The induction of differentiation in teratocarcinoma stem cells by retinoic acid

Strickland, Sidney; Mahdavi, Vijak

doi:10.1016/0092-8674(78)90008-9

Cited by 1,394 publications

(661 citation statements)

References 26 publications

Supporting

Mentioning

639

Contrasting

Unclassified

Order By: Relevance

“…Di erentiation of F9 embryonal carcinoma cells into cells resembling parietal endoderm can be e ected by adding RA into the medium. This di erentiation is accompanied by cell cycle arrest (Strickland & Mahdavi, 1978). Di erentiation of C2C12 myoblasts is induced when cultures are shifted to medium containing low concentrations of mitogens.…”

Section: Resultsmentioning

confidence: 99%

“…C2C12 myoblasts were di erentiated into myotubes by changing growth medium to DMEM with 2% horse serum and 1% glucose (NadalGinard, 1978). F9 di erentiation into cells resembling parietal endoderm was a ected by additional of retinoic acid (®nal concentration 0.3 mM) to the medium (Strickland and Mahdavi, 1978). Neuronal di erentiation of SK-N-SH cells and LAN-1 cells was performed by adding retinoic acid (®nal concentration 20 mM) or DMSO (®nal concentration 1.5%) into the medium (Thiele et al, 1985(Thiele et al, , 1988Abemayor and Sidell, 1989;Tahira et al, 1991;Kranenburg et al, 1995).…”

Section: Cells and Tissue Culturementioning

confidence: 99%

See 1 more Smart Citation

A role of the tuberous sclerosis gene-2 product during neuronal differentiation

et al. 1998

View full text Add to dashboard Cite

Tuberous sclerosis is an autosomal dominant disorder. Besides the development of benign growths (hamartomas) in di erent tissues, one hallmark of this disease is the presence of highly epileptogenic dysplastic lesions in the cerebral cortex (tubers) composed of abnormal shaped neurones. Patients often show evidence of severe mental retardation. Linkage analysis revealed two diseasedetermining genes on chromosome 9 and chromosome 16. The TSC2 gene on chromosome 16 encodes a 1784-amino acid putative tumour suppressor protein, tuberin, that functions as a GTPase-activating protein. Here we show that tuberin expression is upregulated upon induction of neuronal di erentiation in the neuroblastoma cell lines SK-N-SH and LAN-1. This upregulation occurs at post-transcriptional level and is independent of the proliferation status. TSC2 expression is una ected during di erentiation of C2C12 myoblasts into myotubes and of F9 embryonal carcinoma cells into cells resembling parietal endoderm. Antisense inhibition of tuberin expression in SK-N-SH or LAN-1 cells inhibits neuronal di erentiation, but does not a ect the di erentiation of F9 cells. Ectopic overexpression of TSC2 not only reverts the antisense-associated phenotype but furthermore accelerates the neuronal di erentiation process. Our data show for the ®rst time that tuberin plays a critical role in neuronal di erentiation. Such role is consistent with the phenotype of tuberous sclerosis patients, who inherit one defective TSC2 allele, and frequently lose the remaining normal allele in many of the tubers/hamartomas which develop in the central nervous system of these patients.

show abstract

Section: Resultsmentioning

confidence: 99%

Section: Cells and Tissue Culturementioning

confidence: 99%

A role of the tuberous sclerosis gene-2 product during neuronal differentiation

et al. 1998

View full text Add to dashboard Cite

show abstract

“…tissues, including teratocarcinoma [35]. The roles of ADM and PAMP in development need to be explored further.…”

Section: Discussionmentioning

confidence: 99%

Proadrenomedullin NH2-terminal 20 peptide (PAMP) and adrenomedullin bind to teratocarcinoma cells☆

et al. 2000

View full text Add to dashboard Cite

Proadrenomedullin NH 2-terminal 20 peptide (PAMP) and adrenomedullin (ADM) bind to teratocarcinoma cells. The effects of PAMP and ADM on teratocarcinoma cells were investigated. 125 I-PAMP bound to PA1 cells with moderate affinity (K d ϭ 110 nM) to a single class of sites (B max ϭ 110 000/cell). Specific 125 I-PAMP binding was inhibited by PAMP (IC 50 of 100 nM) but not ADM, calcitonin gene-related peptide (CGRP), or amylin. Specific 125 I-ADM binding was inhibited with high affinity by ADM, CGRP, and CGRP(8 -37) (IC 50 values of 10, 10, and 15 nM respectively) but not PAMP or amylin. ADM elevated cAMP (ED 50 value of 100 nM), whereas PAMP had no effect on basal cAMP but inhibited the increase in cAMP caused by 10 nM ADM. Also, the increase in cAMP caused by ADM was inhibited CGRP(8 -37), suggesting that ADM is binding to CGRP receptors. ADM (100 nM) stimulated transiently c-fos mRNA, whereas PAMP (1000 nM) had little effect; however, PAMP inhibited the increase in c-fos mRNA caused by ADM. ADM stimulated [ 3 H]thymidine uptake into PA1 cells, whereas PAMP inhibited the increase in thymidine uptake caused by ADM. These results indicate that ADM and PAMP are both biologically active in teratocarcinoma cells. Published by Elsevier Science Inc.

show abstract

“…1,2 Similarly, tRA induces differentiation and inhibits proliferation of certain cell types, including HL-60 leukemia 3 and F9 embryonal carcinoma cells. 4,5 tRA is being explored as a differentiation therapy in cancer because it induces complete remission in acute promyelocytic leukemia (APL). 6 Unfortunately, APL patients receiving only tRA therapy eventually experience retinoid resistance and clinical relapse.…”

Section: Introductionmentioning

confidence: 99%