Corrigendum to “(R)-FTY720 methyl ether is a specific sphingosine kinase 2 inhibitor: Effect on sphingosine kinase 2 expression in HEK 293 cells and actin rearrangement and survival of MCF-7 breast cancer cells” [Cell. Signal. 23 (2011) 1590–1595]

2012 ◽  
Vol 24 (6) ◽  
pp. 1115
Author(s):  
Keng Gat Lim ◽  
Chaode Sun ◽  
Robert Bittman ◽  
Nigel J. Pyne ◽  
Susan Pyne
Keyword(s):  
Breast Cancer ◽  
Cancer Cells ◽  
Methyl Ether ◽  
Breast Cancer Cells ◽  
Sphingosine Kinase ◽  
Hek 293 ◽  
Sphingosine Kinase 2 ◽  
293 Cells ◽  
Actin Rearrangement ◽  
Mcf 7

scholarly journals PAPOLA contributes to Cyclin D1 mRNA alternative polyadenylation and promotes breast cancer cells proliferation

2021 ◽  
pp. jcs.252304
Author(s):  
Chrysoula Komini ◽  
Irini Theohari ◽  
Andromachi Lambrianidou ◽  
Lydia Nakopoulou ◽  
Theoni Trangas
Keyword(s):  
Breast Cancer ◽  
Cancer Cells ◽  
Breast Cancer Cells ◽  
Triple Negative ◽  
Alternative Polyadenylation ◽  
Hek 293 ◽  
Protein Levels ◽  
293 Cells ◽  
Candidate Target ◽  
Mcf 7

Poly(A) polymerases add the poly(A) tail at the 3’ end of nearly all eukaryotic mRNA, are associated with proliferation and cancer. To elucidate the role of the most studied mammalian poly(A) polymerase α (PAPOLA) in cancer, we assessed its expression in 221 breast cancer samples and found it to correlate strongly with the aggressive triple-negative subtype. Silencing PAPOLA in MCF-7 and MDA-MB-231 breast cancer cells reduced proliferation and anchorage-independent growth by decreasing steady-state CCND1 mRNA and protein levels. Whereas the length of the CCND1 mRNA poly(A) tail was not affected, its 3' untranslated region (3'UTR) lengthened. Overexpressing PAPOLA caused CCND1 mRNA 3'UTR shortening with a concomitant increase in the corresponding transcript and protein, resulting in growth arrest in MCF-7 cells and DNA damage in HEK-293 cells, whereas in the P53 mutant MDA-MB-231 promoted proliferation.Our data suggest PAPOLA as a possible candidate target for the control of tumor growth, mostly relevant to triple-negative tumors, a group characterized by its overexpression and lacking alternative targeted therapies.

scholarly journals Sphingosine Kinase Transmits Estrogen Signaling in Human Breast Cancer Cells

2003 ◽  
Vol 17 (10) ◽  
pp. 2002-2012 ◽  
Author(s):  
Olga A. Sukocheva ◽  
Lijun Wang ◽  
Nathaniel Albanese ◽  
Stuart M. Pitson ◽  
Mathew A. Vadas ◽  
...  
Keyword(s):  
Breast Cancer ◽  
Cell Growth ◽  
Cancer Cells ◽  
Human Breast Cancer ◽  
Breast Cancer Cells ◽  
Sphingosine Kinase ◽  
Human Breast Cancer Cells ◽  
Human Breast ◽  
Mcf 7 ◽  
Cytoplasmic Signaling

Abstract Current understanding of cytoplasmic signaling pathways that mediate estrogen action in human breast cancer is incomplete. Here we report that treatment with 17β-estradiol (E2) activates a novel signaling pathway via activation of sphingosine kinase (SphK) in MCF-7 breast cancer cells. We found that E2 has dual actions to stimulate SphK activity, i.e. a rapid and transient activation mediated by putative membrane G protein-coupled estrogen receptors (ER) and a delayed but prolonged activation relying on the transcriptional activity of ER. The E2-induced SphK activity consequently activates downstream signal cascades including intracellular Ca2+ mobilization and Erk1/2 activation. Enforced expression of human SphK type 1 gene in MCF-7 cells resulted in increases in SphK activity and cell growth. Moreover, the E2-dependent mitogenesis were highly promoted by SphK overexpression as determined by colony growth in soft agar and solid focus formation. In contrast, expression of SphKG82D, a dominant-negative mutant SphK, profoundly inhibited the E2-mediated Ca2+ mobilization, Erk1/2 activity and neoplastic cell growth. Thus, our data suggest that SphK activation is an important cytoplasmic signaling to transduce estrogen-dependent mitogenic and carcinogenic action in human breast cancer cells.

Sphingosine kinase 1 is required for migration, proliferation and survival of MCF-7 human breast cancer cells

FEBS Letters ◽  
2005 ◽  
Vol 579 (24) ◽  
pp. 5313-5317 ◽  
Author(s):  
Sukumar Sarkar ◽  
Michael Maceyka ◽  
Nitai C. Hait ◽  
Steven W. Paugh ◽  
Heidi Sankala ◽  
...  
Keyword(s):  
Breast Cancer ◽  
Cancer Cells ◽  
Human Breast Cancer ◽  
Breast Cancer Cells ◽  
Sphingosine Kinase ◽  
Sphingosine Kinase 1 ◽  
Human Breast Cancer Cells ◽  
Human Breast ◽  
Mcf 7

scholarly journals Epanorin, a lichen secondary metabolite, inhibits proliferation of MCF-7 breast cancer cells

2019 ◽  
Vol 52 (1) ◽  
Author(s):  
Juan Palacios-Moreno ◽  
Cecilia Rubio ◽  
Wanda Quilhot ◽  
M. Fernanda Cavieres ◽  
Eduardo de la Peña ◽  
...  
Keyword(s):  
Breast Cancer ◽  
Cell Cycle ◽  
Cancer Cells ◽  
Cell Line ◽  
Dna Fragmentation ◽  
Secondary Metabolite ◽  
Breast Cancer Cells ◽  
Mutagenic Activity ◽  
Hek 293 ◽  
Mcf 7

Abstract Background Epanorin (EP) is a secondary metabolite of the Acarospora lichenic species. EP has been found in lichenic extracts with antimicrobial activity, and UV-absorption properties have been described for closely related molecules; however, its antiproliferative activity in cancer cells has not yet been explored. It has been hypothesized that EP inhibits cancer cell growth. MCF-7 breast cancer cells, normal fibroblasts, and the non-transformed HEK-293 cell line were exposed to increasing concentrations of EP, and proliferation was assessed by the sulforhodamine-B assay. Results MCF-7 cells exposed to EP were examined for cell cycle progression using flow cytometry, and DNA fragmentation was examined using the TUNEL assay. In addition, EP’s mutagenic activity was assessed using the Salmonella typhimurium reverse mutation assay. The data showed that EP inhibits proliferation of MCF-7 cells, and it induces cell cycle arrest in G0/G1 through a DNA fragmentation-independent mechanism. Furthermore, EP’s lack of overt cytotoxicity in the normal cell line HEK-293 and human fibroblasts in cell culture is supported by the absence of mutagenic activity of EP. Conclusion EP emerges as a suitable molecule for further studies as a potential antineoplastic agent.

2,3,6- Tribromo- 4,5- dihydroxybenzyl Methyl Ether Induces Growth inhibition and apoptosis in MCF-7 human breast cancer cells

2007 ◽  
Vol 30 (9) ◽  
pp. 1132-1137 ◽  
Author(s):  
Ji-Hyeon Lee ◽  
Sang Eun Park ◽  
Mohammad Akbar Hossain ◽  
Min Young Kim ◽  
Mi-Na Kim ◽  
...  
Keyword(s):  
Breast Cancer ◽  
Growth Inhibition ◽  
Cancer Cells ◽  
Methyl Ether ◽  
Human Breast Cancer ◽  
Breast Cancer Cells ◽  
Human Breast Cancer Cells ◽  
Human Breast ◽  
Mcf 7

scholarly journals Restoring Endocrine Response in Breast Cancer Cells by Inhibition of the Sphingosine Kinase-1 Signaling Pathway

Endocrinology ◽  
2009 ◽  
Vol 150 (10) ◽  
pp. 4484-4492 ◽  
Author(s):  
Olga Sukocheva ◽  
Lijun Wang ◽  
Emily Verrier ◽  
Mathew A. Vadas ◽  
Pu Xia
Keyword(s):  
Breast Cancer ◽  
Cancer Cells ◽  
Signaling Pathway ◽  
Human Breast Cancer ◽  
Breast Cancer Cells ◽  
Sphingosine Kinase ◽  
Sphingosine Kinase 1 ◽  
Human Breast Cancer Cells ◽  
Human Breast ◽  
Mcf 7

Abstract We previously demonstrated that sphingosine kinase-1 (SphK1) is an important mediator in the cytoplasmic signaling of estrogens, including Ca2+ mobilization, ERK1/2 activation, and the epidermal growth factor receptor transactivation. Here we report for the first time that SphK1 activity is causally associated with endocrine resistance in MCF-7 human breast cancer cells. Enforced overexpression of human SphK1 in MCF-7 cells resulted in enhanced cell proliferation and resistance to tamoxifen-induced cell growth arrest and apoptosis. Tamoxifen-resistant (TamR) MCF-7 cells selected by prolonged exposure to 4-hydroxytamoxifen, exhibited higher levels in SphK1 expression and activity, compared with the control cells. Inhibition of SphK1 activity by either specific pharmaceutical inhibitors or the dominant-negative mutant SphK1G82D restored the antiproliferative and proapoptotic effects of tamoxifen in the TamR cells. Furthermore, silencing of SphK1, but not SphK2, expression by the specific small interference RNA also restored the tamoxifen responsiveness in the TamR cells. Thus, blockade of the SphK1 signaling pathway may reprogram cellular responsiveness to tamoxifen and abrogate antiestrogen resistance in human breast cancer cells.

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