Expression of cyclin B1 after induction of senescence and cell death in non-small cell lung carcinoma A549 cells

Abstract

Abstract:The purpose of this study was to evaluate the level of mitotic cyclin B1 in the context of senescence and cell death in A549 non-small cell lung carcinoma cells. This was performed through analysis of the cell cycle, the percentage of SA-b-galactosidase-positive, as well as TUNEL-positive cells. Morphological alterations were studied using a transmission electron microscope. Changes in the intracellular level and the presence of cyclin B1 in the nucleus and cytoplasm areas were detected by flow cytometry and confocal fluorescence microscopy, respectively. In the cells exposed to various concentrations of doxorubicin, different kinds of cell death and senescent phenotype were observed. Alterations in the cell cycle and increased polyploidy may be indicative of mitotic catastrophe execution. Changes in cyclin B1 may also be strictly related to its different regulation at mitotic catastrophe and senescence programs.

Air Pollution Particulate Matter Alters Antimycobacterial Respiratory Epithelium Innate Immunity

“…TEM revealed morphological abnormalities, such as microvillus shedding, mitochondrial deformities, and vacuolelike vesicles, characteristics related to senescence in PM 10 -and PM 2.5 -exposed A549 cells (32,56). Senescence is a cellular stage characterized by loss of proliferative capacity without impairment of cell viability and metabolic activity.…”

Adenovirus vector-mediated FAM176A overexpression induces cell death in human H1299 non-small cell lung cancer cells

“…To circumvent this, attempts have been made to develop abrogators of this arrest in the G2 phase. Most DNA-damaging agents, including doxorubicin, cause cell death by triggering G2/M-phase cell cycle arrest and inducing apoptosis (16). Here, we propose for the first time that FAM176A also triggers G2/M-phase cell cycle arrest in the H1299 cell line, which interferes with the DNA damage repair processes, followed by the induction of cell death.…”