Ion Channels in Cell Proliferation and Apoptotic Cell Death

2005 ◽  
Vol 205 (3) ◽  
pp. 147-157 ◽  
Author(s):  
F. Lang ◽  
M. Föller ◽  
K.S. Lang ◽  
P.A. Lang ◽  
M. Ritter ◽  
...  
Keyword(s):  
Cell Proliferation ◽  
Cell Death ◽  
Ion Channels ◽  
Apoptotic Cell ◽  
Apoptotic Cell Death

Ion Channels and Cell Volume in Regulation of Cell Proliferation and Apoptotic Cell Death

2006 ◽  
pp. 142-160 ◽  
Author(s):  
Florian Lang ◽  
Ekaterina Shumilina ◽  
Markus Ritter ◽  
Erich Gulbins ◽  
Alexey Vereninov ◽  
...  
Keyword(s):  
Cell Proliferation ◽  
Cell Death ◽  
Ion Channels ◽  
Cell Volume ◽  
Apoptotic Cell ◽  
Apoptotic Cell Death

Ion Channels, Cell Volume, Cell Proliferation and Apoptotic Cell Death

2008 ◽  
pp. 69-84 ◽  
Author(s):  
Florian Lang ◽  
Erich Gulbins ◽  
Ildiko Szabo ◽  
Alexey Vereninov ◽  
Stephan M. Huber
Keyword(s):  
Cell Proliferation ◽  
Cell Death ◽  
Ion Channels ◽  
Cell Volume ◽  
Apoptotic Cell ◽  
Apoptotic Cell Death ◽  
Volume Cell

C-Myc Is Required for Acute but Not for Chronic Hematopoietic Malignances in Pten-Null Mice.

Blood ◽  
2009 ◽  
Vol 114 (22) ◽  
pp. 1632-1632
Author(s):  
Yinshi Guo ◽  
Christopher Seet ◽  
Chao Niu ◽  
Peter Breslin ◽  
Shubin Zhang ◽  
...  
Keyword(s):  
Cell Proliferation ◽  
Cell Death ◽  
Conflicts Of Interest ◽  
Apoptotic Cell ◽  
Akt Signaling ◽  
Apoptotic Cell Death ◽  
Lymphocytic Leukemia ◽  
Mutant Mice ◽  
Myelogenous Leukemia ◽  
Hematopoietic Stem

Abstract Abstract 1632 Poster Board I-658 c-Myc, the product of an oncogene, is a common target of most leukemic oncoproteins. Deregulation of c-Myc is commonly found in human leukemic blasts. Transgenic over-expression of c-Myc induces myeloid, erythroid, and lymphocytic leukemia in mice, however whether c-Myc is absolutely required for leukemogenesis has not yet been addressed. Pten, a tumor-suppressing phosphatase, inhibits cell proliferation and promotes apoptotic cell death through repression of PI3K-Akt signaling. Inactivating mutations of Pten and deregulation of PI3K/Akt signaling are both involved in the development of both chronic and acute hematopoietic malignances. Mice with Pten deletions in hematopoietic stem cells (HSCs) develop myeloproliferative disorders (MPD) followed by acute T lymphocytic or myeloid leukemia, reminiscent of disease progression in human chronic myelogenous leukemia. Mice with Pten deletions in lymphocytes develop lymphadenopathy (due to a chronic polyclonal lymphoproliferative disorder) as well as CD4+ T lymphocytic lymphoma. The appearance of these diseases in one animal model provides an opportunity to study the pathogenesis of multiple diseases simultaneously. To study whether c-Myc is required for the development of these hematopoietic disorders in Pten-mutant mice, we generated inducible Pten and c-Myc double-knockout mice (Pten-/-c-Myc-/-). By comparing the hematopoietic phenotypes of the Pten-/-c-Myc-/- mice with those of Pten-mutant (Pten-/-) mice, we found that both sets of mice developed MPD and lymphadenopathy, however none of the compound-mutant mice developed acute leukemia or lymphoma. Interestingly, in contrast to the MPD which developed in Pten-/- mice, which is dominated by granulocytes, megakaryocytes predominate in the MPD of Pten-/-c-Myc-/- mice. We have concluded that c-Myc is required for the development of both T lymphocytic lymphoma and the acute leukemic transformation of Pten-/- MPD, but is not essential for the development of chronic myeloid or lymphoid proliferative disorders. Our study suggests that deregulation of PI3K/Akt signaling in Pten-mutant hematopoietic cells protects these cells from apoptotic cell death, which results in chronic proliferative disorders, while the deregulation of c-Myc resulting from additional mutations promotes hematopoietic cell proliferation and blockage of maturation, and is absolutely required for the development of acute hematopoietic malignances. Disclosures No relevant conflicts of interest to declare.

Ion Channels, Cell Volume, and Apoptotic Cell Death

1998 ◽  
Vol 8 (6) ◽  
pp. 285-292 ◽  
Author(s):  
F. Lang ◽  
A. Lepple-Wienhues ◽  
M. Paulmichl ◽  
I. Szabó ◽  
D. Siemen ◽  
...  
Keyword(s):  
Cell Death ◽  
Ion Channels ◽  
Cell Volume ◽  
Apoptotic Cell ◽  
Apoptotic Cell Death

scholarly journals Melatonin decreases cell proliferation, impairs myogenic differentiation and triggers apoptotic cell death in rhabdomyosarcoma cell lines

2015 ◽  
Vol 34 (1) ◽  
pp. 279-287 ◽  
Author(s):  
SILVIA CODENOTTI ◽  
MICHELA BATTISTELLI ◽  
SABRINA BURATTINI ◽  
SARA SALUCCI ◽  
ELISABETTA FALCIERI ◽  
...  
Keyword(s):  
Cell Proliferation ◽  
Cell Death ◽  
Cell Lines ◽  
Apoptotic Cell ◽  
Myogenic Differentiation ◽  
Apoptotic Cell Death ◽  
Rhabdomyosarcoma Cell

scholarly journals Apatinib triggers autophagic and apoptotic cell death via VEGFR2/STAT3/PD-L1 and ROS/Nrf2/p62 signaling in lung cancer

2021 ◽  
Vol 40 (1) ◽  
Author(s):  
Chunfeng Xie ◽  
Xu Zhou ◽  
Chunhua Liang ◽  
Xiaoting Li ◽  
Miaomiao Ge ◽  
...  
Keyword(s):  
Lung Cancer ◽  
Cell Cycle ◽  
Cell Proliferation ◽  
T Cells ◽  
Cell Death ◽  
Colony Formation ◽  
Apoptotic Cell ◽  
Apoptotic Cell Death ◽  
Jurkat T Cells

Abstract Background Recently, a variety of clinical trials have shown that apatinib, a small-molecule anti-angiogenic drug, exerts promising inhibitory effects on multiple solid tumors, including non-small cell lung cancer (NSCLC). However, the underlying molecular mechanism of apatinib on NSCLC remains unclear. Methods MTT, EdU, AO/EB staining, TUNEL staining, flow cytometry, colony formation assays were performed to investigate the effects of apatinib on cell proliferation, cell cycle distribution, apoptosis and cancer stem like properties. Wound healing and transwell assays were conducted to explore the role of apatinib on migration and invasion. The regulation of apatinib on VEGFR2/STAT3/PD-L1 and ROS/Nrf2/p62 signaling were detected. Furthermore, we collected conditioned medium (CM) from A549 and H1299 cells to stimulate phorbol myristate acetate (PMA)-activated THP-1 cells, and examined the effect of apatinib on PD-L1 expression in macrophages. The Jurkat T cells and NSCLC cells co-culture model was used to assess the effect of apatinib on T cells activation. Subcutaneous tumor formation models were established to evaluate the effects of apatinib in vivo. Histochemical, immunohistochemical staining and ELISA assay were used to examine the levels of signaling molecules in tumors. Results We showed that apatinib inhibited cell proliferation and promoted apoptosis in NSCLC cells in vitro. Apatinib induced cell cycle arrest at G1 phase and suppressed the expression of Cyclin D1 and CDK4. Moreover, apatinib upregulated Cleaved Caspase 3, Cleaved Caspase 9 and Bax, and downregulated Bcl-2 in NSCLC cells. The colony formation ability and the number of CD133 positive cells were significantly decreased by apatinib, suggesting that apatinib inhibited the malignant and stem-like features of NSCLC cells. Mechanistically, apatinib inhibited PD-L1 and c-Myc expression by targeting VEGFR2/STAT3 signaling. Apatinib also inhibited PD-L1 expression in THP-1 derived macrophages stimulated by CM from NSCLC cells. Furthermore, apatinib pretreatment increased CD69 expression and IFN-γ secretion in stimulated Jurkat T cells co-cultured with NSCLC cells. Apatinib also promoted ROS production and inhibited Nrf2 and p62 expression, leading to the autophagic and apoptotic cell death in NSCLC. Moreover, apatinib significantly inhibited tumor growth in vivo. Conclusion Our data indicated that apatinib induced autophagy and apoptosis in NSCLC via regulating VEGFR2/STAT3/PD-L1 and ROS/Nrf2/p62 signaling.

Bile salts stimulate intestinal cell proliferation and protect against apoptotic cell death by activation of NF-κB

2003 ◽  
Vol 124 (4) ◽  
pp. A598
Author(s):  
Alex Toledo ◽  
Jon Yamaguchi ◽  
Jian-Ying Wang ◽  
Barbara L. Bass ◽  
Eric D. Strauch
Keyword(s):  
Cell Proliferation ◽  
Cell Death ◽  
Bile Salts ◽  
Apoptotic Cell ◽  
Apoptotic Cell Death ◽  
Intestinal Cell

scholarly journals Depletion of histone methyltransferase KMT9 inhibits lung cancer cell proliferation by inducing non-apoptotic cell death

2020 ◽  
Vol 20 (1) ◽  
Author(s):  
Hannah Maria Baumert ◽  
Eric Metzger ◽  
Matthias Fahrner ◽  
Julie George ◽  
Roman K. Thomas ◽  
...  
Keyword(s):  
Lung Cancer ◽  
Cell Proliferation ◽  
Cell Death ◽  
Cancer Cell ◽  
Apoptotic Cell ◽  
Histone Methyltransferase ◽  
Apoptotic Cell Death ◽  
Cancer Cell Proliferation ◽  
Lung Cancer Cell
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