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Objective To observe the expression levels of serum osteopontin (OPN),adenosine kinase 1 (TK1) and secretory protein Dikkopf 1 (DKK1) in patients with lung cancer and their clinical significances.Methods Lung cancer patients treated in the First Affiliated Hospital of Xi'an Medical University from February 2017 to April 2018 were selected as the lung cancer group (60 cases),and 60 healthy adults who received physical examination in the same period were selected as the control group.The differences of serum OPN,TK1 and DKK1 levels between the lung cancer group and the control group and lung cancer patients with different characteristics were compared.Measurement data were compared by using t test.Results The levels of serum OPN,TK1 and DKK1 in lung cancer patients were (38.56±3.18) μg/L,(4.69±1.03) pmol/L and (3.76±0.89) ng/ml,respectively,which were higher than those in the control group [(15.98±2.06) μg/L,(1.01±0.22)pmol/L,(1.21±0.24) ng/ml;t =-46.162,-27.064,-21.428,all P ＜ 0.01].The levels of serum OPN,TK1 and DKK1 in lung cancer patients of different ages and gender had no statistical differences (all P ＞ 0.05).The levels of serum OPN,TK 1 and DKK1 in stage Ⅲ-Ⅳ lung cancer patients were (57.18 ±3.12) μg/L,(6.26±1.28) pmol/L and (4.98±1.03) ng/ml,respectively,which were higher than those in stage Ⅰ-Ⅱ lung cancer patients [(30.35±2.96) μg/L,(3.49±0.67) pmol/L,(3.01±0.96) ng/ml;t =-34.156,-10.690,-7.665,all P ＜ 0.01].The levels of serum OPN,TK 1 and DKK1 in non-small cell lung cancer (NSCLC) patients were (55.13±5.02) μg/L,(5.96±1.11) pmol/L and (5.02±1.32) ng/ml,respectively,which were higher than those in small cell lung cancer (SCLC) patients [(29.68±3.16) μg/L,(3.13±0.98) pmol/L,(2.86±0.56) ng/ml;t =-22.353,-10.213,-7.688,all P ＜ 0.01].Conclusion The levels of serum OPN,TK1 and DKK1 in patients with lung cancer are higher,which are related to the type and stage of lung cancer.
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Objective To examine the expressions of multidrug resistance gene (MDR)-1 and P-glycoprotein (P-gp) in nasopharyngeal squamous cell carcinoma CNE1 cell line before and after X-ray exposure.Methods CNE1 cells were exposed to X-ray.After the irradiation,the CNE1 cells were cultured for 24 hours and tested.The mRNA expressions of MDR-1 in CNE1 cells were measured by semi-quantitative real-time polymerase chain reaction (RT-PCR) before and after X-ray exposure,and the protein expressions of P-gp in CNE1 cells were detected by Western blotting.The protein expressions of P-gp in CNE1 cells were observed by confocal microscope before and after X-ray exposure.Results The results of RT-PCR showed that the absorbance (A) values of MDR-1 mRNA in CNE1 cells were 0.17 ±0.01 and 0.34 ±0.03 before and after irradiation,and the difference was statistically significant (t =16.541,P ＜ 0.001).The results of Western blotting showed that the A values of P-gp protein in CNE1 cells were 0.02 ± 0.01 and 0.04 ± 0.01,and the difference was statistically significant (t =4.612,P =0.016).The green fluorescence intensity of P-gp protein in CNE1 cells after X-ray irradiation was higher than that before X-ray irradiation by confocal microscope.Conclusion X-ray irradiation can cause the high expressions of MDR-1 and P-gp in CNE1 cells,suggesting that X-ray irradiation can induce the occurrence of multidrug resistance in CNE1 cells.
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Objective To investigate the relationship between multidrug resistance of X-ray irradiated human nasopharyngeal squanous carcinoma cell line CNE1 and platelet endothelial cell adhesion molecule-1 (PECMA-1)/phosphatidylinositol 3-kinase (PI3K)/protein kinase B (AKT)/Bcl-2 signaling pathway.Methods ①The CNE1 cells were cultured in incubator.Exponentially growing CNE1 cells were exposed to 50 Gy ionizing radiation administered in 25 fractions,2 Gy per fraction,once every two days,and the CNE1/R cells were collected.②CNE1/R cells were cultured for 24 h,and divided into three groups:the control group,experimental group one (CNE1/R cells were processed through 1 ∶ 600 PECAM-1 antibody for 24 h) and experimental group two (CNE1/R cells were processed through 10 μmol/L PI3K inhibitor LY294002 for 24 h).③The half maximal inhibitory concentration (IC50) values of the control group and two experimental groups of CNE1/R cells were detected by methyl thiazolyl tetrazolium (MTT).④The mRNA expressions of PI3K and Bcl-2 in the control group and experimental group one were measured by semi-quantitative reverse transcription-polymerase chain reaction (RT-PCR).⑤The mRNA expressions of AKT and Bcl-2 in the control group and experimental group two were measured by semi-quantitative RT-PCR.Results ①The IC50 of the control group,experimental group one and two were (2.99 ± 0.02) μg/ml,(1.50 ± 0.03) μg/ml and (1.60 ±0.05)μg/ml,and the difference among the three groups was statiatically signficant (F =4 381.263,P =0.000).The IC50 of the two experimental groups were obviously lower than that of the control group (t =116.885,P =0.000;t =73.006,P =0.000).②The semi-quantitative values of PI3K in the control group and experimental group one were 1.66 ±0.01 and 0.90 ±0.05 (t =50.394,P =0.000),and the semi-quantitative values of Bcl-2 were 1.66 ±0.02 and 0.71 0.05 (t =183.165,P =0.000),and the differences were statistically significant.③The semi-quantitative values of AKT of control group and experimental group two were 1.53 ± 0.01 and 0.72 ± 0.01 (t =135.281,P =0.000),and the semi-quantitative values of Bel-2 were 1.66 ± 0.02 and 0.63 ± 0.02 (t =128.814,P =0.000),and the differences were statistically significant.Conclusion PECAM-1 induced multidmg resistance of human nasopharyngeal squamous cell carcinoma CNE1 cells may be related to the activity of Bcl-2 through the signal pathway of PI3K/AKT.
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[ ABSTRACT] AIM:To investigate the effects of c-Met on the proliferation and the sensitivity to chemotherapeutic drugs of triple negative breast cancer cells.METHODS: Doxorubicin-resistant cells ( MDA-MB-231/ADR) were estab-lished.The expression of c-Met at mRNA and protein levels in the MDA-MB-231/ADR cells and parental MDA-MB-231 cells was detected by real-time PCR and Western blotting.c-Met siRNA and plasmid or AKT siRNA were transfected into the cancer cells.The cell proliferation and the sensitivity to doxorubicin were determined by MTT assay.RESULTS:The expression of c-Met at mRNA and protein levels in MDA-MB-231/ADR cells was significantly higher than that in parental MDA-MB-231 cells.Transfection with pBABE-puro TPR-MET plasmid into the MDA-MB-231 cells induced cell prolifera-tion and resistance to doxorubicin.Meanwhile, inhibition of c-Met in the MDA-MB-231/ADR cells by siRNA reversed the doxorubicin-resistance.In addition, over-expression of c-Met led to higher phosphorylation level of AKT, which was in-volved in the effects of c-Met on the MDA-MB-231 cell proliferation and doxorubicin-resistance.CONCLUSION: c-Met may have the potential as a therapeutic target in the treatment of triple negative breast cancer.
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Objective To detect the levels of AKAP12 methylation by methylation‐specific high‐resolution melting curve(MS‐HRM ) in peripheral blood in patients with colorectal cancer and investigate its clinical significance .Methods We used MS‐HRM technology to detect the levels of AKAP12 methylation in peripheral blood in 60 lung cancer patients ,and analyzed the relationship between the levels of AKAP12 methylation and pathological parameters of lung cancer patients .Results 34(56 .7% ) of the 60 lung cancer patients were found to be methylated at the AKAP12 promoter region by MS‐HRM ,the methylation levels of 18 cases ranged between 1% -20% ,14 cases ranged between 20% -60% ,2 cases ranged between 60% -100% .There was no significant differences between the levels of AKAP12 methylation and lung cancer patients′age and gender(P>0 .05) .However ,it was signifi‐cantly higher in the patients with high pathological stage and differentiation degree (P<0 .05) .Conclusion AKAP12 promoter re‐gion methylation was related to tumor progression and malignant degree .