kml001
KML001 Inhibits Cell Proliferation and Invasion in Pancreatic Cancer Cells through Suppression of NF-κB and VEGF-C.
Yang MH1, Kim HT2, Lee KT3, Yang S4, Lee JK2, Lee KH2, Rhee JC2.
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Abstract
Pancreatic cancer is an aggressive malignancy with poor prognosis and the efficacy of chemotherapy is limited.
KML001 (sodium meta-arsenite) has been demonstrated to have anticancer activity against some solid cancer cells.
The aim of the present study was to determine the effect of KML001 on cell proliferation, migration,
and invasion of pancreatic cancer cells.
The Dojindo Cell Counting Kit-8 assay was used to determine the inhibition of pancreatic cancer cell proliferation by drugs.
Cell migration and invasion were examined using 24-well inserts and Matrigel™-coated invasion chambers.
The activity of nuclear factor-kappa B (NF-κB) p65, vascular endothelial growth factor-C (VEGF-C),
and matrix metalloproteinase-9 (MMP-9) were measured by enzyme-linked immunosorbent assay (ELISA).
KML001 inhibited the proliferation of pancreatic cancer cells in a dose- and time-dependent manner.
KML001 also inhibited the migration and invasion of pancreatic cancer cells in a dose-dependent mannr.
KML001 significantly decreased NF-κB p65 and VEGF-C activities in the pancreatic cancer cells.
KML001 inhibited cell proliferation, migration, and invasion in pancreatic cancer cells.
Suppression of NF-κB and VEGF-C activation may partly be associated with the anticancer activity of KML001.
These results suggest that KML001 could be a novel potential therapeutic agent for treatment of pancreatic cancer.
Copyright© 2014 International Institute of Anticancer Research (Dr. John G. Delinassios), All rights reserve
췌장암은 예후와 공격적인 악성 종양과 화학 요법의 효과는 제한적이다. KML001 (sodium meta-arsenite) has been demonstrated to have anticancer activity against some solid cancer cells. KML001 (나트륨 메타 아비 산염)은 일부 고형암 세포에 대한 항암 활성이 입증되었습니다. The aim of the present study was to determine the effect of KML001 on cell proliferation, migration, and invasion of pancreatic cancer cells. 본 연구의 목적은 세포 증식, 이동, 및 췌장암 세포의 침윤에 KML001의 효과를 결정하는 것이었다. The Dojindo Cell Counting Kit-8 assay was used to determine the inhibition of pancreatic cancer cell proliferation by drugs. Dojindo 셀 카운팅 키트 -8 분석은 약물에 의해 췌장암 세포 증식의 억제를 측정 하였다. Cell migration and invasion were examined using 24-well inserts and Matrigel™-coated invasion chambers. 세포 이동 및 침윤은 24도 삽입 및 마트 리겔 ™ 코팅 침공 챔버를 사용하여 조사 하였다. The activity of nuclear factor-kappa B (NF-κB) p65, vascular endothelial growth factor-C (VEGF-C), and matrix metalloproteinase-9 (MMP-9) were measured by enzyme-linked immunosorbent assay (ELISA). 핵 인자 - 카파 B (NF-κB) P65, 혈관 내피 성장 인자 C (VEGF-C), 및 매트릭스 메탈 로프 -9 (MMP-9)의 활성은 효소 - 연결된 면역 분석 (ELISA)으로 측정 하였다. KML001 inhibited the proliferation of pancreatic cancer cells in a dose- and time-dependent manner. KML001는 복용량 및 시간 의존적으로 췌장암 세포의 증식을 억제 하였다. KML001 also inhibited the migration and invasion of pancreatic cancer cells in a dose-dependent manner. KML001은 또한 투여 량 - 의존적으로 마이그레이션 및 췌장암 세포의 침입을 억제 하였다. KML001 significantly decreased NF-κB p65 and VEGF-C activities in the pancreatic cancer cells. KML001 크게 췌장암 세포에서 NF-κB의 P65와 VEGF-C의 활동을 감소. KML001 inhibited cell proliferation, migration, and invasion in pancreatic cancer cells. KML001은 췌장암 세포에서 세포 증식, 이동 및 침윤을 억제 하였다. Suppression of NF-κB and VEGF-C activation may partly be associated with the anticancer activity of KML001. NF-κB 및 VEGF-C의 활성화의 억제는 대체로 KML001의 항암 활성과 연관 될 수있다. These results suggest that KML001 could be a novel potential therapeutic agent for treatment of pancreatic cancer. 이러한 결과는 KML001 췌장암의 치료에 대한 새로운 가능성 치료제가 될 수 있음을 시사한다.