Objective Ovarian cancer is one of the leading causes of mortality in patients with malignant gynecological tumors. After surgical intervention for ovarian cancer, cisplatin(DDP)-based chemotherapy is the first-line treatment. However, a major challenge to treating ovarian cancer is the development of chemoresistance. Thus, the first aim of this study was to determine whether low-dose radiation could enhance the susceptibility of resistant ovarian cancer cells to DDP. The second aim was to provide new strategies for treating DDP-resistant ovarian cancer by examining its mechanism.Methods A cell counting kit-8(CCK8) assay was performed to measure cell proliferation. Flow cytometry was utilized to quantify the apoptosis of DDP-resistant ovarian cancer cells(SKOV3/DDP) using Annexin V and propidium iodide staining. Real-time quantitative(q PCR) was used to analyze the messenger RNA(m RNA) expression levels of excision repair cross complementing-group 1(ERCC1) and B-cell lymphoma 2(Bcl-2) in SKOV3/DDP.Results The IC_(50) values of the control, conventional-dose, and low-dose groups were 9.367 ± 0.16, 9.289 ± 0.16, and 3.847 ± 0.15, respectively(P < 0.05 vs control group and conventional-dose group). Compared with the control and conventional-dose groups, low-dose radiation resulted in significantly more apoptosis, as detected by flow cytometry(P < 0.05). The relative m RNA expression of ERCC1 and Bcl-2 in the low-dose group was significantly lower than that in the control group and conventional-dose group(P < 0.05). Conclusion Low-dose radiation enhanced the sensitivity of resistant ovarian cancer cells to DDP, possibly by decreasing the DNA repair capacity of tumor cells and promoting apoptosis. Objective Ovarian cancer is one of the leading causes of mortality in patients with malignant gynecological tumors. After surgical intervention for ovarian cancer, cisplatin (DDP) -based chemotherapy is the first-line treatment. However, a major challenge to treating ovarian cancer is the development of chemoresistance. Thus, the first aim of this study was to determine low-dose radiation could enhance the susceptibility of resistant ovarian cancer cells to DDP. The second aim was to provide new strategies for treating DDP-resistant ovarian cancer by examining its Mechanism. Methods A cell counting kit-8 (CCK8) assay was performed to measure cell proliferation. Flow cytometry was utilized to quantify the apoptosis of DDP-resistant ovarian cancer cells (SKOV3 / DDP) using Annexin V and propidium iodide staining. time quantitative (q PCR) was used to analyze the messenger RNA (m RNA) expression levels of excision repair cross complementing-group 1 (ERCC1) and B-cell lymphoma 2 (Bcl-2) in SKOV3 / DDP.Results The IC 50 values ​​of the control, conventional-dose, and low-dose groups were 9.367 ± 0.16, 9.289 ± 0.16, and 3.847 ± 0.15, respectively (P <0.05 vs. control group and conventional- dose group. Compared with the control and conventional-dose groups, low-dose radiation resulted in significantly more apoptosis, as detected by flow cytometry (P <0.05). The relative m RNA expression of ERCC1 and Bcl-2 in the low- The dose group was significantly lower than that in the control group and conventional-dose group (P <0.05). Conclusion Low-dose radiation enhanced the sensitivity of resistant ovarian cancer cells to DDP, possibly by decreasing the DNA repair capacity of tumor cells and promoting apoptosis.