Paclitaxel-exposed ovarian cancer cells induce cancer-specific CD4(+) T cells after doxorubicin exposure through regulation of MyD88 expression
- Authors
- Kim, Jee-Eun; Jang, Min Ja; Jin, Dong-Hoon; Chung, Yoon Hee; Choi, Byung-Sun; Park, Ga Bin; Kim, Yeong Seok; Kim, Seonghan; Hur, Dae Young; Hung, Chien-Fu; Kim, Daejin
- Issue Date
- May-2014
- Publisher
- SPANDIDOS PUBL LTD
- Keywords
- ovarian cancer; paclitaxel; doxorubicin; MyD88; CD4
- Citation
- INTERNATIONAL JOURNAL OF ONCOLOGY, v.44, no.5, pp 1716 - 1726
- Pages
- 11
- Journal Title
- INTERNATIONAL JOURNAL OF ONCOLOGY
- Volume
- 44
- Number
- 5
- Start Page
- 1716
- End Page
- 1726
- URI
- https://scholarworks.bwise.kr/cau/handle/2019.sw.cau/12302
- DOI
- 10.3892/ijo.2014.2308
- ISSN
- 1019-6439
1791-2423
- Abstract
- Ovarian cancer has the highest mortality rate among gynecological malignancies due to high chemoresistance to the combination of platinum with taxane. Immunotherapy against ovarian cancer is a promising strategy to develop from animal-based cancer research. We investigated changes in the immunogenicity of paclitaxel-exposed ovarian cancer cells following exposure to other chemotherapeutic drugs. Murine ovarian surface epithelial cells (MOSECs) showed some resistance to paclitaxel, a first-line therapy for ovarian cancer. However, MOSECs pre-exposed to paclitaxel died through apoptosis after incubation with doxorubicin or cisplatin for 2 h. Injected into mice, the paclitaxel-exposed MOSECs post-treated with doxorubicin induced more MOSEC-specific CD4(+) T cells and extended survival for a greater time than MOSECs treated with paclitaxel alone; and bone marrow-derived dendritic cells (BMDCs) expressed higher levels of co-stimulatory molecules and produced IL-12 after co-culture with paclitaxel-exposed MOSECs treated with doxorubicin. We also observed that in paclitaxel-exposed MOSECs treated with doxorubicin, but not cisplatin, the expression of MyD88 and related target proteins decreased compared to paclitaxelexposed MOSECs only, while in BMDCs co-cultured with these MOSECs the expression of myeloid differentiation primary response gene 88 (MyD88) increased. These findings suggest that paclitaxel pre-exposed cancer cells treated with doxorubicin can induce significant apoptosis and a therapeutic antitumor immune response in advanced ovarian cancer.
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