Knockdown of SASS6 reduces growth of MDA-MB-231 triple-negative breast cancer cells through arrest of the cell cycle at the G2/M phase

Spindle assembly abnormal protein 6 homolog (SASS6) is crucial for centriole duplication; however, the role of SASS6 in the proliferation of cancer cells remains unclear. In the present study, the expression and functional role of SASS6 in triple negative breast cancer (TNBC) was assessed. Immunohistochemical staining was performed using an anti-SASS6 antibody in TNBC and normal tissues. Lentivirus-mediated RNA interference was used to knockdown SASS6 in MDA-MB-231 TNBC cells. Cell viability was determined using an MTT assay, and cell cycle distribution and apoptosis were measured using flow cytometry. Additionally, PathScan intracellular signaling arrays were used to detect the presence of intracellular signaling molecules. The results revealed that SASS6 expression was increased in TNBC tissues compared with the control tissue. Moreover, SASS6 knockdown significantly suppressed the growth of MDA-MB-231 cells. MDA-MB-231 cell cycle progression was arrested at the G2/M phase and cyclin dependent kinase 1 (CDK1), cyclin B1 and PCNA expression in MDA-MB-231 cells was decreased following SASS6 knockdown. Furthermore, the phosphorylation of STAT3, BAD and rpS6 was reduced following SASS6 knockdown. A strong correlation between SASS6 and CDK1 expression was observed in TNBC tissues based on immunohistochemical staining analysis (R=0.989; P<0.001). In conclusion, the present study revealed the crucial role of SASS6 in promoting MDA-MB-231 cell growth, regulating cell cycle progression and its ability to downregulate the CDK1/cyclin B1 signaling pathway, thus highlighting the potential of SASS6 as a therapeutic target for treatment of TNBC, and merits further investigation in animal models or in preclinical and clinical studies.

Automated summary

The present study demonstrated the important role of SASS6 in promoting MDA-MB-231 cell growth, regulating cell cycle progression, and downregulating the CDK1/cyclin B1 signaling pathway in TNBC. SASS6 knockdown resulted in inhibited cell growth, G2/M phase arrest, and decreased expression of key cell cycle regulators and signaling molecules. These findings suggest the potential therapeutic target of SASS6 in TNBC treatment, warranting further investigation in preclinical and clinical studies.