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논문 기본 정보

자료유형
학술저널
저자정보
Hwang, Ki Eun (Department of Internal Medicine, Institute of Wonkwang Medical Science, Wonkwang University School of Medicine) Park, Chul (Department of Internal Medicine, Institute of Wonkwang Medical Science, Wonkwang University School of Medicine) Seol, Chang Hwan (Department of Internal Medicine, Institute of Wonkwang Medical Science, Wonkwang University School of Medicine) Hwang, Yu Ri (Department of Internal Medicine, Institute of Wonkwang Medical Science, Wonkwang University School of Medicine) Hwang, June Seong (Department of Internal Medicine, Institute of Wonkwang Medical Science, Wonkwang University School of Medicine) Jung, Jae Wan (Department of Internal Medicine, Institute of Wonkwang Medical Science, Wonkwang University School of Medicine) Choi, Keum Ha (Department of Pathology, Wonkwang University School of Medicine) Jeong, Eun Taik (Department of Internal Medicine, Institute of Wonkwang Medical Science, Wonkwang University School of Medicine) Kim, Hak Ryul (Department of Internal Medicine, Institute of Wonkwang Medical Science, Wonkwang University School of Medicine)
저널정보
대한결핵 및 호흡기학회 Tuberculosis and Respiratory Diseases 결핵 및 호흡기 질환 제75권 제2호
발행연도
2013.1
수록면
59 - 66 (8page)

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Background: This study was conducted in order to elucidate the effects of docetaxel on the growth of peroxiredoxin 1 (Prx1) knockdown A549 xenograft tumors and further tested the role of Prx1 as a predictor for how a patient would respond to docetaxel treatment. Methods: Effects of docetaxel on the growth of scrambled- and shPrx1-infected A549 xenograft tumors in nude mice were measured. Moreover, immunohistochemical expression of Prx1 was evaluated in paraffin-embedded tissues from 24 non-small cell lung cancer patients who had received docetaxel-cisplatin regimens as a first-line treatment. Results: Docetaxel treatment in Prx1 knockdown xenograft tumor resulted in reduced tumors growth compared with other groups. Prx1 knockdown increased the production of cleaved caspases-8 and -9 in the control itself compared to scramble tumors. Moreover, docetaxel treatment in Prx1 knockdown tissue led to an increased protein band. Phosphorylated Akt was found in Prx1 scramble tissues. Phosphorylated FOXO1 was detected in the docetaxel treatment group. On the other hand, Prx1 knockdown completely suppressed the Akt-FOXO1 axis. The median progression-free survival (PFS) of patients with low Prx1 expression was 7 months (95% confidence interval [CI], 6.0-7.7), whereas the median progression-free survival of patients with high Prx1 expression was 4 months (95% CI, 4.0-5.0). However, high Prx1 expression was not associated with decreased PFS (p=0.114). Conclusion: Our findings suggest that elevated Prx1 provides resistance to docetaxel treatment through suppression of FOXO1-induced apoptosis in A549 xenograft tumors, but may not be related with the predictive significance for response to docetaxel treatment.
#PRDX1 Protein, Human #Docetaxel #Lung Neoplasms

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