We show mTORC3’s tumorigenicity in a rhabdomyosarcoma mouse model in which transgenic ETV7 expression accelerates tumor onset and promotes tumor penetrance. Discovery of mTORC3 represents an mTOR paradigm shift and identifies a novel target for …

Furthermore, mTORC3 includes ETS transcription factor ETV7, which is crucial for the binding of mTOR and plays an essential role in the assembly of mTORC3 within the cytoplasm . It has been noted that mTORC3 is robustly activated in cancer. The loss of mTORC3 expression in cancer cells has displayed marked sensitivity to rapamycin.

Oct 2, 2023 · Harwood et al. have identified another rapamycin-insensitive complex known as mTORC3. The E26 transformation-specific transcription factor ETV7 was found to interact with mTOR in the cytoplasmic...

Tumor cells that assemble mTORC3 have a proliferative advantage and become resistant to rapamycin, indicating that inhibiting mTORC3 may have a therapeutic impact on cancer. Here, we investigate which domains or amino acid residues of ETV7 and …

Sep 12, 2018 · We show mTORC3's tumorigenicity in a rhabdomyosarcoma mouse model in which transgenic ETV7 expression accelerates tumor onset and promotes tumor penetrance. Discovery of mTORC3 represents an mTOR paradigm shift and identifies a novel target for anticancer drug development.

Jan 27, 2024 · Our laboratory recently discovered a new mTOR complex, called mTORC3, distinct from the two canonical mTOR complexes, mTORC1, and mTORC2, which causes accelerated proliferation and increased malignancy of cancer cells. Understanding how mTORC3 is controlled is an important approach to designing cancer therapies targeting mTORC3.

Sep 12, 2018 · Geneticists discovered that mTORC3 aids cancers' resistance to rapamycin and related drugs, offering the promise of new drug therapies to treat cancers.

Jul 5, 2019 · As a core component of several distinct complexes including mTOR complex 1 (mTORC1), mTOR complex 2 (mTORC2), and a putative mTOR complex 3 (mTORC3), mTOR has critical roles in diverse biological processes, such as cell proliferation, survival, autophagy, metabolism, and immunity [2, 3].

Despite these insights, the full mechanism of action of rapamycin remained elusive until 1994, when biochemical studies identified the mechanistic (formerly “mammalian”) target of rapamycin (mTOR) as the direct target of the rapamycin-FKBP12 complex in mammals (Brown et al., 1994; Sabatini et al., 1994; Sabers et al., 1995) and revealed it to be the homolog of the yeast TOR/DRR genes that ...

We show mTORC3’s tumorigenicity in a rhabdomyosarcoma mouse model in which transgenic ETV7 expression accelerates tumor onset and promotes tumor penetrance.