Background: Breast cancer, a malignant tumor with its highest incidence in women, affects physical and mental health, and can even be life-threatening. In recent years, its incidence has continued to grow, accompanied by a trend of younger onset. XRCC1  is well known as a DNA-repair gene, and its abnormal expression is related to the occurrence of various malignant tumors. 
Methods: In this study, we detected XRCC1  expression and investigated its association with the XRCC1  rs1799782 polymorphism. XRCC1  was overexpressed to investigate its effect on in breast cancer cells. CCK8 and clone formation efficiency assay were used to detect cell proliferation. Transwell assay was performed to confirm cell migration and invasion. Flow cytometry was used to detect cell apoptosis. 
Results: In 118 breast cancer samples, CC genotype frequency was 49.15% (58 of 118), CT genotype frequency was 42.37% (50 of 118), and TT genotype frequency was 8.48% (ten of 118). Lymphatic metastasis was associated with a higher frequency of XRCC1  rs1799782 polymorphism (P <0.05), and breast cancer patients with positive PR, HER2, and negative ER had high XRCC1  rs1799782 frequency (P <0.05). Meanwhile, XRCC1  had low expression in breast cancer (74.6%, 88 of 118) and high expression in ER-negative, PR-negative, HER2-positive and Ki67-low-expression patients. XRCC1  rs1799782 may play an important role in the development and metastasis of breast cancer. These results differ from previous studies that did not suggest that rs1799782 is effective in breast cancer. We also investigated the role of XRCC1  in breast cancer progression. 
Conclusion: We have proved that XRCC1  can inhibit proliferation and invasion and promote apoptosis of breast cancer cells. XRCC1  expression was regulated by the JNK pathway. We found that the JNK inhibitor SP600125 significantly inhibited the growth of breast cancer cells, and consider it a potential drug for breast cancer.
Keywords: MCF7, gene expression, proliferation, apoptosis, JNK pathway