Mouse Anti-Human LGALS3 Hybridoma [II28-5]

Lung cancer is one of the leading causes of cancer-related mortality worldwide. MicroRNAs (miRNAs) are endogenous non-coding small RNAs that repress the expression of a broad array of target genes. Many efforts have been made to therapeutically target miRNAs in lung cancer treatments. In the present study, we revealed that low miR-548c expression in lung cancer was correlated with poorer prognosis in patients with lung cancer; miR-548c could inhibit lung cancer cell viability and proliferation. Moreover, miR-548c inhibited LGALS3 and TLR-4 expression through direct targeting; LGALS3 acted as a ceRNA to modulate TLR-4 expression by sponging miR-548c expression. Through miR-548c suppression of Galectin-3 and TLR-4, miR-548c exerted its inhibitory effect on lung cancer cells. What's more, Galectin-3-mediated TLR-4 signaling activation was involved in miR-548c regulation of lung cancer cell proliferation. Taken together, this miR-548c/Galectin-3/TLR-4 axis might represent an attractive target for the treatment of lung cancer.

Purpose Galectin-3 is a M-r 31,000 protein that belongs to a family of carbohydrate-binding proteins. Galectin-3 has already been associated with protection against apoptosis through cell to cell or cell to matrix adhesion processes. It seems that galectin-3 plays an important role in tumor progression, cell growth, invasion and metastasis. Galectin-3 is the only member of the chimeric galectins that has an N-terminal glycine and proline domain and a C-terminal carbohydrate recognition domain that allows galectin-3 to accommodate larger structures such us polylactosaminoglycans and intervene to DNA damage repair process. In this systematic review, our primary goal is to identify the effect of galectin-3 expression in association with drug resistance and apoptosis inhibition in breast cancer. Materials and methods Scopus and PubMed databases were searched on 26 November 2018 using the following combination of keywords: (galectin-3 OR gal-3 OR LGALS3) AND (breast cancer) AND (chemoresistance OR (drug resistance) OR chemosensitivity). All the articles in English, regardless the time of publication, text availability and species included were initially accepted. Results In the majority of the included studies, the expression of galectin-3 had a protective role in cell survival via different pathways such as the response to DNA damage and repair or the inhibition of apoptosis after treatment with a chemotherapeutic agent. Conclusion Galectin-3 expression in breast tumors might be an important factor in the selection of the most suitable treatment.