Traditional wisdom suggests that galectins play pivotal roles at different steps in cancer progression. Galectins are particularly well known for their ability to increase the invasiveness of cancer cells and their resistance to drug-induced cell death. They also contribute to the development of local and systemic immunosuppression, allowing cancer cells to escape the host's immunological defense. This is particularly true in glioma, the most common primary intracranial tumor. Abnormally high production of extracellular galectins in glioma contributes to the establishment of a strong immunosuppressive environment that favors immune escape and tumor progression. Considering the recent development and success of immunotherapy in halting cancer progression, it is logical to foresee that galectin-specific drugs may help to improve the success rate of immunotherapy for glioma. This provides a new perspective to target galectins, whose intracellular roles in cancer progression have already been investigated thoroughly. In this review, we discuss the mechanisms of action of galectins at different steps of glioma progression and the potential of galectin-specific drugs for the treatment of glioma.
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http://dx.doi.org/10.3390/cancers13215533 | DOI Listing |
Discov Oncol
January 2025
Department of Clinical Laboratory, Laboratory Medicine Center, Zhejiang Provincial People's Hospital (Affiliated People's Hospital), Hangzhou Medical College, Hangzhou, Zhejiang, China.
Gastric cancer (GC), one of the most common and heterogeneous malignancies, is the second leading cause of cancer death worldwide and is closely related to dietary habits. Fatty acid is one of the main nutrients of human beings, which is closely related to diabetes, hypertension and other diseases. However, the correlation between fatty acid metabolism and the development and progression of GC remains largely unknown.
View Article and Find Full Text PDFSci Rep
January 2025
The Queen's Medical Center, 1301 Punchbowl Street, QET 4M, Honolulu, Hawai'i, 96813, USA.
High flow nasal cannula (HFNC) can reduce the need for intubation in patients with coronavirus disease-19 (COVID-19) pneumonia induced acute hypoxemic respiratory failure (AHRF), but predictors of HFNC success could be characterized better. C-reactive protein (CRP) and D-dimer are associated with COVID-19 severity and progression. However, no one has evaluated the use of serial CRP and D-dimer ratios to predict HFNC success.
View Article and Find Full Text PDFNaunyn Schmiedebergs Arch Pharmacol
January 2025
Department of Respiratory and Critical Care Medicine, Guangdong Provincial Hospital of Traditional Chinese Medicine, No. 111, Dade Road, Guangzhou, 510120, China.
Berberine (BBR) has been proved to inhibit the malignant progression of non-small cell lung cancer (NSCLC), but the underlying molecular mechanism still needs to be further revealed. NSCLC cells (A549 and H1299) were treated with BBR. CCK8 assay, colony formation assay, flow cytometry, TUNEL staining and transwell assay were used to examine cell proliferation, apoptosis and invasion.
View Article and Find Full Text PDFApoptosis
January 2025
Department of Pathology, Fudan University Shanghai Cancer Center, Shanghai, China.
Cancer-associated fibroblasts (CAFs) significantly influence tumor progression and therapeutic resistance in colorectal cancer (CRC). However, the distributions and functions of CAF subpopulations vary across the four consensus molecular subtypes (CMSs) of CRC. This study performed single-cell RNA and bulk RNA sequencing and revealed that myofibroblast-like CAFs (myCAFs), tumor-like CAFs (tCAFs), inflammatory CAFs (iCAFs), CXCL14CAFs, and MTCAFs are notably enriched in CMS4 compared with other CMSs of CRC.
View Article and Find Full Text PDFNPJ Precis Oncol
January 2025
Zentalis Pharmaceuticals, Inc., San Diego, CA, USA.
Upregulation of Cyclin E1 and subsequent activation of CDK2 accelerates cell cycle progression from G1 to S phase and is a common oncogenic driver in gynecological malignancies. WEE1 kinase counteracts the effects of Cyclin E1/CDK2 activation by regulating multiple cell cycle checkpoints. Here we characterized the relationship between Cyclin E1/CDK2 activation and sensitivity to the selective WEE1 inhibitor azenosertib.
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