Association of Galectin-3 but not Laminin in Tamoxifen-Induced Growth Suppression in Breast Cancer MCF-7 Cells

Authors: Raychoudhury S* , Segree A , Flemmings S and Nagdas S

DOI: 10.23880/ijbp-16000267

Volume 10, Issue 2

Abstract

Tamoxifen (TAM), a selective estrogen receptor modulator, competes with estrogen for binding to estrogen receptor (ER) sites, thereby inhibiting estrogen-induced proliferation in ER-positive breast cancer cells. However, long-term treatment with TAM often leads to resistance, and its mechanisms, particularly involving biochemical markers, remain unclear. This study investigated the effects of TAM (10⁻⁶ M and 10⁻⁸ M) compared to 17β-estradiol (10⁻⁶ M and 10⁻⁸ M) on galectin-3 and laminin expressions in ER-positive MCF-7 breast cancer cells. The MTT assays showed that 10⁻⁶ M TAM significantly reduced cell viability and altered cellular morphology. Indirect immunofluorescence microscopy revealed that galectin-3 was present on the cell surface and in the nucleus; however, its localization was diminished after 48 hours of TAM (10⁻⁶ M) exposure. Western blot analysis showed no change in galectin-3 expression at 24 hours but a significant reduction at 48 and 72 hours. In contrast, laminin expression remained unchanged. ELISA results further confirmed reduced galectin-3 but not laminin levels after 48 hours of TAM treatment. These findings suggest that galectin-3, but not laminin, is involved in TAM-induced suppression of MCF-7 cell growth and may serve as a biochemical marker for TAM responsiveness.

Keywords: MCF-7 Cells; Western Blot; Fluorescence Microscopy; Galectin-3, Laminin

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