scholarly journals Correction to: 125I seeds irradiation inhibits tumor growth and induces apoptosis by Ki-67, P21, survivin, livin and caspase-9 expression in lung carcinoma xenografts

2021 ◽  
Vol 16 (1) ◽  
Author(s):  
Qing Jin ◽  
Cunzhi Lin ◽  
Xinhong Zhu ◽  
Yiwei Cao ◽  
Caihong Guo ◽  
...  
Keyword(s):  
Tumor Growth ◽  
Lung Carcinoma ◽  
Caspase 9 ◽  
Ki 67 ◽  
125I Seeds

scholarly journals 125I seeds irradiation inhibits tumor growth and induces apoptosis by Ki-67, P21, survivin, livin and caspase-9 expression in lung carcinoma xenografts

2020 ◽  
Vol 15 (1) ◽  
Author(s):  
Qing Jin ◽  
Cunzhi Lin ◽  
Xinhong Zhu ◽  
Yiwei Cao ◽  
Caihong Guo ◽  
...  
Keyword(s):  
Lung Cancer ◽  
Caspase 3 ◽  
Human Lung ◽  
Human Lung Cancer ◽  
Caspase 8 ◽  
125I Seed ◽  
Caspase 9 ◽  
Ki 67 ◽  
125I Seeds ◽  
Seed Irradiation

Abstract Background Lung cancer is a fatal disease and a serious health problem worldwide. Patients are usually diagnosed at an advanced stage, and the effectiveness of chemotherapy for such patients is very limited. Iodine 125 seed (125I) irradiation can be used as an important adjuvant treatment for lung carcinoma. The purpose of this study was to examine the role of irradiation by 125I seeds in human lung cancer xenograft model and to determine the underlying mechanisms involved, with a focus on apoptosis. Methods 40 mice with A549 lung adenocarcinoma xenografts were randomly divided into 4 groups: control group (n = 10), sham seed (0 mCi) implant group (n = 10), 125I seed (0.6 mCi) implant group (n = 10) and 125I seed (0.8 mCi) implant group (n = 10), respectively. The body weight and tumor volume, were recorded every 4 days until the end of the study. Apoptotic cells were checked by terminal deoxynucleotidyl transferase dUTP nick end labeling (TUNEL) assay and activities of caspase-3 and caspase-8 enzyme were tested. Expression of P21, survivin, livin, caspase-9 and proliferating cell nuclear antigen (Ki-67) was detected with immunohistochemical staining. Results The results of TUNEL staining assays showed that 125I seed irradiation suppresses the growth of lung cancer xenografts in nude mice and induced apoptosis. The activity of caspase-3 and caspase-8 was significantly higher. The expression levels Ki67, survivin and livin were substantially downregulated, while P21 and caspase-9 protein expression were significantly increased following 125I seed irradiation. This study revealed that 125I seed irradiation could significantly change apoptosis-related protein in human lung cancer xenografts. Conclusions Overall, our study demonstrates that radiation exposure by 125I seeds could be a new treatment option for lung cancer.

scholarly journals 125 I seeds irradiation inhibits tumor growth and induces apoptosis by Ki-67, P21, Survivin，Livin and Caspase-9 expression in lung carcinoma xenografts

2020 ◽  
Author(s):  
Qing Jin ◽  
Cunzhi Lin ◽  
Xinhong Zhu ◽  
Yiwei Cao ◽  
Caihong Guo ◽  
...  
Keyword(s):  
Lung Cancer ◽  
Lung Carcinoma ◽  
Caspase 3 ◽  
Human Lung ◽  
Human Lung Cancer ◽  
Caspase 8 ◽  
125I Seed ◽  
Caspase 9 ◽  
Ki 67 ◽  
Seed Irradiation

Abstract Background: Lung cancer is a fatal disease and a serious health problem worldwide. Patients are usually diagnosed at an advanced stage, and the effectiveness of chemotherapy for such patients is very limited. Iodine 125 seed(125I) irradiation can be used as an important adjuvant treatment for lung carcinoma. The purpose of this study was to examine the role of irradiation by 125I seeds in human lung cancer xenograft model and to determine the underlying mechanisms involved, with a focus on apoptosis. Methods: 40 mice with A549 lung adenocarcinoma xenografts were randomly divided into 4 groups: control group (n=10), sham seed (0 mCi) implant group (n=10), 125I seed (0.6 mCi) implant group (n=10) and 125I seed (0.8 mCi) implant group (n=10), respectively. The body weight and tumor volume, were recorded every four days until the end of the study. Apoptotic cells were checked by terminal deoxynucleotidyl transferase dUTP nick end labeling (TUNEL) assay and activities of caspase-3 and caspase-8 enzyme were tested. Expression of P21, survivin, livin, caspase-9 and proliferating cell nuclear antigen (Ki-67) was detected with immunohistochemical staining. Results: The results of TUNEL staining assays showed that 125I seed irradiation suppresses the growth of lung cancer xenografts in nude mice and induced apoptosis. The activity of caspase-3 and caspase-8 was significantly higher. The expression levels Ki67, survivin and livin were substantially downregulated, while P21 and caspase-9 protein expression were significantly increased following 125I seed irradiation. This study revealed that 125I seed irradiation could significantly change apoptosis-related protein in human lung cancer xenografts. Conclusions: Overall, our study demonstrates that radiation exposure by 125I seedscould be a new treatment option for lung cancer.

scholarly journals 125 I seeds irradiation inhibits tumor growth and induces apoptosis by Ki-67, P21, Survivin，Livin and Caspase-9 expression in lung carcinoma xenografts

2020 ◽  
Author(s):  
Lijun Wang ◽  
Cunzhi Lin ◽  
Qing Jin ◽  
Xinhong Zhu ◽  
Yiwei Cao ◽  
...  
Keyword(s):  
Lung Cancer ◽  
Caspase 3 ◽  
Human Lung ◽  
Human Lung Cancer ◽  
Caspase 8 ◽  
125I Seed ◽  
Caspase 9 ◽  
Ki 67 ◽  
125I Seeds ◽  
Seed Irradiation

Abstract Background: Lung cancer is a fatal disease and a serious health problem worldwide. Patients are usually diagnosed at an advanced stage, with the effectiveness of chemotherapy for such patients being very limited. Iodine 125 seed(125I) irradiation can be used as an important adjuvant treatment for lung carcinoma. The purpose of this study was to examine the effects of irradiation by 125I seeds in human lung cancer xenograft model and to determine the underlying mechanisms involved, with a focus on apoptosis. Methods: A group of 40 mice bearing A549 lung adenocarcinoma xenografts were randomly divided into 4 groups: control group (n=10), sham seed (0 mCi) implant group (n=10), 125I seed (0.6 mCi) implant group (n=10) and 125I seed (0.8 mCi) implant group (n=10), respectively. The body weight and tumor volume, was recorded every four days until the end of the study. Apoptotic cells were checked with terminal deoxynucleotidyl transferase dUTP nick end labeling (TUNEL) assay and activities of caspase-3 and caspase-8 enzyme were tested. Expression of P21, survivin, livin, caspase-9 and proliferating cell nuclear antigen (Ki-67) was detected with immunohistochemical staining. Results: The results of TUNEL staining assays shows that 125I seed irradiation suppresses the growth of lung cancer xenografts in nude mice and induces apoptosis. The activity of caspase-3 and caspase-8 was significantly higher. The expression levels Ki67, survivin and livin were substantially downregulated, while P21 and caspase-9 protein expression was significantly increased following 125I seed irradiation. This study revealed that 125I seed irradiation could significantly change apoptosis-related protein in human lung cancer xenograft. Conclusions: Overall, our study demonstrates that radiation exposure by 125I seeds has been expected as a new treatment option for lung cancer.

scholarly journals LncRNA SNHG12 regulates the radiosensitivity of cervical cancer through the miR-148a/CDK1 pathway

2020 ◽  
Vol 20 (1) ◽  
Author(s):  
Chen Wang ◽  
Shiqing Shao ◽  
Li Deng ◽  
Shelian Wang ◽  
Yongyan Zhang
Keyword(s):  
Cell Cycle ◽  
Cervical Cancer ◽  
Tumor Growth ◽  
Luciferase Reporter ◽  
Tunel Staining ◽  
Cell Cycle Distribution ◽  
Ki 67 ◽  
In Vivo Experiments ◽  
Potential Biomarker

Abstract Background Radiation resistance is a major obstacle to the prognosis of cervical cancer (CC) patients. Many studies have confirmed that long non-coding RNAs (lncRNAs) are involved in the regulation of radiosensitivity of cancers. However, whether small nucleolar RNA host gene 12 (SNHG12) regulates the radiosensitivity of CC remains unknown. Methods Quantitative real-time polymerase chain reaction was used to measure the expression levels of SNHG12 and microRNA-148a (miR-148a). The radiosensitivity of cells was evaluated by clonogenic assay. Flow cytometry and caspase-3 activity assay were performed to assess the apoptosis ability and cell cycle distribution of cells. Besides, dual-luciferase reporter and RNA immunoprecipitation assay were used to verify the interaction between miR-148a and SNHG12 or cyclin-dependent kinase 1 (CDK1). Also, the protein levels of CDK1, CCND1 and γ-H2AX were detected by western blot analysis. Furthermore, in vivo experiments were conducted to verify the effect of SNHG12 on CC tumor growth. Ki-67 and TUNEL staining were employed to evaluate the proliferation and apoptosis rates in vivo. The hematoxylin and eosin (HE) staining were employed to evaluate the tumor cell morphology. Results SNHG12 was upregulated in CC tissues and cells, and its knockdown improved the radiosensitivity by promoting the radiation-induced apoptosis and cell cycle arrest of CC cells. Also, miR-148a could be sponged by SNHG12 and could target CDK1. MiR-148a inhibitor or CDK1 overexpression could invert the promotion effect of silenced-SNHG12 on CC radiosensitivity. Meanwhile, SNHG12 interference reduced the tumor growth of CC, increased miR-148a expression, and inhibited CDK1 level in vivo. Conclusion LncRNA SNHG12 promoted CDK1 expression to regulate the sensitivity of CC cells to radiation through sponging miR-148a, indicating that SNHG12 could be used as a potential biomarker to treat the radiotherapy resistance of CC patients.

scholarly journals new bIologIcal model of moderate InhIbItIon of tumor and metastases growth wIth prolonged leukopenIa In mIce

2016 ◽  
Vol 1 (5) ◽  
pp. 121-125
Author(s):  
Зуева ◽  
Elena Zueva ◽  
Разина ◽  
Tatyana Razina ◽  
Ермакова ◽  
...  
Keyword(s):  
Tumor Growth ◽  
Lung Carcinoma ◽  
Lewis Lung Carcinoma ◽  
Tumor Therapy ◽  
Biological Model ◽  
Tumor Growth Inhibition ◽  
Lewis Lung ◽  
Inhibition Of Tumor Growth ◽  
Toxic Manifestation ◽  
Cyclophosphamide Dose

A new biological model of moderate inhibition of tumor growth and metastases with prolonged leukopenia on C57Bl/6 mice with the Lewis Lung Carcinoma was designed. The model was created by the injection of cyclophosphamide (dose 83.3mg/kg) on 6th, 12th, 18th days after tumor cells transplantation on animals. Experiment showed that 3-fold cyclo-phosphamide use leads to growth of primary tumor and metastases inhibition. Tumor growth inhibition was 34% on 21st day after cyclophosphamide inject. The number of metastases decreased by 4.7times (p<0,01). Metastatic area reduced. Metastasis frequency made 100%. In addition, the course of cyclophosphamide application caused inhibition of granulocytic and lymphoid hematopoiesis. The reducing the number of segmented neutrophils and lymphocytes was showed on the 3rd day after 1, 2 and 3 injections of cyclophosphamide. The model can be used to study the efficacy of drugs in tumor therapy and in correction of such toxic manifestation of chemotherapy as leukopenia.

EXTH-72. TRANSLATIONAL INVESTIGATION OF TD139 FOR THE TREATMENT OF HIGH-GRADE MENINGIOMA

2021 ◽  
Vol 23 (Supplement_6) ◽  
pp. vi179-vi180
Author(s):  
Connor Stephenson ◽  
Katie Ross ◽  
William Vandergrift III ◽  
Abhay Varma ◽  
Bruce Frankel ◽  
...  
Keyword(s):  
T Cells ◽  
Tumor Growth ◽  
Cytotoxic T Cells ◽  
Transglutaminase 2 ◽  
Treg Cells ◽  
Orphan Receptor ◽  
High Grade ◽  
Ki 67 ◽  
Western Blots

Abstract BACKGROUND High-Grade Meningioma (HGM), such as atypical and anaplastic meningiomas, represent a subgroup of meningiomas with histologic and clinical features suggesting aggressive behavior with a penchant for recurrence, even after surgical resection. Here, we postulate that high levels of Galectin-3 (Gal-3) affect the cellular composition and are at the root of the profoundly immunosuppressive tumor microenvironment of HGM. Our study aimed to validate the effect of the Gal-3 inhibitor (TD139) in in vivo. METHODS In vivo MGS2 murine models of HGM were utilized to assess efficacy of treatment with TD139 via intravenous injection. We used ELISA spot, RT-PCR and western blots techniques. MRI and immunohistochemistry -staining methods were used to detect tumor growth in in vivo following TD139 treatments. RESULTS Our results demonstrated a significantly elevated level of Gal-3 in both HGM tissue and serum when compared to non-tumor patients. Furthermore, Epithelial membrane antigen, Ki-67, and Transglutaminase 2 were highly expressed in HGM, whereas the number of observed cytotoxic T-cells in HGM was markedly decreased. When human PBMCs were activated with anti-CD3 (1µg/ml) and anti-CD28 (2µg/ml) antibodies and treated with recombinant Gal-3 protein (500ng/ml) for 96hr, we found reduced expression of T-Box Transcription Factor 21 and RAR Related Orphan Receptor C mRNA with concurrent upregulated expression of GATA Binding protein 3 and Forkhead box P3 mRNA. These findings support the concept that Gal-3 skews the differentiation of CD4+ T cells towards Th2 and Treg cells. In vivo treatment of TD139 (1mg/kg per day for 14 days) showed significant decrease (∼35%) in MGS2 tumor growth in orthotopic allograft model (at Day 41) and increased survival via multiple mechanism. Additionally, we observed an upregulation of CD38 (M1 macrophages) and CD8+ T cells in treated cells. CONCLUSIONS These findings suggest that TD139 may be an effective approach in the treatment of HGM patients.

scholarly journals BAP31 Promotes Tumor Cell Proliferation by Stabilizing SERPINE2 in Hepatocellular Carcinoma

2020 ◽  
Vol 8 ◽  
Author(s):  
Xiyang Zhang ◽  
Dongbo Jiang ◽  
Shuya Yang ◽  
Yuanjie Sun ◽  
Yang Liu ◽  
...  
Keyword(s):  
Hepatocellular Carcinoma ◽  
Cell Proliferation ◽  
Tumor Growth ◽  
Tumor Cell ◽  
Colony Formation ◽  
Clinical Stage ◽  
Tumor Cell Proliferation ◽  
Ki 67 ◽  
Hcc Cells

Hepatocellular carcinoma (HCC) patients are mostly diagnosed at an advanced stage, resulting in systemic therapy and poor prognosis. Therefore, the identification of a novel treatment target for HCC is important. B-cell receptor-associated protein 31 (BAP31) has been identified as a cancer/testis antigen; however, BAP31 function and mechanism of action in HCC remain unclear. In this study, BAP31 was demonstrated to be upregulated in HCC and correlated with the clinical stage. BAP31 overexpression promoted HCC cell proliferation and colony formation in vitro and tumor growth in vivo. RNA-sequence (RNA-seq) analysis demonstrated that serpin family E member 2 (SERPINE2) was downregulated in BAP31-knockdown HCC cells. Coimmunoprecipitation and immunofluorescence assays demonstrated that BAP31 directly binds to SERPINE2. The inhibition of SERPINE2 significantly decreased the BAP31-induced cell proliferation and colony formation of HCC cells and phosphorylation of Erk1/2 and p38. Moreover, multiplex immunohistochemistry staining of the HCC tissue microarray showed positive associations between the expression levels of BAP31, SERPINE2, its downstream gene LRP1, and a tumor proliferation marker, Ki-67. The administration of anti-BAP31 antibody significantly inhibited HCC cell xenograft tumor growth in vivo. Thus, these findings suggest that BAP31 promotes tumor cell proliferation by stabilizing SERPINE2 and can serve as a promising candidate therapeutic target for HCC.

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