Treatment of Vemurafenib-Resistant SKMEL-28 Melanoma Cells with Paclitaxel

Nguyen, Dinh Thang; Phan, Tuan Nghia; Kumasaka, Mayuko Y.; Yajima, Ichiro; Kato, Masashi

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자료유형: 학술저널

저자정보: Nguyen, Dinh Thang (Department of Biochemistry and Plant Physiology, Key Laboratory of Enzyme and Protein Technology, VNU University of Science, Vietnam National University) Phan, Tuan Nghia (Department of Biochemistry and Plant Physiology, Key Laboratory of Enzyme and Protein Technology, VNU University of Science, Vietnam National University) Kumasaka, Mayuko Y. (Department of Occupational and Environmental Health, Nagoya University Graduate School of Medicine) Yajima, Ichiro (Department of Occupational and Environmental Health, Nagoya University Graduate School of Medicine) Kato, Masashi (Department of Occupational and Environmental Health, Nagoya University Graduate School of Medicine)

저널정보: 아시아태평양암예방학회 Asian Pacific journal of cancer prevention : APJCP Asian Pacific journal of cancer prevention : APJCP 제16권 제2호

발행연도: 2015.1

수록면: 699 - 705 (7page)

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Vemurafenib has recently been used as drug for treatment of melanomas with $BRAF^{V600E}$ mutation. Unfortunately, treatment with only vemurafenib has not been sufficiently effective, with recurrence after a short period. In this study, three vemurafenib-resistant $BRAF^{V600E}$ melanoma cell lines, $A375P^R$, $A375M^R$ and SKMEL-$28^R$, were established from the original A375P, A375M and SKMEL-28 cell lines. Examination of the molecular mechanisms showed that the phosphorylation levels of MEK and ERK, which play key roles in the RAS/RAF/MEK/ERK signaling pathway, were reduced in these three cell lines, with increased phosphorylation levels of pAKTs limited to SKMEL-$28^R$ cells. Treatment of SKMEL-$28^R$ cells with 100 nM paclitaxel resulted in increased apoptosis and decreased cellular proliferation, invasion and colony formation via reduction of expression levels of EGFR and pAKTs. Moreover, vemurafenib-induced pAKTs in SKMEL-$28^R$ were decreased by treatment with an AKT inhibitor, MK-2206. Taken together, our results revealed that resistance mechanisms of $BRAF^{V600E}$-mutation melanoma cells to vemurafenib depended on the cell type. Our results suggested that paclitaxel should be considered as a drug in combination with vemurafenib to treat melanoma cells.

#Melanoma #vemurafenib #paclitaxel #treatment resistance #$BRAF^{V600E}$ #EGFR #AKT

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Nguyen, Dinh Thang

소속기관 Department of Biochemistry and Plant Physiology, Key Laboratory of Enzyme and Protein Technology, VN