Recent studies have demonstrated that intravenous transplantation or local injection of bone marrow cells can induce unexpected changes of their fate. The results of these experiments showed that after transplantation or injecton, some of tissue specific somatic cells such as hepatocytes, skeleton, cardiac muscle cells and brain cells expressed the donor cell-specific genes, such as Y chromosome. There are two hypotheses that can explain this phenomenon. One is bone marrow stem cell transdifferentiation and the other is spontaneous cell fusion.

Objective One of the major obstacle to the successful treatment of cancer in clinic is the drug-resistance phenotype.In this study,the effect of realgar(REA) on the induction of apoptosis and the reversal of drug resistance were investigated. Methods Human breast cancer line MCF-7 and its adriamycin(ADM) resistant counterpart MCF-7/ADM cells were used in this study.15mg/L REA and 25mg/L REA were selected as non-cytotoxic dose and low-cytotoxic to MCF-7/ADM cells respectively by MTT assay.Then,they were adopted to affect the growth of MCF-7/ADM cells. MTT assay was used to analyze the effect of REA on drug sensitivity to ADM.The cells apoptosis was detected by transmission electron microscope and flow cytornetry.The expressions of anti-apoptosis protein Bcl-2 were detected by flow cytometry.Finally,the intracellular accumulation of ADM in MCF-7/ADM cells was detected by fluorescent-spectrophotometry. Results REA reversed the drug-resistance of ADM in MCF-7/ADM cells with dose-dependent relationship.When 15mg/L REA or 25mg/L REA was added into the culture,the 50% inhibitory concentration(IC_(50)) of ADM in MCF-7/ADM cells was reduced from 30.4mg/L to 13.2mg/L and 10.8mg/L(P

Objective In many types of epithelial tumors,down-regulation or mutation of the epithelial cell-adherent molecule E-cadherin is associated with an increased invasiveness that can be prevented by the forced expression of the cell-adherent molecule.This suggests that E-cadherin is a latestage tumor suppressor that prevents invasion and metastasis.This study was to investigate cell invasion and migration status of human ovary serous cystadeno carcinoma HO-8910 cell line when the E-cadherin expression was down-regulated with RNA interference(RNAi) technology. Methods E-cadherin siRNA was transfected into HO-8910 cells to inhibit the expression of E-cadherin.The effect of RNAi was detected by immunofluoresence assay and Western blotting.The invasive ability of the cancer cells was determined by Transwell assay. Results After RNAi,the expressions of E-cadherin were significantly decreased from 63.7% to 11.9%(P

Objective L-selectin is an important adhesion molecule,which is the lymph cell's homing receptor specifically expressed on leukocytes.A non-lymphoma cell line-HCa-F has the high potential ability of metastasis to peripheral lymph nodes,whose character is similar to lymphoma's.We want to explore whether the HCa-F cell's metastasis mechanism is also similar to lymphoma's,that is to say,whether HCa-F cell can also express L-selectin and the expression of L-selectin bring about the lymph node metastasis character. Methods First,?-fetoprotein,CD3 and CD20's monoclonal antibodies were used to identify the origin of HCa-F cell;then we analysed whether the HCa-F cell can express L-selectin by means of flow cytometry analysis,RT-PCR,and Western blotting;finally,Stamper-Woodruff method was used to examine the L-selectin's function. Results Immunostaining showed that the HCa-F cell was ?-fetoprotein positive,CD3 and CD20 negative cell line,which suggests that it is a liver cell line.And results of flow cytometry,RT-PCR,and Western blotting showd that HCa-F cell can express L-selectin.Additionally,anti-L-selectin's antibody can inhibit the adhesion between HCa-F cells and frozen section of mouse lymph node.Conclusion L-selectin expressed on HCa-F cells is a functional molecule which can facilitate HCa-F cell's metastasis to lymph nodes.

Objective To explore the effect of ?-elemece on the reverse of drug resistance and the expression of P-glycoprotein(P-gp) in MDR K562/ADM cells. Methods MTT method was used to detect the sensitivity of cell and its reverse of drug resistance.Immunohistochemistry and immunoelectron microscopy were for observing the expression of P-gp.It's quantitative analysis was determined by flow cytometry.All experimental data were dealt with by SPSS(10.0 production pacility) soft ware. Results 1.Non-cytotoxic dose of ?-elemece(4.0?mg/L) could obviously decrease the IC-(50) value of K562/ADM cells to ADM.The reversing fold was 2.18;2.The level of P-gp expression was higher in K562/ADM cells than that in its parent K562 cells.Our studies also showed that the distribution of P-gp was on membrane of K562/ADM cells;3.Non-cytotoxic dose of ?-elemece(4.0?mg/L) could remarkably decrease the P-gp expression in MDR K562/ADM cells.Conclusion\ ?-elemece could evidently reverse drug resistance of K562/ADM to ADM.Decreasing the P-gp expression in drug resistance cell is one of the main mechanism of reversion.

Objective To study the expression of ABC gene family of MCF 7/ADM cells as compared to parental cell line MCF 7/S, and its reversion by realgar of the expressed genes. Methods Expression of ABC family genes was examined by RT PCR, and cell growth by MTT test. Results The expression of ABC gene family was positive in MCF 7/ADM cells compared to MCF 7/S cells; Realgar can down regulate the expression ABC gene family in MCF 7/ADM cells; the IC 50 of ADM to MCF 7/ADM cells was decreased.Conclusion ABC gene family was responsible for the induced resistance of MCF 7/ADM cells to ADM; Realgar is able to reverse partly the multidrug resistance of the human breast cancer cell line MCF 7/ADM. [

OBJECTIVE: To observe the effects of psoralen plus ultraviolet-A light (PUVA) on K562 cells and the relative mechanism. METHODS: The effects of psoralen, ultraviolet-A light and PUVA on K562 cells were assayed by monotetrazolium test (MTT). DNA content was analyzed by flow cytometry (FCM). The apoptotic rates of K562 cells treated with 40 and 80 microg/ml psoralen for 24 and 48 hours were assayed by Annexin-V-FITC/PI reagent kit on FCM respectively. The ultrastructures of apoptotic cells were observed by a transmission electron microscope (TEM). RESULTS: Either single psoralen therapy or single ultraviolet-A irradiation had inhibiting effect on K562 cells. The inhibiting effect of PUVA on K562 cells was stronger than that of the single psoralen therapy or single ultraviolet-A light irradiation (P<0.05). Apoptotic peak (AP) was detected by FCM. TEM test showed that K562 cells treated with PUVA were smaller, having condensed cell nucleus, assembled chromatin, disintegrated nucleus body and the majority of the cells appeared to be apoptotic conformation. CONCLUSION: Psoralen has inhibiting effect on K562 cells, and the effect of PUVA is more significant. It is suggested that 10 min irradiation and 40 microg/ml terminal concentration of psoralen be probably the best choice for PUVA. The inhibiting effect of PUVA is due to apoptosis.

OBJECTIVETo investigate the effect of drug resistance by arsenic trioxide (As(2)O(3)) and its possible mechanism in human breast cancer cell line MCF-7/ADM.

METHODSCytotoxicity of As(2)O(3) and the sensibility to adriamycin (ADM) in MCF-7/ADM cell line, a ADM-resistance cell line of human breast cancer, were studied through MTT assay. The concentration of intracellular ADM was detected by spectrofluorometry. With MCF-7/ADM cells treated with As(2)O(3) in combination with ADM, the glutathione-s-transferase (GST) activity was measured by biochemical method. The expression of GST-pi mRNA was assessed by RT-PCR.

RESULTSThe non-cytotoxic dose of As(2)O(3) was 0.2 micro mol/L and the low cytotoxic dose was 0.8 micro mol/L to MCF-7/ADM cell line. 0.2 micro mol/L As(2)O(3) could significantly increase the intracellular accumulation of ADM in MCF-7/ADM cell line (P < 0.05). The medium inhibition concentration (IC(50)) was obviously reduced from 53.74 micro mol/L to 25.0 micro mol/L, with a reversal ratio of 2.1 as compared to its parental cell line. Before and after 0.2 micro mol/L, 0.8 micro mol/L As(2)O(3) were given, GST activities were decreased from 29.68 +/- 0.29 U/ml to 19.29 +/- 2.10 U/m l and 12.66 +/- 2.78 U/ml (P < 0.05). In addition, MCF-7/ADM cell line had overexpression of GST-pi mRNA. A significant down regulation of GST-pi mRNA was observed in MCF-7/ADM cells when As(2)O(3) and ADM (21.55 micro mol/L) were given for 24 hours.

CONCLUSIONAs(2)O(3) is able to enhance the cytotoxicity of ADM and partly reverse the ADM resistance of MCF-7/ADM cell line of human breast cancer, which may be related to the variation of GST-pi enzyme.

Antineoplastic Agents ; pharmacology ; Arsenicals ; pharmacology ; Breast Neoplasms ; Dose-Response Relationship, Drug ; Doxorubicin ; pharmacology ; Drug Resistance, Multiple ; Drug Resistance, Neoplasm ; Female ; Gene Expression ; Glutathione S-Transferase pi ; Glutathione Transferase ; genetics ; Humans ; Isoenzymes ; genetics ; Oxides ; pharmacology ; RNA, Messenger ; Reverse Transcriptase Polymerase Chain Reaction ; Tumor Cells, Cultured