INPP4B acts as a tumor suppressor in various epithelial cancers by inhibiting PI3K/Akt signaling. Unexpectedly, tumor-promoting features of INPP4B in leukemia and breast cancer have been recently uncovered. In this spotlight, we discuss the seemingly paradoxical nature of INPP4B-mediated signaling in cancer.
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http://dx.doi.org/10.1016/j.molmed.2015.06.006 | DOI Listing |
Cell Commun Signal
January 2025
Department of General Biochemistry, Faculty of Biochemistry, Biophysics and Biotechnology, Jagiellonian University, Krakow, Poland.
The RNase activity of MCPIP1 is essential for regulating cellular homeostasis, proliferation, and tumorigenesis. Our study elucidates the effects of downregulation of MCPIP1 expression and an RNase-inactivating mutation (D141N) on normal epithelial kidney cells, indicating that MCPIP1 expression is a key factor that suppresses neoplastic transformation. We observed that either expression downregulation or mutation of MCPIP1 significantly increased its clonogenicity and altered the expression of cancer stem cell (CSC) markers and factors involved in epithelial-to-mesenchymal transition (EMT).
View Article and Find Full Text PDFJ Transl Med
January 2025
School of Medicine, Shanghai Baoshan Luodian Hospital, Shanghai University, Shanghai, 201908, China.
This review seeks to elucidate the therapeutic potential of tumor necrosis factor receptor 1 (TNFR1) and enhance our comprehension of its role in disease mechanisms. As a critical cell-surface receptor, TNFR1 regulates key signaling pathways, such as nuclear factor kappa-B (NF-κB) and mitogen-activated protein kinase (MAPK), which are associated with pro-inflammatory responses and cell death. The intricate regulatory mechanisms of TNFR1 signaling and its involvement in various diseases, including inflammatory disorders, infectious diseases, cancer, and metabolic syndromes, have attracted increasing scholarly attention.
View Article and Find Full Text PDFCell Commun Signal
January 2025
Digestive Disease Center, The First Affiliated Hospital of Jiamusi University, Jiamusi, Heilongjiang Province, 154000, China.
Background: Programmed cell death ligand 1 (PD-L1) expression on immune cells is correlated with the efficacy of immune checkpoint inhibitor (ICI) therapy in various types of cancer. Platelets are important components of the tumour microenvironment (TME) and are widely involved in the development of many types of cancer including colorectal cancer (CRC). However, the role of PD-L1 positive platelets in ICI therapy for CRC remains unknown.
View Article and Find Full Text PDFBMC Cancer
January 2025
Department of Otorhinolaryngology, Shenzhen Key Laboratory of Otorhinolaryngology, Longgang Otorhinolaryngology Hospital, Shenzhen Institute of Otorhinolaryngology, No. 3004 Longgang Avenue, Shenzhen, Guangdong, China.
Background: To investigate the role of the translocase of the outer mitochondrial membrane 40 (TOM40) in oral squamous cell carcinoma (OSCC) with the aim of identifying new biomarkers or potential therapeutic targets.
Methods: TOM40 expression level in OSCC was evaluated using datasets downloaded from The Cancer Genome Atlas (TCGA), as well as clinical data. The correlation between TOM40 expression level and the clinicopathological parameters and survival were analyzed in TCGA.
Nat Med
January 2025
Department of Hematology/Oncology, Cell and Gene Therapy, Scientific Institute for Research, Hospitalization and Healthcare (IRCCS), Bambino Gesù Children's Hospital, Rome, Italy.
Allogeneic chimeric antigen receptor (CAR) T cells targeting disialoganglioside-GD2 (ALLO_GD2-CART01) could be a therapeutic option for patients with relapsed or refractory, high-risk neuroblastoma (r/r HR-NB) whose tumors did not respond to autologous GD2-CART01 or who have profound lymphopenia. We present a case series of five children with HR-NB refractory to more than three different lines of therapy who received ALLO_GD2-CART01 in a hospital exemption setting. Four of them had previously received allogeneic hematopoietic stem cell transplantation.
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