The modulation of growth by HMBA in PKC overproducing HT29 colon cancer cells.
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Summary
Although HMBA markedly inhibited the growth of the control cells, no inhibition was seen with the HT29-PKC7 cells, which may be relevant to the use of HMBA in combination with other agents in the therapy of specific cancers.
- Type
- article
- Published
- 1991-12-16
- Cited by
- 8
- References
- 11
- OpenAlex
- https://openalex.org/W1755860
- Semantic Scholar
- https://api.semanticscholar.org/CorpusID:31095228
Keywords
Humanities, Art
References
- Differential expression of protein kinase C isozymes and erythroleukemia cell differentiation.
- Overexpression of protein kinase C in HT29 colon cancer cells causes growth inhibition and tumor suppression
- Antagonistic interactions of hexamethylene bisacetamide in combination with 1-beta-D-arabinofuranosylcytosine, adriamycin and harringtonine on the growth and differentiation of HL-60 cells in vitro.
- Induction of differentiation in mouse neuroblastoma cells by hexamethylene bisacetamide.
- The molecular heterogeneity of protein kinase C and its implications for cellular regulation
- Transport by the (Na+, K+) ATPase: Modulation by differentiation inducers and inhibition of protein synthesis in the MDCK kidney epithelial cell line
- Differentiation-defective mutants of mouse embryonal carcinoma cells: response to hexamethylenebisacetamide and retinoic acid.
- Induction of the expression of differentiation-related antigens on human colon carcinoma cells by stimulating protein kinase C.
- Bryostatins: potent, new mitogens that mimic phorbol ester tumor promoters.
- Induction of morphological and functional differentiation of human promyelocytic leukemia cells (HL‐60) by compounds which induce differentiation of murine leukemia cells
- Phase I and pharmacologic study of hexamethylene bisacetamide in patients with advanced cancer.
Cited by
- Alteration of membrane fatty acid composition and inositol phosphate metabolism in HT-29 human colon cancer cells.
- Expression patterns of protein kinase C isoenzymes are characteristically modulated in chronic pancreatitis and pancreatic cancer.
- Towards selective pharmacological modulation of protein kinase C--opportunities for the development of novel antineoplastic agents.
- Expression of protein kinase C isoenzymes in colorectal cancer tissue and their differential activation by different bile acids
- Protein kinase C isoenzyme patterns characteristically modulated in early prostate cancer.
- Overexpression of protein kinase C-beta1 isoenzyme suppresses indomethacin-induced apoptosis in gastric epithelial cells.
- EXPRESSIO NO FPROTEI NKINAS E Cb 1CONFER SRESISTANCE T OTNFa -AN DPACLITAXEL-INDUCE DAPOPTOSI SI NHT-29 COLO NCARCINOM ACELLS
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