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Hsp72 mediates TAp73α anti-apoptotic effects in small cell lung carcinoma cells.

Nyman U, Muppani NR, Zhivotovsky B, Joseph B - J. Cell. Mol. Med. (2011)

Bottom Line: However, the precise mechanism by which TAp73α exerts its pro-survival effect is yet unclear.Finally, we revealed that TAp73β counteracts the anti-apoptotic effect of TAp73α by preventing Hsp72 induction.Our results thus provide additional evidence for the potential oncogenic role of TAp73α, and extend the understanding of the mechanism for its anti-apoptotic effect.

View Article: PubMed Central - PubMed

Affiliation: Department of Oncology-Pathology, Cancer Centrum Karolinska, Karolinska Institutet, Stockholm, Sweden.

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Hsp72 represses TAp73β pro-apoptotic effect. (A) H82 cells were transfected with Hsp72 expression vector and extracts were analysed as described in Figure 2A. (B) H82 cells were co-transfected with EGFP and Hsp72 vector (green), and samples assayed as described in Figure 2B. (C) H82 cells were co-transfected with EGFP, Hsp72 vector and empty vector or TAp73β. Samples were treated, stained and assayed as described in Figure 2D. Figures are mean ± S.D. of three independent experiments, where *P < 0.05, **P < 0.01 and ***P < 0.001.
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fig03: Hsp72 represses TAp73β pro-apoptotic effect. (A) H82 cells were transfected with Hsp72 expression vector and extracts were analysed as described in Figure 2A. (B) H82 cells were co-transfected with EGFP and Hsp72 vector (green), and samples assayed as described in Figure 2B. (C) H82 cells were co-transfected with EGFP, Hsp72 vector and empty vector or TAp73β. Samples were treated, stained and assayed as described in Figure 2D. Figures are mean ± S.D. of three independent experiments, where *P < 0.05, **P < 0.01 and ***P < 0.001.

Mentions: Given that TAp73α is able to induce Hsp72 expression and that the anti-apoptotic activity of TAp73α seems to be dependent on this induction, and since it is known from before that the p73 isoforms can interact and regulate the activity of each other [16, 29], we sought to investigate whether the overexpression of Hsp72 could counteract the pro-apoptotic function of TAp73β upon drug-induced apoptosis. Transfection of H82 cells with Hsp72 vector lead to an enhanced expression of Hsp72 protein, as shown by immunoblot (Fig. 3A) and confocal imaging (Fig. 3B). Subsequent transfection of H82 cells with Hsp72 reduced the level of VP16-induced apoptosis (Fig. 3C, black and grey bars). Moreover, co-transfection of TAp73β together with Hsp72 abolished TAp73β pro-apoptotic effect upon VP16 treatment. Hence, TAp73β augmentation of drug-induced apoptosis can be repressed by simultaneous co-expression of Hsp72.


Hsp72 mediates TAp73α anti-apoptotic effects in small cell lung carcinoma cells.

Nyman U, Muppani NR, Zhivotovsky B, Joseph B - J. Cell. Mol. Med. (2011)

Hsp72 represses TAp73β pro-apoptotic effect. (A) H82 cells were transfected with Hsp72 expression vector and extracts were analysed as described in Figure 2A. (B) H82 cells were co-transfected with EGFP and Hsp72 vector (green), and samples assayed as described in Figure 2B. (C) H82 cells were co-transfected with EGFP, Hsp72 vector and empty vector or TAp73β. Samples were treated, stained and assayed as described in Figure 2D. Figures are mean ± S.D. of three independent experiments, where *P < 0.05, **P < 0.01 and ***P < 0.001.
© Copyright Policy
Related In: Results  -  Collection

Show All Figures
getmorefigures.php?uid=PMC4373366&req=5

fig03: Hsp72 represses TAp73β pro-apoptotic effect. (A) H82 cells were transfected with Hsp72 expression vector and extracts were analysed as described in Figure 2A. (B) H82 cells were co-transfected with EGFP and Hsp72 vector (green), and samples assayed as described in Figure 2B. (C) H82 cells were co-transfected with EGFP, Hsp72 vector and empty vector or TAp73β. Samples were treated, stained and assayed as described in Figure 2D. Figures are mean ± S.D. of three independent experiments, where *P < 0.05, **P < 0.01 and ***P < 0.001.
Mentions: Given that TAp73α is able to induce Hsp72 expression and that the anti-apoptotic activity of TAp73α seems to be dependent on this induction, and since it is known from before that the p73 isoforms can interact and regulate the activity of each other [16, 29], we sought to investigate whether the overexpression of Hsp72 could counteract the pro-apoptotic function of TAp73β upon drug-induced apoptosis. Transfection of H82 cells with Hsp72 vector lead to an enhanced expression of Hsp72 protein, as shown by immunoblot (Fig. 3A) and confocal imaging (Fig. 3B). Subsequent transfection of H82 cells with Hsp72 reduced the level of VP16-induced apoptosis (Fig. 3C, black and grey bars). Moreover, co-transfection of TAp73β together with Hsp72 abolished TAp73β pro-apoptotic effect upon VP16 treatment. Hence, TAp73β augmentation of drug-induced apoptosis can be repressed by simultaneous co-expression of Hsp72.

Bottom Line: However, the precise mechanism by which TAp73α exerts its pro-survival effect is yet unclear.Finally, we revealed that TAp73β counteracts the anti-apoptotic effect of TAp73α by preventing Hsp72 induction.Our results thus provide additional evidence for the potential oncogenic role of TAp73α, and extend the understanding of the mechanism for its anti-apoptotic effect.

View Article: PubMed Central - PubMed

Affiliation: Department of Oncology-Pathology, Cancer Centrum Karolinska, Karolinska Institutet, Stockholm, Sweden.

Show MeSH
Related in: MedlinePlus