The Proto-oncogene c-myc and c-myb has been shown to be crucial in the development of the hematopoietic system. The changes in the expression of c-myc are concerned the cell proliferation and differentiation, the expression products of which play an important regulatory role in cell growth, differentiation or malignant transformation. The c-myb involves in transcription and affects cell proliferation, differentiation, apoptosis. More recently, the researches on proto-oncogene c-myc, c-myb in hematopoietic regulation have gradually increased along with development of molecular biology, molecular immunology and cell biology. Scientists point out that the directive differentiation of erythroid and megakaryocytic progenitors, and platelet abnormalities all relate to the level of their expressions. The most common thrombocytopathy includes thrombocytopenia, thrombocytosis and so on. The etiology and the mechanism of these diseases are unknown. This article reviews the structure, function and the expression of c-myc and c-myb in platelet diseases and their significance.
Blood Platelet Disorders ; genetics ; metabolism ; Humans ; Proto-Oncogene Proteins c-myb ; genetics ; metabolism ; Proto-Oncogene Proteins c-myc ; genetics ; metabolism

Animals ; Gene Amplification ; Genes, myc ; Humans ; Lymphoma, B-Cell ; genetics ; metabolism ; pathology ; Mutagenesis, Insertional ; Proto-Oncogene Proteins c-myc ; metabolism ; Translocation, Genetic

OBJECTIVETo study the clinical significance of P53, C-MYC and BCL-6 abnormality in the patients with diffuse large B cell lymphoma (DLBCL).

METHODSFrom July 2011 to January 2013, 80 patients with DLBCL were admitted in our hospital and were chosen as study objects, their clinical data were collected. The abnormality of P53, C-MYC and BCL-6 was examined by using I-FISH for all the patients. The correlation of abnormality of P53, C-MYC and BCL-6 with clinical staging, curative efficacy and prognosis of the patients were analyzed.

RESULTSOut of 80 patients 27 patients (33.75%) had P53 deletion, 24 patients (30.00%) had C-MYC rearrangement/amplification, and 46 patients (57.50%) had BCL-6 rearrangement. The P53 deletion, C-MYC rearrangement/amplification and BCL-6 rearrangement significantly correlated with staging, curative effect and prognosis of the patients (P < 0.05).

CONCLUSIONThe curative efficacy and prognosis of the DLBCL patients with abnormality of P53, C-MYC and BCL-6 have been confirmed to be unsatisfactory.

DNA-Binding Proteins ; genetics ; metabolism ; Humans ; In Situ Hybridization, Fluorescence ; Lymphoma, Large B-Cell, Diffuse ; diagnosis ; genetics ; metabolism ; Prognosis ; Proto-Oncogene Proteins c-bcl-6 ; Proto-Oncogene Proteins c-myc ; genetics ; metabolism ; Tumor Suppressor Protein p53 ; genetics ; metabolism

This study was aimed to investigate the effects of SUV39H1 siRNA on proliferation and apoptosis of acute myelogenous leukemia KG-1 cell line. The small interfering RNA (siRNA) targeting SUV39H1 gene was designed and transfected into KG-1 cells by Lipofectamine(TM) 2000. Cell growth affected by SUV39H1 siRNA was determined by MTS method. Cell apoptosis was measured by flow cytometry. The expressions of P15 and anti-apoptosis protein such as BCL-2, procaspase-9, procaspase-3 and C-MYC were detected by Western blot. The results indicated that siRNA targeting SUV39H1 inhibited proliferation of KG-1 cells. Proliferated rates were (76.43 ± 1.98)%, (51.31 ± 1.84)%, (37.31 ± 1.61)%, (18.94 ± 3.22)% respectively after transfection with SUV39H1 siRNA at 30, 60, 120, 240 nmol/L for 48 h, while P15 expression was upregulated. Apoptotic cells significantly increased, apoptotic rates were (40.2 ± 5.1)%, (56.8 ± 4.8)%, (71.6 ± 5.6)% respectively after transfection with siRNA targeting SUV39H1 at 30, 60, 120 nmol/L (P < 0.05). The protein expression of BCL-2, procaspase-9, procaspase-3, C-MYC was downregulated after transfection. It is concluded that the siRNA targeting SUV39H1 inhibits cell growth and induces cell apoptosis of KG-1 cell line, which may be a new therapeutic target in human leukemia.
Apoptosis ; genetics ; Caspase 3 ; metabolism ; Caspase 9 ; metabolism ; Cell Line, Tumor ; Cell Proliferation ; Humans ; Methyltransferases ; genetics ; Proto-Oncogene Proteins c-bcl-2 ; metabolism ; Proto-Oncogene Proteins c-myc ; metabolism ; RNA Interference ; RNA, Small Interfering ; genetics ; Repressor Proteins ; genetics

OBJECTIVETo study the effects of cadmium on hepatocellular DNA damage, expression of proto-oncogenes c-myc, c-fos, and c-jun as well as apoptosis in rats.

METHODSCadmium chloride at the doses of 5, 10, and 20 micromol/kg was given to rats by i.p. and there were 5 male SD rats in each group. Hepatocellular DNA damage was measured by single cell gel electrophoresis (or comet assay), while expression of proto-oncogenes c-myc, c-fos, and c-jun in rat hepatocytes were measured by Northern dot hybridization. C-Myc, c-Fos, and c-Jun were detected with immuno-histochemical method. Hepatocellular apoptosis was determined by TUNEL (TdT-mediated dUTP Nick End Labelling) and flow cytometry.

RESULTSAt the doses of 5, 10, and 20 micromol/kg, cadmium chloride induced DNA damage in rat hepatocytes and the rates of comet cells were 50.20%, 88.40%, and 93.80%, respectively. Results also showed an obvious dose-response relationship between the rates of comet cells and the dose of cadmium chloride (r = 0.9172, P < 0.01). Cadmium chloride at the doses of 5, 10, and 20 micromol/kg induced expression of proto-oncogenes c-myc, c-fos, and c-jun. The positive brown-yellow signal for c-myc, c-fos, and c-jun was mainly located in the cytoplasm of hepatocytes with immunohistochemical method. TUNEL-positive cells were detected in cadmium-treated rat livers. Apoptotic rates (%) of cadmium-treated liver cells at the doses of 5, 10, and 20 micromol/kg were (17.24 +/- 2.98), (20.58 +/- 1.35), and (24.06 +/- 1.77) respectively, being significantly higher than those in the control. The results also displayed an obvious dose-response relationship between apoptotic rates and the dose of cadmium chloride (r = 0.8619, P < 0.05).

CONCLUSIONCadmium at 5-20 micromol/kg can induce hepatocellular DNA damage, expression of proto-oncogenes c-myc, c-fos, and c-jun as well as apoptosis in rats.

Animals ; Apoptosis ; drug effects ; Cadmium ; toxicity ; DNA Damage ; Gene Expression Regulation ; drug effects ; Hepatocytes ; cytology ; drug effects ; metabolism ; Male ; Proto-Oncogene Proteins ; genetics ; metabolism ; Proto-Oncogene Proteins c-fos ; genetics ; metabolism ; Proto-Oncogene Proteins c-jun ; genetics ; metabolism ; Proto-Oncogene Proteins c-myc ; genetics ; metabolism ; Rats ; Rats, Sprague-Dawley

OBJECTIVE: To study the mechanism of apoptosis in laryngeal carcinoma cell induced by Stat3 antisense oligodeoxynucleotide (ASODN). METHOD: The designed Stat3 ASODN was transferred into laryngeal carcinoma Hep-2 cell by lipofection. Expression of Bcl-2, Bax and C-Myc were detected by Western blot and PCR. RESULT: Western blot and PCR results demonstrated that Stat3 ASODN could significantly increased the expression of Bax and decreased the expression of Bcl-2 and C-Myc when the concentration of antisense oligodeoxynucleotide were heightened. CONCLUSION Stat3 ASODN participate in apoptosis by enhancing the expression of Bax and reducing the expression of Bcl-2 and C-Myc.
Apoptosis ; genetics ; Cell Line, Tumor ; Gene Expression Regulation, Neoplastic ; Humans ; Oligodeoxyribonucleotides, Antisense ; genetics ; Proto-Oncogene Proteins c-bcl-2 ; metabolism ; Proto-Oncogene Proteins c-myc ; metabolism ; STAT3 Transcription Factor ; genetics ; bcl-2-Associated X Protein ; metabolism

This study was aimed to investigate the effect of SU11248 on proliferation and apoptosis of leukemia cell line K562 in vitro and its mechanism. The inhibitory effect of 3.2 µg/ml SU11248 on K562 proliferation was tested by MTT assay. The ability of SU11248 to induce apoptosis of K562 cells was examined by TUNEL and DNA ladder. The expression of C-MYC, hTERT and BCR-ABL mRNA in K562 cells was detected by RT-PCR. The protein expression of Akt and p-Akt in K562 cells was detected by Western blot. The results showed that the proliferation of K562 cells was obviously inhibited by 3.2 µg/ml SU11248 in a time-dependent manner. SU11248 could induce K562 cells apoptosis in dose-and time-dependent manner. The mRNA expression of C-MYC, hTERT and BCR-ABL was reduced significantly by SU11248 in a time-dependent manner (P < 0.05). Western blot detection showed that the expression of p-Akt protein in K562 cells decreased in dose-and time-dependent manner after SU11248 treatment, but the expression of Akt was not significantly changed. It is concluded that SU11248 can inhibit the growth of K562 cells efficiently through inducing apoptosis, its mechanism may be closely relate with the expression down-regulation of C-MYC, hTERT, BCR-ABL and the inhibition of Akt phosphorylation.
Apoptosis ; drug effects ; Cell Proliferation ; drug effects ; Fusion Proteins, bcr-abl ; metabolism ; Humans ; Indoles ; pharmacology ; K562 Cells ; Proto-Oncogene Proteins c-akt ; metabolism ; Proto-Oncogene Proteins c-myc ; metabolism ; Pyrroles ; pharmacology ; RNA, Messenger ; genetics ; Telomerase ; metabolism

In this study, the effect of heparin-derived oligosaccharide (HDO) on bovine vascular smooth muscle cell (VSMC) proliferation and signal transduction mechanism involved were investigated. The levels of PKC-alpha protein and mRNA were determined by cell-based ELISA, RT-PCR, Western blotting and immunocytochemical methods. Meanwhile, mRNA levels of c-jun, c-myc and c-fos were assayed by RT-PCR method. The results showed that HDO inhibited newborn calf serum (NCS)-induced expression of PKC-alpha and proto-oncogenes, which may be one of the mechanisms for the inhibition of VSMC proliferation by HDO. Flow cytometry analysis indicated that HDO blocked NCS-induced cell cycle progression by arresting cells at G0/G1 phase. The results imply that HDO inhibits VSMC proliferation by moderating the gene level of PKC-alpha, eventually inhibiting proto-oncogene mRNA expression and blocking G1/S transition.
Animals ; Cattle ; Cell Cycle ; drug effects ; Cell Proliferation ; drug effects ; Cells, Cultured ; G1 Phase ; drug effects ; Heparin ; pharmacology ; Muscle, Smooth, Vascular ; cytology ; metabolism ; Oligosaccharides ; pharmacology ; Protein Kinase C-alpha ; genetics ; metabolism ; Proto-Oncogene Proteins c-fos ; genetics ; metabolism ; Proto-Oncogene Proteins c-jun ; genetics ; metabolism ; Proto-Oncogene Proteins c-myc ; genetics ; metabolism ; RNA, Messenger ; metabolism ; Signal Transduction

This study was aimed to explore the effects of Notch ligand DLL4 on the protein expression of the transcription factor YY1 and proto-oncogene c-Myc, as well as K562 cell proliferation. The experiment was divided into 3 groups: normal control, negative control (pBudCE4.1-transfected) and experimental (pBudCE4.1-DLL4-transfected) groups. At 48 hours after transfection, the expression level of DLL4, YY1 and c-Myc proteins in K562 cells of each group were detected by Western blot and indirect immunocytochemical method; the CCK-8 method was used to detect proliferation of K562 cells; at 48 hours after transfection, cell cycle distribution and apoptosis of K562 cells were detected by flow cytometry. The results showed that the protein expression of DLL4, YY1 and c-Myc in K562 cells of every group were found. The protein expression levels of DLL4, YY1 and c-Myc in the experimental group cells were significantly higher than that in control groups (p < 0.05). The cell number in G(0)/G(1) phase increased in the experimental group and was higher than that in the control groups (p < 0.001), and the number of apoptotic cells were also increased (p < 0.001). It is concluded that DLL4 gene was successfully transfected into K562 cells, which increased the protein expression levels of transcription factor YY1 and proto-oncogene c-Myc, leading to the cell proliferation slower in experiment group, inducing the cell cycle arrested in G(0)/G(1) phase and increasing apoptosis.
Cell Cycle ; Cell Proliferation ; Humans ; Intercellular Signaling Peptides and Proteins ; genetics ; K562 Cells ; Proto-Oncogene Proteins c-myc ; metabolism ; Transfection ; YY1 Transcription Factor ; metabolism

Oncogene and antioncogene play contrary effects on the cell growth and proliferation controlling process, and cancer occurs when the presence of imbalance expression between them. That means there is yin-yang relationship between oncogene (yang) and antioncogene (yin), and also inside both of them. Taking the oncogene myc and antioncogene p53 for example, the yin gene p53 acts, in the yin side, to promote cell apoptosis and inhibit cell growth, while in the yang side, it facilitates for repairing the injured DNA to keep cell survival; the yang gene myc, promoting cell growth and proliferation in the yang side and inducing cell apoptosis in the yin side. To elucidate the yin-yang reactions between oncogene and antioncogene would be of important significance in the all-round and profound research of cancer.
Genes, Tumor Suppressor ; Humans ; Medicine, Chinese Traditional ; Neoplasms ; genetics ; Oncogenes ; genetics ; Proto-Oncogene Proteins c-myc ; metabolism ; Tumor Suppressor Protein p53 ; metabolism ; Yin-Yang