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- Neurons in ALS patients often degenerate due to the buildup of misfolded proteins, with heat shock proteins (HSPs) playing a key role in managing protein health.
- Recent findings link mutations in a gene encoding an HSP co-chaperone to rare ALS forms, highlighting unclear disease mechanisms.
- Research shows that mutations lead to impaired RNA metabolism in motor neurons and increased vulnerability to stress, while boosting HSF1 expression could protect these neurons and could offer a potential ALS treatment approach.
HSF1 is a prognostic determinant and therapeutic target in intrahepatic cholangiocarcinoma.
J Exp Clin Cancer Res
September 2024
Department of Medicine, Surgery, and Pharmacy, University of Sassari, via P. Manzella 4, Sassari, 07100, Italy.
Article Synopsis
- Intrahepatic cholangiocarcinoma (iCCA) is a highly aggressive liver cancer with poor treatment options, prompting research into new therapies targeting the Heat Shock Factor 1 (HSF1) transcription factor.
- Studies showed that HSF1 levels are significantly elevated in various stages of iCCA and correlate with worse patient outcomes, while inhibiting HSF1 delayed tumor development in mouse models.
- The HSF1 inhibitor KRIBB-11 was effective in slowing iCCA cell growth, inducing cell death, and reducing key metabolic functions in cancer cells, highlighting its potential as a therapeutic avenue.
HSF1 renders NK cells too stressed to respond.
Nat Cell Biol
October 2024
Department of Biomolecular Sciences, The Weizmann Institute of Science, Rehovot, Israel.
Mint3-depletion-induced energy stress sensitizes triple-negative breast cancer to chemotherapy via HSF1 inactivation.
Cell Death Dis
December 2023
Department of Cancer Biology, Institute of Biomedical Science, Kansai Medical University, Osaka, Japan.
Given the lack of therapeutic targets, the conventional approach for managing triple-negative breast cancer (TNBC) involves the utilization of cytotoxic chemotherapeutic agents. However, most TNBCs acquire resistance to chemotherapy, thereby lowering the therapeutic outcome. In addition to oncogenic mutations in TNBC, microenvironment-induced mechanisms render chemoresistance more complex and robust in vivo.
View Article and Find Full Text PDFHsf1 and the molecular chaperone Hsp90 support a 'rewiring stress response' leading to an adaptive cell size increase in chronic stress.
Elife
December 2023
Département de Biologie Moléculaire et Cellulaire, Université de Genève, Genève, Switzerland.
Cells are exposed to a wide variety of internal and external stresses. Although many studies have focused on cellular responses to acute and severe stresses, little is known about how cellular systems adapt to sublethal chronic stresses. Using mammalian cells in culture, we discovered that they adapt to chronic mild stresses of up to two weeks, notably proteotoxic stresses such as heat, by increasing their size and translation, thereby scaling the amount of total protein.
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