The investigation of tumor microenvironment (TME) is essential to better characterize the complex cellular crosstalk and to identify important immunological phenotypes and biomarkers. The niche is a crucial contributor to neoplasm initiation, maintenance and progression. Therefore, a deeper analysis of tumor surroundings could improve cancer diagnosis, prognosis and assertive treatment. Thus, the WNT family exerts a critical action in tumorigenesis of different types of neoplasms due to dysregulations in the TME. WNT5A, an evolutionary WNT member, is involved in several cellular and physiopathological processes, in addition to tissue homeostasis. The WNT5A protein exerts paradoxical effects while acting as both an oncogene or tumor suppressor by regulating several non-canonical signaling pathways, and consequently interfering in cell growth, cytoskeletal remodeling, migration and invasiveness. This review focuses on a thorough characterization of the role of WNT5A in neoplastic transformation and progression, which may help to understand the prognostic potentiality of WNT5A and its features as a therapeutic target in several cancers. Additionally, we herein summarized novel findings on the mechanisms by which WNT5A might favor tumorigenesis or suppression of cancer progression and discussed the recently developed treatment strategies using WNT5A as a protagonist.
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http://dx.doi.org/10.1016/j.biopha.2022.113599 | DOI Listing |
Osteoarthr Cartil Open
March 2025
Université de Lorraine, CNRS (French National Centre for Scientific Research), IMoPA (Molecular Engineering and Articular Physiopathology), F-54000, Nancy, France.
Objective: Osteoarthritis (OA) is the most common form of chronic joint disease, affecting mainly the elderly population. This disorder is caused by cartilage degeneration with complex changes in the chondrocyte phenotype. Inorganic pyrophosphate (PPi) was shown to counteract the detrimental effect of interleukin (IL)-1β challenging in an in vitro OA model based on rat articular chondrocytes.
View Article and Find Full Text PDFCell Genom
January 2025
National Clinical Research Center for Obstetric & Gynecologic Diseases, Department of Obstetrics and Gynecology, Peking Union Medical College Hospital, Chinese Academy of Medical Sciences & Peking Union Medical College, Beijing 100730, China. Electronic address:
Endometriosis is a chronic condition with limited therapeutic options. The molecular aberrations promoting ectopic attachment and interactions with the local microenvironment sustaining lesion growth have been unclear, prohibiting development of targeted therapies. Here, we performed single-cell and spatial transcriptomic profiling of ectopic lesions and eutopic endometrium in endometriosis.
View Article and Find Full Text PDFMol Carcinog
January 2025
Department of Thoracic Oncology Surgery, Clinical Oncology School of Fujian Medical University, Fujian Cancer Hospital, Fuzhou, China.
A-to-I RNA editing is a pervasive mechanism in the human genome that affects the regulation of gene expression and is closely associated with the pathogenesis of numerous diseases. This study elucidates the regulatory mechanism of A-to-I edited miR-1304-3p in esophageal squamous cell carcinoma (ESCC). Western blot, immunohistochemistry, and RT-qPCR assays were employed to quantify protein and mRNA expression.
View Article and Find Full Text PDFiScience
December 2024
Anhui Province Key Laboratory of Basic and Translational Research of Inflammation-related Diseases, Bengbu, China.
Curr Pharm Des
January 2025
Hubei Key Laboratory of Tumor Microenvironment and Immunotherapy, China Three Gorges University, Yichang, Hubei, China.
Background: The Prickle2 (Pk2) gene shows promising potential in uncovering the underlying causes of epilepsy, a neurological disorder that is currently not well understood. This paper utilizes the online tool PubMed to gather and condense information on the involvement of PCP channels and the associated roles of PCP pathway molecules in the onset of epilepsy. These findings are significant for advancing epilepsy treatment.
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