Abstract
Breast cancer is the most common and deadliest cancer that affects females around the world. Triple‐negative breast cancer (TNBC) is a subtype of cancer characterized by the lack of progesterone, estrogen, and Her2 receptors expression. TNBC have the worst prognosis because of its elevated growth rate, limited options for treatment, rapid development of chemoresistance, and its high metastatic potential. Recent studies have correlated Shugoshin‐1 (SGO1) with epithelial‐to‐mesenchymal transition and tumor growth in cancer; however, none of the studies published so far were done in breast cancer. Therefore, we aimed to identify the role of SGO1 in tumor growth of TNBC. We hypothesize that tumor growth will be reduced in shSGO1, given its biological role in other cancers. To test our hypothesis, 2.5x106 MDA‐MB‐231 cell containing either shRNA Control or shRNA SGO1 were injected into female NSG mice that were 6‐8 weeks old. Tumors were allowed to growth for an 8‐weeks period. Following this timepoint, mice were sacrificed to harvest tumors (primary and secondary). Protein lysates were isolated from tumor samples and SGO1 depletion was characterized by Western blot. Tumors were measured, embedded in paraffin, sectioned, and stained with Hematoxylin and Eosin. A student t‐ test was used to evaluate statistical significance. Our results show that the average tumor size for shRNA Control group (n=10) was significantly higher than for shRNA SGO1 group (n=10) at any time point once the tumors were palpable. At the end‐point measurement the average tumor size for shRNA Control group was 848 mm3, while for shRNA SGO1 was 50 mm3. These results suggest that silencing SGO1 reduces tumor growth. Therefore, SGO1 may be a potential line of treatment for TNBC.
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