• Title/Summary/Keyword: cell arrest

Search Result 888, Processing Time 0.032 seconds

Increased HoxB4 Inhibits Apoptotic Cell Death in Pro-B Cells

  • Park, Sung-Won;Won, Kyung-Jong;Lee, Yong-Soo;Kim, Hye-Sun;Kim, Yu-Kyung;Lee, Hyeon-Woo;Kim, Bo-Kyung;Lee, Byeong-Han;Kim, Jin-Hoi;Kim, Dong-Ku
    • The Korean Journal of Physiology and Pharmacology
    • /
    • v.16 no.4
    • /
    • pp.265-271
    • /
    • 2012
  • HoxB4, a homeodomain-containing transcription factor, is involved in the expansion of hematopoietic stem cells and progenitor cells in vivo and in vitro, and plays a key role in regulating the balance between hematopoietic stem cell renewal and cell differentiation. However, the biological activity of HoxB4 in other cells has not been reported. In this study, we investigated the effect of overexpressed HoxB4 on cell survival under various conditions that induce death, using the Ba/F3 cell line. Analysis of phenotypical characteristics showed that HoxB4 overexpression in Ba/F3 cells reduced cell size, death, and proliferation rate. Moreover, the progression from early to late apoptotic stages was inhibited in Ba/F3 cells subjected to HoxB4 overexpression under removal of interleukin-3-mediated signal, leading to the induction of cell cycle arrest at the G2/M phase and attenuated cell death by Fas protein stimulation in vitro. Furthermore, apoptotic cell death induced by doxorubicin-treated G2/M phase cell-cycle arrest also decreased with HoxB4 overexpression in Ba/F3 cells. From these data, we suggest that HoxB4 may play an important role in the regulation of pro-B cell survival under various apoptotic death environments.

Cell Cycle Arrest and Cytochrome c-mediated Apoptotic Induction in A549 Human Lung Cancer Cells by MCS-C2, an Analog of Sangivamycin

  • Kang, Jeong-Hwa;Lee, Dong-Keun;Lee, Chul-Hoon
    • Journal of Microbiology and Biotechnology
    • /
    • v.20 no.2
    • /
    • pp.433-437
    • /
    • 2010
  • In the course of screening for novel modulators of cell cycle progression and apoptosis as anticancer drug candidates, we generated an analog of sangivamycin, MCS-C2, which was elucidated as 4-amino-6-bromo-7-cyclopentyl-7H-pyrrolo[2,3-d]pyrimidine-5-carboxamide. In the present study, we evaluated the molecular mechanisms of MCSC2-induced cell cycle arrest and apoptosis in A549 human lung cancer cells. To investigate the effects of MCS-C2 on cell cycle progression in A549 cells, we measured the DNA content of A549 cells treated with $5\;{\mu}M$ MCS-C2 using flow cytometry. The analysis revealed an appreciable $G_2$ phase arrest in treated cells. This event was associated with significant upregulation of p53 and $p21^{Cip1}$. In addition, the TUNEL assay was used to examine apoptotic induction in treated cells, and the effects of MCS-C2 on the expression of apoptosis-associated proteins were examined by Western blot. Apoptotic induction in MCS-C2-treated A549 cells was associated with cytochrome c release from mitochondria, which in turn resulted in the activation of caspase-9 and -3 and the cleavage of poly(ADP-ribose) polymerase (PARP). Based on these results, we conclude that MCS-C2 is a candidate therapeutic agent for the treatment of human lung cancer via upregulation and activation of p53.

Anti-Proliferative Effect of Polysaccharides from Salicornia herbacea on Induction of G2/M Arrest and Apoptosis in Human Colon Cancer Cells

  • Ryu, Deok-Seon;Kim, Seon-Hee;Lee, Dong-Seok
    • Journal of Microbiology and Biotechnology
    • /
    • v.19 no.11
    • /
    • pp.1482-1489
    • /
    • 2009
  • In this study, we investigated the anti-proliferative effect of polysaccharides from Salicornia herbacea on HT-29 human colon cancer cells. Crude polysaccharides from S. herbacea (CS) were prepared by extraction with hot steam water, and fine polysaccharides from S. herbacea (PS) were obtained through further size exclusion chromatography. The anti-proliferative effect of CS and PS were measured using the MTS assay, apoptosis analysis, cell cycle analysis, and RT-PCR. HT-29 cells were treated with CS or PS at different dosages (0.5, 1, 2, 4 mg $ml^{-1}$) for 24 or 48 h. CS and PS inhibited proliferation and stimulated apoptosis of cells in a dose-dependent manner. Flow cytometric analysis after Annexin V-FITC and PI staining revealed that treatment with CS or PS increased total apoptotic death of cells to 24.99% or 91.59%, respectively, in comparison with the control (13.51 %). PS increased early apoptotic death substantially - up to 12 times more than the control. Treatment with CS or PS resulted in a concentration-dependent increase of the G2/M cell population of the cell cycle as determined by flow cytometry. G2/M arrest was induced significantly with the highest concentration (4 mg $ml^{-1}$) of PS. RT-PCR was performed to study the correlation between G2/M arrest and transcription of cell cycle control genes. The anti-proliferative activity of CS and PS was accompanied by inhibition of cyclin B1, and Cdc 2 mRNA. Moreover, both CS and PS induced expression of the p53 tumor suppressor gene and the Cdk inhibitor p21. These results suggest that polysaccharides from S. herbacea have anti-cancer activity in human colon cancer cells.

Temporal and Spatial Regulation of Cell Cycle Genes during Maize Sex Determination (옥수수 성 결정에 있어서 세포주기 유전자들의 시간적, 공간적 조절)

  • Lee, Jung-Ro;Kim, Jong-Cheol
    • Journal of Life Science
    • /
    • v.16 no.5
    • /
    • pp.828-833
    • /
    • 2006
  • Maize (Zea mays L.) pistil cell death and stamen cell arrest are pivotal process on the sex determination, which diverges from bisexual state of floral meristem to unisexual state in staminate or pistillate floret. We investigated the temporal and spatial distribution of cell cycle gene expression during maize sex determination. The positive regulatory genes of cell cycle, cyclin A, cyclin B, cyclin dependent kinase (CDK) and Mad2 were highly expressed in the developing pistil and stamen but the expression was disappeared in the dying pistil and arresting stamens. In contrast, the negative regulatory genes of cell cycle, Wee1 and CDK inhibitor (CKI) were expressed in the arresting stamens in the wild-type ear and tasselseed2 mutant tassel, however, these genes were not detected in dying pistil although the cyclin B gene expression was disappeared. These results suggest that both the pistil cell death and stamen cell arrest process in maize sex determination are involved in cell cycle regulation, but the different expression patterns of negative regulatory cell cycle genes in the arresting stamens and aborting pistils suggest that the two processes may have distinctive modes of action.

Involvement of G1 arrest and caspase-3 activation in apoptosis induced by bovine lactoferricin

  • Yoo, Yung-Choon;Lee, Kyung-Bok
    • Proceedings of the PSK Conference
    • /
    • 2002.10a
    • /
    • pp.325.2-325.2
    • /
    • 2002
  • We investigated the effect of bovine lactoferricin (Lfcin-B) on cell cycle regulation and caspase activation in tumor cells. Treatment with Lfcin-B resulted in the production of intracellular reactive oxygen species (ROS) during apoptosis of THP-1 cells. Biochemical analysis revealed that Lfcin-B-induced apoptosis. the cell cycle arrest and caspase activation were completely abrogated by addition of an antioxidant such as N-acetylcysteine(NAC). (omitted)

  • PDF

Sensitization of Radiation-Induced Cell Death by Genistein (제니스틴에 의한 방사선유발 세포사멸 민감도증가)

  • Kim, Tae Rim;Kim, In Gyu
    • Journal of Radiation Industry
    • /
    • v.4 no.1
    • /
    • pp.91-94
    • /
    • 2010
  • A number of epidemiological studies as well as biological experiments, showed that genistein, one of the isoflavone, prevents prostate cancer occurrence. In this study, we showed that genistein inhibited the cell proliferation of human promyeoltic leukemia HL-60 cells and induced G2/M phase arrest. In addition, combination of genistein treatment and ${\gamma}$-irradiation displayed synergistic effect in apoptotic cell death of HL-60 cells. This means that the repair of genistein-induced DNA damage was hindered by ${\gamma}$-radiation and thus cell death was increased. In conclusion, genistein is one of the important chemicals that sensitize radiation-induced cell death.