Gene interactions and pathways from curated databases and text-mining
Cancer Lett 2013, PMID: 23528835

Sustained overexpression of Redd1 leads to Akt activation involved in cell survival.

Jin, Hyeon-Ok; Hong, Sung-Eun; Kim, Jae-Hee; Choi, Ha-Na; Kim, Karam; An, Sungkwan; Choe, Tae-Boo; Hwang, Chang-Sun; Lee, Jae-Ho; Kim, Jong-Il; Kim, Hyun-Ah; Kim, Eun-Kyu; Noh, Woo Chul; Hong, Young-Joon; Hong, Seok-Il; Lee, Jin Kyung; Park, In-Chul

Herein, we show that the constitutive overexpression of Redd1, a negative regulator of mTORC1, induces Akt activation in lung cancer cells. Akt phosphorylation was reduced to basal levels by Rictor siRNA, suggesting the involvement of mTORC2 in this process. Perifosine and PP242, selective inhibitors of Akt and mTORC1/2, respectively, efficiently suppressed the Akt phosphorylation that was induced by the sustained overexpression of Redd1 and increased the sensitivity of the cells to cisplatin. Therefore, the sustained overexpression of Redd1 leads to mTORC1 inhibition and to consequent Akt activation that is involved in cell survival. This finding highlights the importance of Akt activation as a therapeutic target to overcome resistance to chemotherapy.

Diseases/Pathways annotated by Medline MESH: Lung Neoplasms
Document information provided by NCBI PubMed

Text Mining Data

Akt ⊣ Redd1: " Sustained overexpression of Redd1 leads to Akt activation involved in cell survival "

Redd1 ⊣ Akt: " Herein, we show that the constitutive overexpression of Redd1 , a negative regulator of mTORC1, induces Akt activation in lung cancer cells "

mTORC1 — Redd1: " Herein, we show that the constitutive overexpression of Redd1 , a negative regulator of mTORC1 , induces Akt activation in lung cancer cells "

Akt ⊣ Redd1: " Perifosine and PP242, selective inhibitors of Akt and mTORC1/2, respectively, efficiently suppressed the Akt phosphorylation that was induced by the sustained overexpression of Redd1 and increased the sensitivity of the cells to cisplatin "

Akt ⊣ Redd1: " Therefore, the sustained overexpression of Redd1 leads to mTORC1 inhibition and to consequent Akt activation that is involved in cell survival "

mTORC1 → Redd1: " Therefore, the sustained overexpression of Redd1 leads to mTORC1 inhibition and to consequent Akt activation that is involved in cell survival "

Manually curated Databases

No curated data.