Publications by authors named "C Lodillinsky"
RSK3 switches cell fate: from stress-induced senescence to malignant progression.
J Exp Clin Cancer Res
November 2023
Background: TGFβ induces several cell phenotypes including senescence, a stable 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. Our aim was to identify mechanisms promoting TGFβ-induced senescence escape.
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- Some changes in the nuclear envelope (the outer layer of the cell's nucleus) can lead to diseases like muscular dystrophies and speed up aging.
- This study shows that if the nuclear envelope gets damaged, it can harm DNA and make non-cancerous cells stop growing and help cancer cells become more invasive.
- The researchers found that a special enzyme called TREX1 moves into the nucleus when the envelope breaks, causing the DNA damage that can spread cancer in crowded areas in the body.
Article Synopsis
- MT1-MMP helps breast cancers spread by breaking down the extracellular matrix, while NME1/NM23-H1 is a metastasis suppressor whose role in local invasion isn't fully understood.
- NME1 levels are higher in early-stage DCIS but drop in more invasive tumor types, and there's an inverse relationship between NME1 and MT1-MMP levels in aggressive breast cancer cases.
- Blocking NME1 function accelerates tumor invasiveness by increasing MT1-MMP on the cell surface, enhancing ECM degradation and boosting the invasive capabilities of breast cancer cells.
Bladder cancer (BC) is the ninth most common cancer worldwide, but molecular changes are still under study. During tumor progression, Epithelial cadherin (E-cadherin) expression is altered and β-catenin may be translocated to the nucleus, where it acts as co-transcription factor of tumor invasion associated genes. This investigation further characterizes E-cadherin and β-catenin associated changes in BC, by combining bioinformatics, an experimental murine cell model (MB49/MB49-I) and human BC samples.
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- - The study investigates the relationship between inducible nitric oxide synthase (iNOS) expression and immunosuppressive protein S100A9 in human bladder cancer (BC), finding both proteins linked to poor prognosis and BCG treatment failure.
- - In a mouse model of bladder cancer, iNOS and S100A9 were also expressed, leading to an immunosuppressive environment, with fewer cytotoxic immune cells and more suppressor cells observed in tumor-bearing mice.
- - Combining BCG treatment with the nitric oxide inhibitor l-NAME showed enhanced tumor control by further reducing tumor growth and improving the immune response, increasing cytotoxic cells while decreasing suppressor cells compared to BCG treatment alone.