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RSK3 switches cell fate: from stress-induced senescence to malignant progression

ABSTRACT: RSK3 switches cell fate: from stress-induced senescence to malignant progression

PROVIDER: PRJNA1017821 | ENA |

REPOSITORIES: ENA

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RSK3 switches cell fate: from stress-induced senescence to malignant progression

Project description:TGFβ signaling induces several cell phenotypes including cellular senescence, a stable form of cell cycle arrest accompanied by a secretory program, and epithelial-mesenchymal transition (EMT) in normal epithelial cells. During carcinogenesis cells lose the ability to undergo senescence in response to TGFβ but they maintain an EMT, which can contribute to tumor progression and resistance. A screen with active kinases in HMECs upon TGFβ treatment identified that the serine threonine kinase RSK3, or RPS6KA2, reverted TGFβ-induced senescence. Interestingly, RSK3 expression decreased in response to TGFβ in a SMAD3-dependent manner, and its constitutive expression rescued SMAD3-induced premature senescence, indicating that decrease of RSK3 itself contributes to TGFβ-induced senescence. Mechanistically, using transcriptomic analyses and affinity purification coupled to mass spectrometry-based proteomics, we unveiled that RSK3 regulates senescence by inhibiting NF-κΒ pathway through the decrease in proteasome-mediated IκBα degradation. Strikingly, senescent TGFβ-treated HMEC display features of epithelial to mesenchymal transition (EMT) and during RSK3-induced senescence escape HMEC conserve EMT features. Importantly, RSK3 expression correlates with EMT and invasion, and anti-correlates with senescence and NF-κΒ in human claudin-low breast tumors and its expression accelerates formation of breast invasive tumors in the mouse mammary gland. We conclude that RSK3 switches cell fate from senescence to malignancy in response to TGFβ signals.

2023-10-01 | GSE243320 | GEO

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Sirt6 attenuates chondrocyte senescence and osteoarthritis progression

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CD146 accelerates malignant progression of phyllodes tumor cells

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CD146 accelerates malignant progression of phyllodes tumor cells

Project description:Breast malignant phyllodes tumors (PTs) are rapid-progressing tumors, known to lack effective treatment and suitable prognostic markers as well as elaborate studies. Herein,we found that level of CD146 is progressively elevated with malignant progression of PTs and is an independent predictor for prognosis of PT patients.Mechanistically, CD146 activates the PI3K/AKT signaling pathway, thereby enhancing malignant behaviors of PT cells.This study unveils a CD146-PI3K/AKT axis in modulating the malignant progression of PTs, and open avenues to develop a novel target for precise prognosis and treatment for breast malignant PTs.

2023-12-01 | GSE227380 | GEO

The extent of liver injury determines hepatocyte fate toward senescence or cancer

Project description:Induction of hepatocyte senescence is known to inhibit hepatocellular carcinoma (HCC). Until now, it has not been clear how the degree of liver injury dictates hepatocyte senescence and carcinogenesis. In this study, we investigated whether the severity of injury determines cell fate decisions between hepatocyte senescence and carcinogenesis. After testing of different degrees of liver injury, we found that hepatocyte senescence is strongly induced in the setting of severe acute liver injury. Longer-term, moderate liver injury did not result into hepatocyte senescence, but instead led to a significant incidence of HCC. In addition, carcinogenesis was significantly reduced by the induction of severe acute injury after chronic moderate liver injury. We conclude that severe acute liver injury leads to hepatocyte senescence along with a low incidence of HCC, whereas chronic moderate injury allows hepatocytes to proliferate rather than to enter into senescence, and correlates with a high incidence of HCC. This study improves our understanding in hepatocyte cell fate decisions and suggests a potential clinical strategy to induce senescence to treat HCC.

2018-12-20 | GSE108328 | GEO

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