ArticleBMC cancer2016
The deficiency of galectin-3 in stromal cells leads to enhanced tumor growth and bone marrow metastasis.
Article in BMC cancer, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 9 papers.
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Who cites it
9 citing papers in PubMed, 18 citations in OpenAlex.
- Revisiting Multi-Omics Data to Unravel Galectins as Prognostic Factors in Head and Neck Squamous Cell Carcinoma.Biomedicines · 2024Article
- The Expression of Galectin-3 in Tumor and Cancer-Associated Fibroblasts in Invasive Micropapillary Breast Carcinomas: Relationship with Clinicopathologic Parameters.European journal of breast health · 2021Article
- Galectins in Cancer and the Microenvironment: Functional Roles, Therapeutic Developments, and Perspectives.Biomedicines · 2021Review
- Elevated Soluble Galectin-3 as a Marker of Chemotherapy Efficacy in Breast Cancer Patients: A Prospective Study.International journal of breast cancer · 2020Article
- Characterization of Cancer-Induced Nociception in a Murine Model of Breast Carcinoma.Cellular and molecular neurobiology · 2019Article
- Galectin-3 Regulates the Expression of Tumor Glycosaminoglycans and Increases the Metastatic Potential of Breast Cancer.Journal of oncology · 2019Article
- Silencing TRIM37 inhibits the proliferation and migration of non-small cell lung cancer cells.RSC advances · 2018Article
- Pro-tumoral immune cell alterations in wild type andOncotarget · 2018Article
- Pediatric Ependymoma: A Proteomics Perspective.Cancer genomics & proteomicsArticle
Corrections and comments
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Authors and funding
8 authors at 4 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
backgroundGalectin-3 is a multifunctional β-galactoside-binding lectin that once synthesized, is expressed in the nucleus, cytoplasm, cell surface and in the extracellular environment. Because of its unique structure, galectin-3 can oligomerize forming lattice upon binding to multivalent oligossacharides and influence several pathologic events such as tumorigenesis, invasion and metastasis.
methodsIn our study, balb/c Lgals3+/+ and Lgals3-/- female mice were inoculated in the fourth mammary fat pad with 4T1 breast cancer cell line. The primary tumor, inguinal lymph nodes and iliac bone marrow were evaluated 15, 21 and 28 days post-injection. The primary tumor growth was evaluated by measuring the external diameter, internal growth by ultrasound and weight of the excised tumor. The presence of cancer cells in the draining lymph nodes and iliac crest bone marrow were performed by immunohistochemistry, PCR and clonogenic metastatic assay.
resultsIn this study we demonstrated that the deletion of galectin-3 in the host affected drastically the in vivo growth rate of 4T1 tumors. The primary tumors in Lgals3-/- mice displayed a higher proliferative rate (p < 0,05), an increased necrotic area (p < 0,01) and new blood vessels with a wider lumen in comparison with tumors from Lgals3+/+ mice (P < 0,05). Moreover, we detected a higher number of 4T1-derived metastatic colonies in the lymph nodes and the bone marrow of Lgals3-/- mice (p < 0,05). Additionally, healthy Lgals3-/- control mice presented an altered spatial distribution of CXCL12 in the bone marrow, which may explain at least in part the initial colonization of this organ in Lgals3-/- injected with 4T1 cells.
conclusionsTaken together, our results demonstrate for the first time that the absence of galectin-3 in the host microenvironment favors the growth of the primary tumors, the metastatic spread to the inguinal lymph nodes and bone marrow colonization by metastatic 4T1 tumor cells.
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