1.A systematic review of the mechanisms and influence factors of cancer-related fatigue
Xinxue TIAN ; Yanhui CUI ; Xiaohong KANG ; Weiwei LI ; Zhanhui MIAO ; Ping LU
Journal of Chinese Physician 2018;20(7):1108-1111
Cancer-related fatigue (CRF) is one of the most common symptoms in clinical cancer patients.It is associated with cancer itself or with cancer-related therapies.It is a persistent and subjective tiredness experience.It not only affects the patient;s physical,psychological and physical condition,social function,quality of life,but also may cause interruption of cancer-related treatment and affect the patient's life.However,the etiology and mechanism of CRF are not fully understood.Many foreign scholars believe that the occurrence of CRF may be related to anemia,obesity,tumor type,insomnia,inflammatory cytokines,hypothalamic-pituitary-adrenal axis and so on.As cancer patients demand higher quality of life,CRF are increasingly receiving medical attention.In this paper,the related factors and mechanisms of CRF are stated.
2.The six-year operation faults statistics analysis and prediction of Philips Brilliance big bore CT
Shouyu WANG ; Xiaochun WANG ; Xiaoqing HUO ; Peng WU ; Bo LIU ; Zhanhui MIAO ; Ping LU
Chinese Journal of Radiation Oncology 2020;29(11):1000-1002
Objective:To analyze the 6-year operation faults of PHILIPS Brilliance big bore CT, identify the common problems, make corresponding maintenance plans, reduce the incidence of failures, and carry out simulation prediction of the occurrence rate of failures in the next few years.Methods:The failure data of Brilliance big bore CT from June 2012 to June 2018 were collected, and the curve estimation function in SPASS 19.0 software and the pareto diagram were used to analyze the relationship between the number of failures, time and failure types, and the prediction was made.Results:A total of 28 faults occurred during the 6-year opeation of Brilliance big bore CT. During the first half year, five times of faults occurred with the highest fault rate and then tended to stabilize. The linear function model was obtained using the curve estimation: y=-0.033 x+ 2.099( y for the number of fault, unit for times, x for the unit of time for half a year), the model of R2=0.003. In the next three years, approximately twice faults occurred within half year. The pareto chart showed that 16 faults occurred during data collection, including 3 faults in the treatment bed and 3 faults in the power supply system, respectively. The accumulative ratio of the above three faults was 71.4%, which were the main fault sources. Conclusion:The fault statistical analysis of Brilliance big bore CT is helpful for department maintenance personnel to better understand CT, develop effective maintenance programs, reduce the occurrence of faults, and predict the incidence of faults in the future.
3. Mechanism of long non-coding RNA-metastasis associated lung adenocarcinoma transcript 1 induced invasion and metastasis of esophageal cancer cell EC-109
Qingqin ZHANG ; Yanhui CUI ; Ying WANG ; Weizheng KOU ; Fei CAO ; Xiangjun CAO ; Zhanhui MIAO ; Xiaohong KANG
Chinese Journal of Oncology 2017;39(6):405-411
Objective:
To investigate the effect and mechanism of long non-coding RNA-metastasis associated lung adenocarcinoma transcript 1, (LncRNA-MALAT1) on invasion and metastasis of esophageal cancer cell EC-109.
Methods:
EC-109 cells were transfected with lentiviral vector carrying short hairpin RNA of MALAT1( shRNA-MALAT1) or a nonspecific shRNA control (shRNA-control). The expressions of MALAT1, microRNA-200a, ZEB1 and ZEB2 were detected by qRT-PCR. The effect of shRNA-MALAT1 on invasion of EC-109 cells was determined by transwell assay. The expressions of components of epithelial-msenchymal transition pathway in EC-109 cells were determined by immunofluorescence array and western blotting. The expression relationship between MALAT1 and miR-200a in EC-109 cells was detected by dual-luciferase reporter assay.
Results:
The result of qRT-PCR showed that the expressions levels of MALAT1, ZEB1 and ZEB2 in shRNA-MALAT1 group were 0.43±0.06, 0.64±0.04 and 0.51±0.04, respectively, significantly lower than 0.97±0.08, 1.06±0.07 and 0.98±0.05 in shRNA-control group and 1 in control group, respectively(all
4. Mechanism of MALAT1 induced osimertinib resistance in HCC827 lung cancer cells
Xiaohong KANG ; Yuanyuan GAO ; Ying WANG ; Yanhui CUI ; Kelei ZHAO ; Weizheng KOU ; Zhanhui MIAO ; Fei CAO ; Yabin GONG
Chinese Journal of Oncology 2019;41(4):257-262
Objective:
To test the effect of metastasis associated in lung adenocarcinoma transcript 1 (MALAT1) and/or osimertinib on the proliferation and apoptosis of HCC827 cells, and explore the potential mechanism of MALAT1 induced resistance to osimertinib.
Methods:
We transfected HCC827 cells with LV-vector or LV-over/MALAT1. Stable transfected cells (HCC827/Vector, HCC827/MALAT1) were selected by adding puromycin. HCC827/MALAT1 cells were further transfected with the shRNA-negative control (NC) or shRNA-human epidermal growth factor receptor 3 (ERBB3) plasmid. The effects of overexpression of MALAT1, knockdown of ERBB3 and/or osimertinib on the proliferation of HCC827 cells were evaluated by 3-(4, 5-dimethyl-2-thiazolyl)-2, 5-diphenyl-2H tetrazolium bromide (MTT) assay. Cell apoptosis induced by MALAT1 overexpression, knockdown of ERBB3 and/or osimertinib treatment were analyzed by flow cytometry analysis. The expressions of EGFR and ERBB3 signal pathway related proteins in HCC827 cells treated with overexpression of MALAT1, knockdown of ERBB3 and/or osimertinib treatment were detected by western blot.
Results:
The MTT assay showed that sensitivity to osimertinib of HCC827/MALAT1 cells were significantly repressed. The 50% inhibitive concentration (IC50) of osimertinib >4 000 nmol/L in HCC827/MALAT1 cells. However, knockdown of ERBB3 facilitated the anti-proliferation effect of osimertinib, and the IC50 of osimertinib in shRNA-ERBB3 cells was (17.27±3.21) nmol/L. The results of flow cytometry analysis showed that the apoptotic rate of HCC827/MALAT1 cells induced by 10 nmol/L osimertinib was (8.38±0.92)%, significantly lower than (27.17±5.83)% of knockdown of ERBB3 (
5. Upregulation of PLOD2 promotes invasion and metastasis of osteosarcoma cells
Fei CAO ; Xiaohong KANG ; Yanhui CUI ; Ying WANG ; Kelei ZHAO ; Yanan WANG ; Weizheng KOU ; Zhanhui MIAO ; Xiangjun CAO
Chinese Journal of Oncology 2019;41(6):435-440
Objective:
To investigate the relationship of procollagen-lysine 2-oxoglutarate 5-dioxygenase 2 (PLOD2) expression and the clinical characteristics of osteosarcoma, and explore the potential mechanism of tumour metastasis promoted by PLOD2.
Methods:
The expression of PLOD2 in osteosarcoma tissues and paired adjacent tissues were detected by immunohistochemistry and qRT-PCR. Correlation of PLOD2 expression in osteosarcoma with the clinical pathologic features was analyzed by Chi square test and Kaplan-Meier analysis.Fibrillar collagen formation and collagen deposition in the tumor tissues were detected by picrosirius red staining. We transfected U-2OS cells with LV-vector, LV-over/PLOD2, sh-NC and sh-PLOD2. The expression of PLOD2 was detected by qRT-PCR. The impact of POLD2 on U-2OS cell invasion was determined by wound-healing assay and Transwell migration assay. The expressions of PLOD2/FAK/JAK2-STAT3 signal pathway related proteins were detected by western blotting.
Results:
The high expression level of PLOD2 in osteosarcoma tissues was 72.5%, significantly higher than 0% in paired adjacent noncancerous tissues (