Background/aims: The molecular mechanism of dormancy initiation of cancer stem cells (CSCs) is not clear. This study was to explore the molecular mechanism by which CSCs switch from mitotic division to quiescence.
Methods: MTT assays, flow cytometry, Western blotting, qRT-PCR, and immunofluorescence staining were used to test cell viability, cell cycle and expression of -box and WD repeat domain-containing 7 (Fbxw7), -myc, S phase kinase associated protein-2 (Skp2), cyclin-dependent kinase inhibitor 1B (p27), octamer-binding transcription factor 3/4 (Oct3/4), and catenin gene in 5-fluorouracil (5-FU)-treated A549 cells.
Objective: We aimed to investigate how the embryonic stem cell-related gene Oct3/4 changes during the injury-repair process of distal pulmonary epithelium induced by 5-fluorouracil (5-Fu).
Methods: We have developed the lung injury model induced by 5-Fu and observed the dynamic changes of Oct3/4 by indirect immunofluorescence, Western blot, and quantitative real-time PCR. Immunofluorescence double staining was used to compare the positions of Oct3/4(+) cells and other reported alveolar epithelial stem cells.
Background: Oct4 is a major transcription factor related to stem cell self-renewal and differentiation. To fulfill its functions, it must be able to enter the nucleus and remain there to affect transcription. KPNA2, a member of the karyopherin family, plays a central role in nucleocytoplasmic transport.
View Article and Find Full Text PDFMost adult stem cells are in the G0 phase of the cell cycle, accounting for only a small percentage of the cells in the tissue. Thus, isolation of stem cells from tissues for further study represents a major challenge. The anti-tumor drug 5-fluorouracil (5-FU) selectively kills proliferating cells, sparing cells in the G0 phase.
View Article and Find Full Text PDFShanghai Kou Qiang Yi Xue
February 2006
Purpose: To investigate the inhibitive effect of COX-2 inhibitor NS-398 on cancer cell growth of human tongue squamous cell carcinoma.
Methods: MTT assay was used to study the inhibitive effect of NS-398 on the growth of Tca8113 cells, and to investigate the time-effect relationship and dose-effect relationship between NS-398 and Tca8113 cells. The effect of NS-398 on cell cycle changes of Tca8113 was studied by flow cytometry (FCM).