지원사업
학술연구/단체지원/교육 등 연구자 활동을 지속하도록 DBpia가 지원하고 있어요.
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연구자들이 자신의 연구와 전문성을 널리 알리고, 새로운 협력의 기회를 만들 수 있는 네트워킹 공간이에요.
논문 기본 정보
- 자료유형
- 학술저널
- 저자정보
- 발행연도
- 2010.1
- 수록면
- 42 - 47 (6page)
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Purpose :Maspin is a tumor suppressor protein that has been reported to stimulate the cell death of cancer and inhibit the metastasis of cancer. The present study aimed to explore the survival pathway by which maspin modulates the resistance of human lung cancer cells to chemotherapeutic drugs, and the consequences of maspin gene therapy in an animal model.
Materials and Methods :NCI-H157 and A549 cells were transfected with either a mock vector (pCMVTaq4C), maspin (pCMV-maspin), siControl or siMaspin. RT-PCR and Western blot analysis were performed to study the expressions of survival proteins in lung cancer. cDNA microarray analysis was carried out to compare the maspin-modulated gene expression between the xenograft tumors derived from the lung cancer cells that were stably transfected with pCMVTaq4C or pCMV-maspin. Maspin gene therapy was performed by intra-tumoral injections of pCMVTaq4C or pCMV-maspin into the pre-established subcutaneous tumors in nude mice.
Results :Maspin significantly decreased the survival to doxorubicin and etoposide, whereas did not affect the survival to cisplatin in the NCI-H157 cells. Interestingly, transfection with a maspin plasmid resulted in a significant reduction of the phosphorylation of Akt in the NCI-H157 cells, whereas knockdown of maspin increased the phosphorylation of Akt in the A549 cells. Microarray analysis of the xenograft tumors revealed a specific gene expression profile, demonstrating that maspin is associated with the differential expressions of PTEN and IGF2R. Direct transfer of pCMV-maspin into the tumor significantly retarded the tumor growth in the animal experiments (p=0.0048).
Conclusion :Lung cancer cells lacking maspin could be resistant to chemotherapeutic drugs such as doxorubicin or etoposide, at least in part by maintaining Akt phosphorylation.
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참고문헌 (19)
참고문헌 신청
/ 2000 / Hendrix MJ. De-mystifying the mechanism(s) of maspin / Nat Med 6 : 374 ~ 376
Beale PJ / 2000 / BCL-2 family protein expression and platinum drug resistance in ovarian carcinoma / Br J Cancer 82 : 436 ~ 440
Hettinga JV / 1996 / Heat-shock protein expression in cisplatin-sensitive and -resistant human tumor cells / Int J Cancer 67 : 800 ~ 807
Jang H / 2008 / Maspin polymorphism associated with susceptibility to apoptosis and in vivo tumorigenesis / Int J Mol Med 22 : 333 ~ 338
Jung HH / 2005 / STAT1 and Nmi are downstream targets of Ets-1 transcription factor in MCF-7 human breast cancer cell / FEBS Letters 579 : 3941 ~ 3946
Beale PJ / 2000 / BCL-2 family protein expression and platinum drug resistance in ovarian carcinoma / Br J Cancer 82 : 436 ~ 440
Hettinga JV / 1996 / Heat-shock protein expression in cisplatin-sensitive and -resistant human tumor cells / Int J Cancer 67 : 800 ~ 807
Jang H / 2008 / Maspin polymorphism associated with susceptibility to apoptosis and in vivo tumorigenesis / Int J Mol Med 22 : 333 ~ 338
Jung HH / 2005 / STAT1 and Nmi are downstream targets of Ets-1 transcription factor in MCF-7 human breast cancer cell / FEBS Letters 579 : 3941 ~ 3946
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