글로벌 연구동향
방사선생물학
본문글자크기
![[Oncotarget] STAT3-survivin signaling mediates a poor response to radiotherapy in HER2-positive breast cancers.](/enewspaper/upimages/admin_20160317182235_R.png)
2016년 03월호
[Oncotarget] STAT3-survivin signaling mediates a poor response to radiotherapy in HER2-positive breast cancers.KIRAMS / 김재성*, 노우철*
- 출처
- Oncotarget
- 등재일
- 2016 Jan 9
- 저널이슈번호
- doi: 10.18632/oncotarget.6855. [Epub ahead of print]
- 내용
- Although radiotherapy resistance is associated with locoregional recurrence and distant metastasis in breast cancers, clinically relevant molecular markers and critical signaling pathways of radioresistant breast cancer are yet to be defined. Herein, we show that HER2-STAT3-survivin regulation is associated with radiotherapy resistance in HER2-positive breast cancers. Depletion of HER2 by siRNA sensitized HER2-positive breast cancer cells to irradiation by decreasing STAT3 activity and survivin, a STAT3 target gene, expression in HER2-positive breast cancer cells. Furthermore, inhibition of STAT3 activation or depletion of survivin also sensitized HER2-positive breast cancer cells to irradiation, suggesting that the HER2-STAT3-survivin axis is a key pathway in radiotherapy resistance of HER2-positive breast cancer cells. In addition, our clinical analysis demonstrated the association between HER2-positive breast cancers and radiotherapy resistance. Notably, we found that increased expression of phosphorylated STAT3, STAT3, and survivin correlated with a poor response to radiotherapy in HER2-positive breast cancer tissues. These findings suggest that the HER2-STAT3-survivin axis might serve as a predictive marker and therapeutic target to overcome radiotherapy resistance in HER2-positive breast cancers.
AbstractAuthor information
Kim JS1, Kim HA2, Seong MK2, Seol H3, Oh JS4, Kim EK5, Chang JW6, Hwang SG1, Noh WC2.1Division of Radiation Cancer Research, Korea Institute of Radiological and Medical Sciences, Seoul, Korea.2Department of Surgery, Korea Cancer Center Hospital, Korea Institute of Radiological and Medical Sciences, Seoul, Korea.3Department of Pathology, Korea Cancer Center Hospital, Korea Institute of Radiological and Medical Sciences, Seoul, Korea.4Department of Genetic Engineering, Sungkyunkwan University, Suwon, Korea.5Department of Surgery, Breast Cancer Center, Seoul National University Bundang Hospital, Seoul National University College of Medicine, Gyeonggi-do, Korea.6Stem Cell Regenerative Medicine Center, Research Institute for Future Medicine, Samsung Medical Center, Seoul, Korea.
- 키워드
- HER2; STAT3; breast cancer; radioresistance; survivin
- 연구소개
- 전 세계 여성암 발병률 1위인 유방암은 수술 후 방사선 치료 및 호르몬 요법을 시행하게 되는데, 일부 환자들의 경우 방사선 치료 후 암이 재발되어 생존율이 낮아지는 등 치료에 한계가 있었습니다. 본 연구는 암세포의 성장과 증식에 관여하는 것으로 알려진 “STAT3-survivin”이 활성화 될수록 HER2+ 유방암 세포가 방사선 치료 이후 재발되는데 관계함을 규명한 논문입니다. 또한 방사선 치료 후 HER2+ 재발환자의 유방암 조직과 완치환자의 유방암 조직에서 확인한 결과, HER2+ 재발환자 조직에서 STAT3-survivin의 발현이 높다는 사실이 확인하였으며, 향후 이들을 활용하여 방사선 치료시 좀 더 정확한 진단을 하는데 활용할 수 있을 것으로 기대합니다.
- 덧글달기
- 이전글 [Oncotarget] Lanatoside C suppressed colorectal cancer cell growth by inducing mitochondrial dysfunction and increased radiation sensitivity by impairing DNA damage repair.
- 다음글 [Cancer Res] HSPB1 Inhibits the Endothelial-to-Mesenchymal Transition to Suppress Pulmonary Fibrosis and Lung Tumorigenesis.
