expression features of PPP2R5C in hematological malignancies. In the present study, we analyzed the expression level of the PPP2R5C gene in leukemia samples. In comparison with healthy controls (1.24 ± 1.09), significantly higher expression of PPP2R5C was found in the AML (2.06 ± 0.85) (p = 0.0076), CML (6.78 ± 2.75) (p < 0.0001), T-ALL/NHL (3.73 ± 3.66) (p = 0.0062) and B-CLL (2.21 ± 1.22) (p = 0.0417) groups (Figure 2). A high tendency toward expression of PPP2R5C was detected in the B-ALL group (1.39 ± 1.31); however, the expression was not significantly different from that in the controls (p = 0.7089) (Figure 2). The expression level of PPP2R5C in the CML-CR group (1.75 ± 0.55) decreased significantly in comparison with the CML group (p < 0.0001), but showed no significant difference compared with the healthy group (p = 0.2895). Although the expression level of PPP2R5C gene decreased in the AML-CR (1.53 ± 0.60) and B-ALL groups (0.54 ± 0.27), there was no significant difference compared with the AML (p = 0.1100) and B-ALL groups (p = 0.2142) or with healthy controls. Overexpression of PPP2R5C was found in T-cell lines like Hut-78, CCRF, Jurkat, Molt-3 and Molt-4, and the expression level was 5-9 times higher than that from healthy CD3+ T cells (Figure 3A). Interesting, the tendency of the expression level of PPP2R5C in Raji, Daudi, NB4 and K562 cells was accordant to the results from primary leukemia cells (Figure 3B), which showed higher expression level of PPP2R5C in K562 (CML cell line), and lower expression level in B-cell lines (Raji and Daudi).


Expression and distribution of PPP2R5C gene in leukemia.

Zheng H, Chen Y, Chen S, Niu Y, Yang L, Li B, Lu Y, Geng S, Du X, Li Y - J Hematol Oncol (2011)

Expression level of PPP2R5C gene in PBMCs from different leukemia patients and healthy individuals (HI).
© Copyright Policy - open-access
Related In: Results  -  Collection

License
Show All Figures
getmorefigures.php?uid=PMC3117819&req=5

Figure 3: Expression level of PPP2R5C gene in PBMCs from different leukemia patients and healthy individuals (HI).
Mentions: PPP2R5C as a potential tumor suppressor plays a crucial role in cell proliferation and differentiation [4]. Based on our recent finding of a novel gene rearrangement from TRAJ7 to PPP2R5C, it could be interesting to analyze the expression features of PPP2R5C in hematological malignancies. In the present study, we analyzed the expression level of the PPP2R5C gene in leukemia samples. In comparison with healthy controls (1.24 ± 1.09), significantly higher expression of PPP2R5C was found in the AML (2.06 ± 0.85) (p = 0.0076), CML (6.78 ± 2.75) (p < 0.0001), T-ALL/NHL (3.73 ± 3.66) (p = 0.0062) and B-CLL (2.21 ± 1.22) (p = 0.0417) groups (Figure 2). A high tendency toward expression of PPP2R5C was detected in the B-ALL group (1.39 ± 1.31); however, the expression was not significantly different from that in the controls (p = 0.7089) (Figure 2). The expression level of PPP2R5C in the CML-CR group (1.75 ± 0.55) decreased significantly in comparison with the CML group (p < 0.0001), but showed no significant difference compared with the healthy group (p = 0.2895). Although the expression level of PPP2R5C gene decreased in the AML-CR (1.53 ± 0.60) and B-ALL groups (0.54 ± 0.27), there was no significant difference compared with the AML (p = 0.1100) and B-ALL groups (p = 0.2142) or with healthy controls. Overexpression of PPP2R5C was found in T-cell lines like Hut-78, CCRF, Jurkat, Molt-3 and Molt-4, and the expression level was 5-9 times higher than that from healthy CD3+ T cells (Figure 3A). Interesting, the tendency of the expression level of PPP2R5C in Raji, Daudi, NB4 and K562 cells was accordant to the results from primary leukemia cells (Figure 3B), which showed higher expression level of PPP2R5C in K562 (CML cell line), and lower expression level in B-cell lines (Raji and Daudi).

Bottom Line: Significantly higher expression of PPP2R5C was found in AML, CML, T-ALL, and B-CLL groups in comparison with healthy controls.High expression of PPP2R5C was detected in the B-ALL group; however, no significant difference was found compared with the healthy group.The expression level of PPP2R5C in the CML-CR group decreased significantly compared with that in the de novo CML group and was not significantly different from the level in the healthy group.

View Article: PubMed Central - HTML - PubMed

Affiliation: Institute of Hematology, Medical College, Jinan University, Guangzhou, People's Republic of China.

ABSTRACT

Background: Recently, we clarified at the molecular level novel chromosomal translocation t(14;14)(q11;q32) in a case of Sézary syndrome, which caused a rearrangement from TRAJ7 to the PPP2R5C gene. PPP2R5C is one of the regulatory B subunits of protein phosphatase 2A (PP2A). It plays a crucial role in cell proliferation, differentiation, and transformation. To characterize the expression and distribution of five different transcript variants of the PPP2R5C gene in leukemia, we analyzed the expression level of PPP2R5C in peripheral blood mononuclear cells from 77 patients with de novo leukemia, 26 patients with leukemia in complete remission (CR), and 20 healthy individuals by real-time PCR and identified the different variants of PPP2R5C by RT-PCR.

Findings: Significantly higher expression of PPP2R5C was found in AML, CML, T-ALL, and B-CLL groups in comparison with healthy controls. High expression of PPP2R5C was detected in the B-ALL group; however, no significant difference was found compared with the healthy group. The expression level of PPP2R5C in the CML-CR group decreased significantly compared with that in the de novo CML group and was not significantly different from the level in the healthy group. By using different primer pairs that covered different exons, five transcript variants of PPP2R5C could be identified. All variants could be detected in healthy samples as well as in all the leukemia samples, and similar frequencies and distributions of PPP2R5C were indicated.

Conclusions: Overexpression of PPP2R5C in T-cell malignancy as well as in myeloid leukemia cells might relate to its proliferation and differentiation. Investigation of the effect of target inhibition of this gene might be beneficial to further characterization of molecular mechanisms and targeted therapy in leukemia.

Show MeSH
Related in: MedlinePlus