Ting-Yan Lin

Fujian Medical University, Min-hou, Fujian, China

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Publications (5)3.13 Total impact

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    ABSTRACT: The aim of the present study was to observe the effects of sorafenib on the proliferation, apoptosis and invasion of A549/DDP cisplatin‑resistant lung adenocarcinoma cells cultured in vitro. The A549/DDP cisplatin‑resistant lung adenocarcinoma cell strain was cultured in vitro, the cell culture group incubated in culture medium only was set as the control group (Group S0) and the four concentration gradients of sorafenib were added to the culture groups as the experimental groups: S1, 2 µmol/l; S2, 4 µmol/l; S3, 8 µmol/l; and S4, 16 µmol/l. The MTT assay was used to determine the growth inhibition rate of the cells, which were respectively subjected to sorafenib treatment for 24, 48 and 72 h. Flow cytometry was used to determine the rate of apoptosis of cells in each group following sorafenib treatment for 72 h. Furthermore, the Transwell invasion experiment was used to determine the effect on A549/DDP cell invasion following sorafenib treatment for 24 h. Based on the MTT assay, it was found that the inhibition rates of A549/DDP cisplatin‑resistant lung adenocarcinoma cells in groups S1‑4 following sorafenib treatment for 24 h were 4.58±2.82, 14.93±2.62, 37.58±7.13 and 58.39±8.15%, respectively. For 48 h, inhibition rates in S1‑4 were 14.98±2.93, 26.28±7.31, 63.00±3.05 and 78.84±3.96%, respectively, and for 72 h, inhibition rates were 18.80±2.82, 32.71±2.55, 75.51±4.73 and 87.50±3.36%, respectively. The difference in the inhibition rates of cells among the experimental groups for the same incubation time showed statistical significance (P<0.05). Flow cytometric analysis indicated that the rate of apoptosis in the control group was 8.88±0.81% following sorafenib treatment for 72 h, and the rates of apoptosis in groups S1‑4 were, 12.84±0.24, 17.27±0.78, 21.98±0.75 and 49.67±1.38%, respectively. The rate of apoptosis in each experimental group was higher compared with that in the control group (P<0.05). The difference in the rate of apoptosis among the experimental groups was statistically significant (P<0.05). The Transwell assay showed that the number of cells permeating the septum in the control group was 82.7±2.3/high power lens (HP), while the average number of cells permeating septum in groups S1‑4 following treatment with sorafenib for 24 h was 58.2±2.5, 41.3±1.3, 22.6±2.1 and 14.7±1.1/HP, which was significantly lower compared with the control group. The number of cells permeating the septum in each experimental group decreased with the enhancement of the concentration gradient. The differences were statistically significant (P<0.05). In conclusion, sorafenib inhibits the proliferation of A549/DDP cisplatin‑resistant lung adenocarcinoma cells in a time‑ and concentration‑dependent manner. In addition, sorafenib induces apoptosis in A549/DDP cisplatin‑resistant lung adenocarcinoma cells, thus reducing their invasiveness.
    Molecular Medicine Reports 04/2014; · 1.17 Impact Factor
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    ABSTRACT: The aim of the present study was to detect the expression of survivin in human lung cancer and to investigate the influence of its downregulation on the biological behavior of A549 lung cancer cells. The high expression of survivin in human lung cancer was verified by immunohistochemistry. Survivin small interfering RNA (siRNA) and unrelated sequence were synthesized and the siRNA lentiviral vector was constructed. The vector was transfected into A549 lung cancer cells, in which the clone with stable expression was screened out. We blocked the expression of survivin mRNA and protein by RNA interference (RNAi) technique. The downregulation of survivin mRNA and protein expression was confirmed by real-time quantitative PCR and western blotting. The proliferative activity and growth rate of A549 cells were determined by colony formation assay and mononuclear cell direct cytotoxicity assay (MTT assay). The reconstituted basement membrane (RBM) penetrating capacity was determined by cell invasion assay. The cell movement and migratory capacity were detected by wound-healing repair assay. The results showed that the sequence-specific siRNA significantly downregulated the expression of survivin at both the mRNA and protein levels. Downregulation of survivin expression dramatically decreased the invasive and metastatic capacities of the cells, suppressed the proliferation, decelerated the rate of growth, reduced the number of clones on soft agar and decreased the capacity of RBM penetration and migration. In conclusion, survivin, which plays an important role in carcinogenesis and development of lung cancer, can be effectively downregulated using the RNAi technique.
    Experimental and therapeutic medicine 06/2012; 3(6):1010-1014. · 0.34 Impact Factor
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    ABSTRACT: The survivin protein, a member of the inhibitors of apoptosis (IAP) family, has gained popularity as a therapeutic target for cancer due to its selective expression in tumor cells and its significant involvement in tumor cell viability. The aim of this study was to investigate the effect of the survivin-small interfering RNA (siRNA) plasmid on survivin expression in the human lung cancer cell line, A549, and to observe its effects on apoptosis and proliferation of A549 cells. A549 human lung cancer cells were transfected with survivin-targeting siRNA. The downregulation of survivin expression was determined by real-time polymerase chain reaction and western blotting. The proliferation of A549 cells was determined by MTT assay. The apoptotic rate and cell cycle distribution were analyzed by flow cytometry (FCM). Caspase-9 activity was also detected to study the apoptosis of lung cancer cells induced by siRNA against survivin. The sequence-specific siRNA efficiently and specifically downregulated the expression of survivin at both the mRNA and protein levels. Downregulation of survivin expression dramatically suppressed the proliferation of A549 cells and arrested the cells at the G (1)/G (0) phase. Caspase-9 activity was significantly increased in A549 cells transfected with siRNA against survivin. In this study, we found that survivin-specific siRNA can efficiently suppress the expression of survivin, increase apoptosis and inhibit A549 cell proliferation. Our findings further indicate the possibility that the antitumor effects of survivin-siRNA are mediated through the activation of caspase-9.
    Molecular Medicine Reports 04/2012; 5(4):917-22. · 1.17 Impact Factor
  • Xiang-qi Chen, Ting-yan Lin
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    ABSTRACT: To investigate the effects of Interleukin-18 (IL-18) on asthmatic airway inflammation. Thirty healthy adult male guinea pigs were randomly divided into 3 equal groups: asthmatic model group (Group A, undergoing intraperitoneally injection of ovalbumin (OVA) once and spraying of OVA aerosol once a day for 5 days; control group (Group B), undergoing intraperitoneally injection of OVA once and spraying of normal saline aerosol once a day for 5 days; and interleukin (IL)-18 intervention group (Group C, undergoing intraperitoneally injection of OVA once and intraperitoneal injection of IL-18 on the days 1, 3, 8. 10. 15, 17, and 19. Twenty-four hours after the final spraying or IL-18 injection the bronchalveolar lavage fluid (BALF) of the left lungs were obtained. HE staining was conducted to the sediment to examine the numbers of eosinophils, neutrophils, and monocytes. ELISA was used to detect the Th1/Th2 cytokines in the BALF. The left lungs underwent pathological examination. The number of EOS in BALF of Groups A was (98 +/- 58) x 10(6)/L, significantly higher than those of Group B, (12 +/- 10) x 10(6)/L, and Group C, (29 +/- 10) x 10(6)/L (P < 0.01 and P < 0.05). The numbers of neutrophils in the BALF of Group A was (24 +/- 16) x 10(6)/L, significantly higher than those of Group B and C [(9 +/- 7) x 10(6)/L and (10 +/- 5) x 10(6)/L respectively, both P < 0.05]. The concentration of IFN-gamma and IL-2 in group A were both significantly lower than those of Group B and Group C (P < 0.05 and P < 0.01). The concentration of IL-4 in Group A was significantly higher than those of Groups B and C (both P < 0.05). The concentration of IL-5 of Group A was significantly higher than those of Group Bs and C (both P < 0.01). IL-18 effectively inhibits asthmatic airway inflammation by regulating the Th1/Th2 balance.
    Zhonghua yi xue za zhi 07/2005; 85(28):1995-8.
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    ABSTRACT: ObjectiveTo investigate the effects of interleukin-18 (IL-18) on implanted Lewis lung cancer in suppressing angiogenesis and lymphangiogenesis. MethodsOne week after hypodermic inoculation of Lewis cells, sixteen tumor-bearing syngeneic mice were randomly divided into two groups. The mice in the treatment group (group A) were intraperitoneally injected with the IL-18 and in the control group (group B) were intraperitoneally injected with normal saline for 7 days. The mice were killed on day 19. The morphology of the tumors was studied, the growth curve was described and the tumor inhibition rate was calculated. The numbers of metastasized pulmonary colonies were calculated using hematoxylin-eosin (HE) staining. The vascular endothelial growth factor A (VEGF-A), vascular endothelial growth factor C (VEGF-C), microvessel density (MVD) and lymphatic microvessel density (LMVD) in tumor mass were measured by immunohistochemistry staining (IHCS). ResultsIn the group A, the tumor volume, tumor weigh, lung metastatic nodules, expression of VEGF-A and VEGF-C, MVD were all decreased significantly (P<0.01 or P<0.05). The tumor inhibition rate was 75% and the inhibition rate of lung metastatic nodules was 61%. The LMVD in group A was also lower than group B, but without significant difference (P>0.05). ConclusionIL-18 could suppress the tumor growth and metastasis of implanted Lewis lung cancer by way of down-regulating VEGF-A and VEGF-C expression, suppressing angiogenesis and lymphangiogenesis. Key wordsInterleukin-18-Lung cancer-VEGF-LMVD CLC numberR734.2
    Chinese Journal of Cancer Research 22(4):303-309. · 0.45 Impact Factor