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首页> 外文期刊>Journal of Cellular Physiology >Involvement of Akt2/protein kinase B β (PKBβ) in the 8-Cl-cAMP-induced cancer cell growth inhibition
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Involvement of Akt2/protein kinase B β (PKBβ) in the 8-Cl-cAMP-induced cancer cell growth inhibition

机译：Akt2的参与/β蛋白激酶B (PKBβ)8-Cl-cAMP-induced癌症细胞生长抑制

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8-chloro-cyclic AMP (8-Cl-cAMP), which induces differentiation, growth inhibition, and apoptosis in various cancer cells, has been investigated as a putative anti-cancer drug. However, the exact mechanism of 8-Cl-cAMP functioning in cancer cells is not fully understood. Akt/protein kinase B (PKB) genes (Akt1, Akt2, and Akt3) encode enzymes belonging to the serine/threonine-specific protein kinase family. It has been suggested that Akt/PKB enhances cell survival by inhibiting apoptosis. Recently, we showed that 8-Cl-cAMP and 5-aminoimidazole-4-carboxamide ribonucleoside (AICAR) inhibited cancer cell growth through the activation of AMPK and p38 MAPK. Therefore, we anticipated that the phosphorylation of Akt/PKB would be decreased upon treatment with 8-Cl-cAMP. However, treatment with 8-Cl-cAMP and AICAR induced the phosphorylation of Akt/PKB, which was inhibited by ABT702 (an adenosine kinase inhibitor) and NBTI (an adenosine transporter inhibitor). Furthermore, whereas Compound C (an AMPK inhibitor), AMPK-DN (AMPK-dominant negative) mutant, and SB203580 (a p38 MAPK inhibitor) did not block the 8-Cl-cAMP-induced phosphorylation of Akt/PKB, TCN (an Akt1/2/3 specific inhibitor) and an Akt2/PKBβ-targeted siRNA inhibited the 8-Cl-cAMP- and AICAR-mediated phosphorylation of AMPK and p38 MAPK. TCN also reversed the growth inhibition mediated by 8-Cl-cAMP and AICAR. Moreover, an Akt1/PKBα-targeted siRNA did not reduce the phosphorylation of AMPK and p38 MAPK after treatment with 8-Cl-cAMP. These results suggest that Akt2/PKBβ activation promotes the phosphorylation of AMPK and p38 MAPK during the 8-Cl-cAMP- and AICAR-induced growth inhibition.
机译：8-chloro-cyclic AMP (8-Cl-cAMP),导致分化、生长抑制和凋亡在各种癌症细胞,被调查一个假定的抗癌药物。在癌症8-Cl-cAMP机制运作细胞并不完全理解。酶属于丝氨酸/ threonine-specific蛋白激酶家族。有人建议,Akt / PKB增强细胞生存通过抑制细胞凋亡。表明8-Cl-cAMP和5-aminoimidazole-4-carboxamide核糖核苷(爱卡)通过抑制癌细胞增长激活AMPK和p38 MAPK。一种蛋白激酶的磷酸化/ PKB预期会减少8-Cl-cAMP治疗。然而,治疗和8-Cl-cAMP爱卡诱导一种蛋白激酶的磷酸化/ PKB,抑制ABT702(腺苷酸激酶抑制剂)和NBTI(腺苷运输车抑制剂)。AMPK抑制剂),AMPK-DN (AMPK-dominant消极的)突变,SB203580 (p38 MAPK抑制剂)不阻止8-Cl-cAMP-induced磷酸化一种蛋白激酶/ PKB TCN (Akt1/2/3特定抑制剂)和一个Akt2 / PKBβ目标核抑制了8-Cl-cAMP——AICAR-mediated磷酸化AMPK和p38 MAPK。抑制由8-Cl-cAMP和爱卡。此外,一个Akt1 / PKBα目标核没有减少AMPK的磷酸化和p38 MAPK与8-Cl-cAMP治疗后。表明Akt2 / PKBβ激活促进AMPK和p38 MAPK的磷酸化8-Cl-cAMP——AICAR-induced抑制增长。

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