We anticipate that ways to avoid or counteract the drug resistance of excessive p170 expression will be developed for other pediatric tumors and eventually will be applied to chemotherapy for RB patients.
Two key enzymes involved in the synthesis of melatonin, hydroxyindole-O-methyltransferase (HIOMT) and arylalkylamine N-acetyltransferase (AA-NAT), are present in Y79 human retinoblastoma cells.
To reveal the expression of multidrug-resistance associated proteins: glutathione-S-transferase π (GSTπ), P-glycoprotein (P-gp) and vault protein lung resistance protein (LRP) in retinoblastoma (RB) without any conservative treatment before primary enucleation and to correlate this expression with histopathological tumor features.
By using a sensitive immunoperoxidase method, increased P-glycoprotein was detected in five multidrug-resistant and two selectively plant alkaloid-resistant retinoblastoma cell lines and in the intraocular and metastatic tumors from which they were derived.
The aim of this study was to reveal the expression and function of P-glycoprotein and multidrug resistance-associated proteins (MRP), members of the ATP-binding cassette (ABC) superfamily of drug transporters, in cultured human Y79 retinoblastoma cells.
We analyzed P-gp expression in retinoblastoma specimens, enucleated either primarily or after neoadjuvant chemotherapy by immunohistochemistry and immunoblotting, and correlated with the histopathological findings.
On the other hand, at the transporters-inhibiting concentrations, LY2835219 did not alter the expression level of ABCB1 and ABCG2, and the phosphorylation status of retinoblastoma (Rb) pathway in both parental and their resistant cells.
Overall, our study demonstrated the novel role of FoxM1-ABCC4 axis in human RB, which provides insights into the prevention of carboplatin resistance in human RB.
Most of the highly expressed ABC transporter genes are typical markers of cancer cells and might exhibit potential targets for medical treatment of retinoblastoma.
On the other hand, at the transporters-inhibiting concentrations, LY2835219 did not alter the expression level of ABCB1 and ABCG2, and the phosphorylation status of retinoblastoma (Rb) pathway in both parental and their resistant cells.
In order to test if the carboxyl terminal polypeptide of the Retinoblastoma (Rb) tumor suppressor protein, could be used to suppress the growth factor-independent growth phenotype of p210bcr-abl positive myeloid cells, we introduced a truncated form of the 3' end of the Rb cDNA encoding its last 173 amino acid residues (Rb C-box) which localize into the cytoplasm where the p210bcr-abl transforming protein is found, into myeloid cells (32D) which depends on the p210bcr-abl protein for IL3 growth factor-independent growth (32D-p210).
Potential G protein-coupled receptor kinase (GRK) and protein kinase A (PKA) mediation of homologous desensitization of corticotropin-releasing factor type 1 (CRF1) receptors was investigated in human retinoblastoma Y-79 cells.
In contrast, opsin, rod transducin, and S-Antigen mRNAs were not detectable by PCR. beta-actin was present in the mRNA populations of whole eye and retinoblastoma.
The combination of failure of G1 control and of tetraploid checkpoint control can cause RB pocket protein-suppressed cells to rapidly become aneuploid and die after exposure to actin inhibitors, whereas pocket protein-competent cells are spared.
Transcripts of ACVR1C receptor and its ligands (Nodal, Activin A/B, and GDF3) were expressed in six retinoblastoma lines, and evidence of downstream SMAD2 signaling was present in all these lines.
The finding of undetectable ACY-1 expression in SCLC supports the hypothesis that inactivation of all alleles of specific chromosome 3p genes occurs in a SCLC in a fashion analogous to Rb gene inactivation in retinoblastoma, and suggests that the structural gene for ACY-1 may be closely linked to a putative SCLC tumor suppressor gene.
The levels of expression of the viral genome in the Balb/c tumor and in the retinoblastoma line were determined by in vitro translation of RNA isolated from these cells and selected with appropriate restriction endonuclease fragments of Ad12 DNA.