ys-49 and Lung-Neoplasms

ys-49 has been researched along with Lung-Neoplasms* in 1 studies

Other Studies

1 other study(ies) available for ys-49 and Lung-Neoplasms

Article	Year
Synthesized tetrahydroisoquinoline alkaloid exerts anticancer effects at least in part by suppressing NF-κB-regulated proteins in A549 human lung cancer cells. Oncology reports, 2015, Volume: 33, Issue:3 CKD-712, a newly synthesized tetrahydroisoquinoline (THI) and an enantiomer (S form) of YS 49 (a derivative of higenamine) has been reported to suppress nuclear factor-κB (NF-κB) activity in normal cells. In the present study, we investigated the anticancer effects of THI at a low concentration where CKD-712 did not induce cell death in normal cells. At the range of concentrations used, CKD-712 induced cell growth arrest, and inhibited the invasion and motility of A549 cells as determined by cell cycle analysis, a Matrigel-coated chamber assay, and a wound-healing assay, respectively. CKD-712 suppressed MMP-9, but not MMP-2 and other NF-κB-regulated proteins involved in cancer metastasis such as VEGF. Moreover, CKD-712 induced cell cycle arrest at G2M phase by suppressing cyclin A, cyclin B and CDK-1 expression. Taken together, these data suggested that CKD-712 may exert anticancer effects by suppressing NF-κB pathways and inducing cell cycle arrest at G2M phase. Topics: Antineoplastic Agents; Blotting, Western; Cell Cycle Checkpoints; Cell Line, Tumor; Flow Cytometry; Humans; Lung Neoplasms; NF-kappa B; Tetrahydroisoquinolines	2015

Article

Year

Synthesized tetrahydroisoquinoline alkaloid exerts anticancer effects at least in part by suppressing NF-κB-regulated proteins in A549 human lung cancer cells.

Oncology reports, 2015, Volume: 33, Issue:3

CKD-712, a newly synthesized tetrahydroisoquinoline (THI) and an enantiomer (S form) of YS 49 (a derivative of higenamine) has been reported to suppress nuclear factor-κB (NF-κB) activity in normal cells. In the present study, we investigated the anticancer effects of THI at a low concentration where CKD-712 did not induce cell death in normal cells. At the range of concentrations used, CKD-712 induced cell growth arrest, and inhibited the invasion and motility of A549 cells as determined by cell cycle analysis, a Matrigel-coated chamber assay, and a wound-healing assay, respectively. CKD-712 suppressed MMP-9, but not MMP-2 and other NF-κB-regulated proteins involved in cancer metastasis such as VEGF. Moreover, CKD-712 induced cell cycle arrest at G2M phase by suppressing cyclin A, cyclin B and CDK-1 expression. Taken together, these data suggested that CKD-712 may exert anticancer effects by suppressing NF-κB pathways and inducing cell cycle arrest at G2M phase.

Topics: Antineoplastic Agents; Blotting, Western; Cell Cycle Checkpoints; Cell Line, Tumor; Flow Cytometry; Humans; Lung Neoplasms; NF-kappa B; Tetrahydroisoquinolines

2015