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Colorectal cancer (CRC) is the third most deadly cancer diagnosed in both men and women. 5-Fluorouracil (5-FU) treatment frequently causes the CRC cells to become chemoresistance, which has a negative impact on prognosis. Using bioinformatic techniques, this work describes important genes and biological pathways linked to 5-FU resistance in CRC cells.

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HSF1 at the crossroads of chemoresistance: from current insights to future horizons in cell death mechanisms.

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Department of Cell and Cancer Biology, College of Medicine and Life Sciences, The University of Toledo, Toledo, OH, United States.

Heat Shock Factor 1 (HSF1) is a major transcriptional factor regulating the heat shock response and has become a potential target for overcoming cancer chemoresistance. This review comprehensively examines HSF1's role in chemoresistance and its potential as a therapeutic target in cancer. We explore the complex, intricate mechanism that regulates the activation of HSF1, HSF1's function in promoting resistance to chemotherapy, and the strategies used to manipulate HSF1 for therapeutic benefit.

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Gliomas constitute the most prevalent primary central nervous system tumors, often characterized by complex metabolic profile, genomic instability, and aggressiveness, leading to frequent relapse and high mortality rates. Traditional treatments are commonly ineffective because of gliomas increased heterogeneity, invasive characteristics and resistance to chemotherapy. Among several pathways affecting cellular homeostasis, cuproptosis has recently emerged as a novel type of programmed cell death, triggered by accumulation of copper ions.

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Bisecting GlcNAc modification of vesicular GAS6 regulates CAFs activation and breast cancer metastasis.

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Key Laboratory of Resource Biology and Biotechnology in Western China, Ministry of Education, Provincial Key Laboratory of Biotechnology, College of Life Sciences, Northwest University, 229 Taibai North Road, Xi'an, Shaanxi, 710069, P. R. China.

Background: Cancer-associated fibroblasts (CAFs) are a pivotal component of the tumor microenvironment (TME), playing key roles in tumor initiation, metastasis, and chemoresistance. While glycosylation is known to regulate various cellular processes, its impact on CAFs activation remains insufficiently explored.

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