1.Study on gene expression changes of arsenic sulfide treated NB4 cells.
Chunhong GU ; Fangyuan CHEN ; Jieying HAN ; Ye TENG ; Nianxian SHAO ; Renrong OUYANG
Chinese Journal of Hematology 2002;23(1):16-18
OBJECTIVETo compare the gene expression status of NB4 cells before and after arsenic sulfide treatment by cDNA microarray.
METHODSTwo cDNA probes were made from mRNA of untreated or arsenic sulfide treated NB4 cells. The cells were labelled with Cy3 or Cy5 fluorescence dyes individually, hybridized with cDNA microarray, and scanned for fluorescent intensity. The altered gene expression was screened through the analysis of difference in gene expression profile.
RESULTSThirty four genes related to apoptosis, cell cycle and others expressed different after the treatment of arsenic sulfide, 28/34 were up-regulated, 6/34 down-regulated.
CONCLUSIONABC50, PNAS-2 and cyclin G(2) might take part in the process of NB4 cell apoptosis induced by arsenic sulfide.
Arsenicals ; pharmacology ; Gene Expression Regulation, Neoplastic ; drug effects ; Humans ; Oligonucleotide Array Sequence Analysis ; Sulfides ; pharmacology ; Tumor Cells, Cultured ; drug effects ; metabolism
2.Effects of red orpiment on cell morphology and expression of PML mRNA and protein in NB4 and HL-60 cells.
Lu ZHONG ; Fangyuan CHEN ; Jieying HAN ; Nianxian SHAO ; Renrong OUYANG
Chinese Medical Journal 2003;116(1):148-150
OBJECTIVETo investigate the effects of red orpiment on cell morphology, expression of promyelocytic leukemia (PML) mRNA and its protein localization in NB4 and HL-60 cell lines.
METHODSCell morphology was assayed by Wright's staining and fluorescence staining, while PML mRNA expression was determined by RT-PCR. PML protein localization by evaluated by immunofluorescence staining.
RESULTSThe typical apoptosis was found in NB4 and HL-60 cells after treatment with red orpiment. The fusion protein was no longer observed in NB4 cells, PML protein was relocated, and then degraded. In HL-60 cells, PML protein underwent a similar progress. The expression of promyelocytic leukemia (PML) mRNA was not changed in the treated cells.
CONCLUSIONRed orpiment inhibits the proliferation of leukemia cells by inducing them to undergo apoptosis.
Antineoplastic Agents ; pharmacology ; Apoptosis ; drug effects ; Arsenicals ; pharmacology ; HL-60 Cells ; Humans ; Leukemia, Promyelocytic, Acute ; drug therapy ; metabolism ; pathology ; Medicine, Chinese Traditional ; Neoplasm Proteins ; analysis ; genetics ; Nuclear Proteins ; Promyelocytic Leukemia Protein ; RNA, Messenger ; analysis ; Transcription Factors ; analysis ; genetics ; Tumor Cells, Cultured ; Tumor Suppressor Proteins
3.Study of the effects of quercetin on PML gene and protein expression and localization in leukemia cells.
Lu ZHONG ; Fangyuan CHEN ; Jieying HAN ; Nianxian SHAO ; Renrong OUYANG
Chinese Journal of Hematology 2002;23(2):87-90
OBJECTIVETo investigate PML gene and protein expression and localization in leukemia cell lines.
METHODSCell morphology was assayed by Wright and fluorescence stain, PML mRNA expression by RT-PCR, and PML protein localization by immunofluorescence.
RESULTS(1) Differentiation was observed by morphology in NB4 and HL-60 cells after treatment with all-trans retinoic acid (ATRA) while K562 cells did not show. Apoptosis was found in each cell line after treatment with quercetin. (2) After treatment with ATRA, the fusion protein disappeared and PML protein resumed in NB4 cells, while in HL-60 and K562 cells there was no difference from control cells. After treatment with quercetin, the fusion protein disappeared in NB4 cells, then degraded, and so did in HL-60 cells and K562 cells. (3) The expression of PML mRNA had no change in all the three cell lines after treatment with ATRA or quercetin.
CONCLUSIONPML plays a role of differentiation and apoptosis induction in leukemia cells at the translational level. PML in POD plays a role of apoptosis induction and growth control of leukemia cells.
Cell Division ; drug effects ; Dose-Response Relationship, Drug ; Gene Expression Regulation, Neoplastic ; drug effects ; HL-60 Cells ; Humans ; K562 Cells ; Leukemia ; genetics ; metabolism ; pathology ; Neoplasm Proteins ; genetics ; metabolism ; Nuclear Proteins ; Promyelocytic Leukemia Protein ; Quercetin ; pharmacology ; RNA, Messenger ; drug effects ; genetics ; metabolism ; Time Factors ; Transcription Factors ; genetics ; metabolism ; Tretinoin ; pharmacology ; Tumor Cells, Cultured ; Tumor Suppressor Proteins