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Objective@#To investigate whether silencing UCP2 can sensitize cervical cancer cell line Siha to radiation.@*Methods@#Siha cells were transfected with UCP2 siRNA and then irradiated by X-ray. The radiosensitivity of Siha cells was verified by colony formation, CCK-8, apoptosis and immunofluorescence assays. The mitochondrial membrane potential and the production of reactive oxygen species (ROS) were detected to further explore the related mechanism.@*Results@#RT-PCR and Western blot assays showed that the expression of UCP2 in Siha cells was increased after irradiation and the UCP2 siRNA successfully silenced the expression of UCP in cells. According to the survival curves, the D0, Dq, N and SF2 were 1.54, 1.31, 2.31 Gy and 0.52 for siUCP2 group, 2.50, 3.64, 4.30 Gy and 0.83 for blank control group, and 3.34, 2.16, 1.91 Gy and 0.69, for siNC group, respectively. The radiosensitivity enhancement ratio of silent group was 0.62 and 0.46, compared with blank control group and negative control group, respectively. The proliferative activity of cells in the silent group was lower than that in the control group (t=13.2, P<0.05). Apoptosis levels in the silent group were significantly higher than those in the control group after irradiation(t=3.14, P<0.05). At 4 h after irradiation, the ROS production in the silent group was significantly higher than that in the control group (t=19.10, P<0.05). At 24 h after irradiation, the mitochondrial membrane potential of Siha cells in the silent group was significantly lower than that in the control group (t=4.18, P<0.05).@*Conclusions@#The radiosensitivity of Siha cells is enhanced after UCP2 silencing, and thus UCP2 may applicable as a new target for radiosensitization of cervical cancer cells.
ABSTRACT
Objective To investigate whether silencing UCP2 can sensitize cervical cancer cell line Siha to radiation.Methods Siha cells were transfected with UCP2 siRNA and then irradiated by Xray.The radiosensitivity of Siha cells was verified by colony formation,CCK-8,apoptosis and immunofluorescence assays.The mitochondrial membrane potential and the production of reactive oxygen species (ROS) were detected to further explore the related mechanism.Results RT-PCR and Western blot assays showed that the expression of UCP2 in Siha cells was increased after irradiation and the UCP2 siRNA successfully silenced the expression of UCP in cells.According to the survival curves,the D0,Dq,N and SF2 were 1.54,1.31,2.31 Gy and 0.52 for siUCP2 group,2.50,3.64,4.30 Gy and 0.83 for blank control group,and 3.34,2.16,1.91 Gy and 0.69,for siNC group,respectively.The radiosensitivity enhancement ratio of silent group was 0.62 and 0.46,compared with blank control group and negative control group,respectively.The proliferative activity of cells in the silent group was lower than that in the control group (t =13.2,P＜0.05).Apoptosis levels in the silent group were significantly higher than those in the control group after irradiation (t=3.14,P＜0.05).At 4 h after irradiation,the ROS production in the silent group was significantly higher than that in the control group (t=19.10,P＜0.05).At 24 h after irradiation,the mitochondrial membrane potential of Siha cells in the silent group was significantly lower than that in the control group (t =4.18,P ＜ 0.05) Conclusions The radiosensitivity of Siha cells is enhanced after UCP2 silencing,and thus UCP2 may applicable as a new target for radiosensitization of cervical cancer cells.
ABSTRACT
<p><b>BACKGROUND</b>It has been known that Kai1 is one of transmembrane 4 superfamily regulating cell proliferation, adhesion and mobility and its down-regulated expression is closely correlated with progression and prognosis of tumor. Fas ligand (FasL) is one of tumor necrosis factor/nerve growth factor family activating caspase-3, a key proteinase in cell apoptosis and leading immune escape in tumor cells. The aim of this study is to investigate the expression of Kai1 and FasL in non-small cell lung cancer (NSCLC) and to explore their roles and relationship in carcinogenesis and progression of NSCLC.</p><p><b>METHODS</b>Kai1 and FasL expressions were examined in 79 NSCLC tissues and their adjacent normal lung tissues by SP immunohistochemistry. Their expressions were compared with clinicopathological features of NSCLC. The relationship between Kai1 and FasL expressions was also analyzed in NSCLC.</p><p><b>RESULTS</b>Kai1 expression in NSCLC tissue was remarkably lower than that in their adjacent tissue (55.7% vs 82.6%, P < 0.05). However, it was the converse for FasL (73.4% vs 52.2%, P < 0.05). Kai1 expression was not correlated with age and gender of NSCLC patients, tumor location or histological classification (P > 0.05), but negatively with lymph node metastasis and clinicopathological staging and positively with differentiation degree (P < 0.05). FasL expression was not correlated with age and gender of the patients, tumor location or histological classification (P > 0.05), but positively with lymph node metastasis and negatively with differentiation degree (P < 0.05). Kai1 expression was closely correlated with FasL expression in NSCLC (P < 0.05).</p><p><b>CONCLUSIONS</b>Down-regulation of Kai1 expression and up-regulation of FasL may play important roles in carcinogenesis and progression of NSCLC. Kai1 and FasL could be considered as molecular markers to reflect pathobiological behavior of NSCLC. Additionally, close correlation of FasL expression with Kai1 expression in NSCLC provides a novel insight into the regulatory effects of FasL expression on Kai1 expression.</p>