scholarly journals Myeloid cell RelA/p65 promotes lung cancer proliferation through Wnt/β-catenin signaling in murine and human tumor cells

Oncogene ◽  
2013 ◽  
Vol 33 (10) ◽  
pp. 1239-1248 ◽  
Author(s):  
D Li ◽  
C Beisswenger ◽  
C Herr ◽  
J Hellberg ◽  
G Han ◽  
...  
Keyword(s):  
Lung Cancer ◽  
Tumor Cells ◽  
Human Tumor ◽  
Myeloid Cell ◽  
Human Tumor Cells ◽  
Cancer Proliferation

scholarly journals Regulation of KRAS4A/B splicing in cancer stem cells by the RBM39 splicing complex

2019 ◽  
Author(s):  
Wei-Ching Chen ◽  
Minh D. To ◽  
Peter M.K. Westcott ◽  
Reyno Delrosario ◽  
Il-Jin Kim ◽  
...  
Keyword(s):  
Lung Cancer ◽  
Stem Cells ◽  
Cancer Stem Cells ◽  
Er Stress ◽  
Tumor Cells ◽  
Human Tumor ◽  
Cancer Development ◽  
Human Tumor Cells ◽  
Splice Isoforms ◽  
Splice Regulation

AbstractThe KRAS oncogene is expressed as major KRAS4B and minor KRAS4A splice isoforms, the distinct functions of which in cancer are unknown. We demonstrate here that KRAS4A is enriched in cancer stem-like cells, and is activated by hypoxia, whereas KRAS4B is more widely expressed and responds to ER stress. Mice completely lacking either isoform are viable but resistant to lung cancer development, as are Kras4A/B double heterozygous mice expressing both isoforms, but in which splice regulation has been uncoupled. Splicing of KRAS4A, but not KRAS4B, in human tumor cells can be inhibited by treatment with the splice inhibitor indisulam, or by CRISPR/Cas inhibition of the RBM39 splicing complex. Our data suggest that control of KRAS4A/B splicing is a targetable vulnerability in KRAS mutant tumors.

Inhibition by dihydrorifampicin of RNA polymerases I and II isolated from nuclei of Rous sarcoma cells and human tumor cells HEp-2

1979 ◽  
Vol 44 (9) ◽  
pp. 2722-2736 ◽  
Author(s):  
Jindřich Kára ◽  
Zdeněk Hostomský
Keyword(s):  
Tumor Cells ◽  
Human Tumor ◽  
Tumor Cell Line ◽  
Selective Inhibition ◽  
Rna Polymerases ◽  
Embryonic Cells ◽  
Human Tumor Cells ◽  
Ribonucleic Acids ◽  
Rous Sarcoma ◽  
Sarcoma Cells

Dihydrorifampicin, a rifampicin derivative hydrogenated at the 18-19 carbon atoms of the aliphatic ansa chain of the rifampicin molecule, inhibits the enzymatic activity of RNA polymerases I and II, isolated from the nuclei of avian tumor cells (Rous sarcoma) and from the human tumor cell line HEp-2. The RNA polymerases from these tumors have been separated and partially purified by chromatography on DEAE Sephadex A-25 and characterized by the sensitivity to α-amanitin. The [3H]UMP-labeled ribonucleic acids synthesized in the isolated nuclei of Rous sarcoma cells in the presence and absence of DHR were analyzed by sedimentation analysis in sucrose density gradients. It was found that the synthesis of rRNAs and mRNAs is very significantly inhibited by dihydrorifampicin, whereas the synthesis of tRNAs is much less inhibited at the same DHR concentration (100μg/ml). The observed cytostatic effect of DHR on the growth of human tumor cells HEp-2 and embryonic cells in culture is apparently mediated by the selective inhibition of RNA polymerases I and II in human and avian cells. The relationship between the molecular structure of DHR and its affinity to RNA polymerases of eukaryotic cells is discussed.

The Sensitivity of Human Tumor Cells to the Cytotoxicity of Gold Polyacrylate (Aurumacryl)

BIOPHYSICS ◽  
2019 ◽  
Vol 64 (6) ◽  
pp. 930-935 ◽  
Author(s):  
D. B. Korman ◽  
E. I. Nekrasova ◽  
L. A. Ostrovskaya ◽  
O. O. Ryabaya ◽  
N. V. Bluhterova ◽  
...  
Keyword(s):  
Tumor Cells ◽  
Human Tumor ◽  
Human Tumor Cells
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