scholarly journals CircHIPK3 Promotes Thyroid Cancer Tumorigenesis and Invasion through the Mirna-338-3p/RAB23 Axis

2020 ◽  
Author(s):  
Taipengfei Shu ◽  
Lin Yang ◽  
Lijie Sun ◽  
Jixuan Lu ◽  
Xiaorong Zhan
Keyword(s):  
Thyroid Cancer ◽  
Luciferase Reporter ◽  
Human Thyroid ◽  
Normal Tissues ◽  
Reporter Assays ◽  
Proliferation And Metastasis ◽  
Cancer Types ◽  
Thyroid Cancer Cell Lines ◽  
Cancer Tissues

Objective：Thyroid cancer is a common type of endocrine malignancy, and its incidence has been steadily increasing in many regions of the world. Numerous studies have found that the circRNAs in various cancer types are aberrantly expressed, which could be potential biological diagnostic markers and therapeutic targets. The purpose of this study was to investigate the role of circHIPK3 in the development and progression of thyroid cancer and its mechanism. Subject and Methods：qRT-PCR was used to detect the relative expression levels of circHIPK3 in thyroid cancer cell lines (K1, CAL-62, TPC1), human thyroid normal cells (Nthy-ori 3-1), 10 pairs of thyroid cancer tissues and corresponding adjacent normal tissues. CCK-8 and Transwell assays were used to detect the proliferation and metastasis ability of cells. The targeted relationships between circHIPK3-miR-338-3p and miR-338-3p-RAB23 were predicted by bioinformatics analysis and verified by dual-luciferase reporter assays. Results and Conclusion: The downregulation of circHIPK3 significantly reduced the migration, invasion and proliferation of thyroid carcinoma. Then, we demonstrated that circHIPK3 up-regulated the expression of its target gene RAB23 by sponging miR-338-3p to promote the tumorigenesis and invasiveness of thyroid cancer. This study is the first to find that circHIPK3 plays the role of oncogenetic circRNA in thyroid cancer, which may provide new insights into how circRNA affects the progression of thyroid cancer. Our study also showed that circHIPK3 could be a novel biomarker for thyroid cancer.

Expression of insulin-like growth factor receptors in primary human thyroid neoplasms

1989 ◽  
Vol 121 (1) ◽  
pp. 112-120 ◽  
Author(s):  
Tohru Yashiro ◽  
Yoshito Ohba ◽  
Hitomi Murakami ◽  
Takao Obara ◽  
Toshio Tsushima ◽  
...  
Keyword(s):  
Thyroid Cancer ◽  
Binding Capacity ◽  
Specific Binding ◽  
Human Thyroid ◽  
Scatchard Analysis ◽  
Type I ◽  
Single Class ◽  
Normal Tissues ◽  
Igf I ◽  
Cancer Tissues

Abstract. The presence of IGF-I receptors was demonstrated in normal and neoplastic tissues of human thyroid. Binding of [125I]IGF-I to thyroid membranes was dependent on time and temperature of incubation, and maximal binding was achieved at 4°C and 18 h of incubation. [125I] IGF-I binding was dose-dependently displaced by unlabelled IGF-I; half-maximal inhibition occurred at concentrations of 10–20 μg/l. IGF-II and insulin had relative potencies of 5 and 1% compared with IGF-I. Scatchard analysis of binding data revealed a single class of IGF-I receptors with high affinity (Ka: 1.2–8.6 × 109 1/mol) in normal thyroid tissues. Affinity cross-linking and autoradiography demonstrated the type I IGF receptors. Specific binding of [125I] IGF-I in thyroid cancer tissues (9.69 ± 2.07% per 200 μg protein; mean ± sem, N = 8) was significantly (p <0.05) higher than that in the surrounding normal tissues (3.03 ± 0.35%, N = 8). In contrast, there was no difference in the binding between adenoma tissues (4.19 ± 0.53%, N = 5) and the adjacent normal tissues (2.94 ± 0.24%, N = 5). The higher IGF-I binding in cancer tissues was due to an increase in the binding capacity without any change in the affinity. The presence of IGF-I receptors suggests a possible role of IGF-I and its receptors in the growth of thyroid cancer cells.

scholarly journals The expression of translocator protein in human thyroid cancer and its role in the response of thyroid cancer cells to oxidative stress

2012 ◽  
Vol 214 (2) ◽  
pp. 207-216 ◽  
Author(s):  
Joanna Klubo-Gwiezdzinska ◽  
Kirk Jensen ◽  
Andrew Bauer ◽  
Aneeta Patel ◽  
John Costello ◽  
...  
Keyword(s):  
Oxidative Stress ◽  
Valproic Acid ◽  
Thyroid Cancer ◽  
Cell Lines ◽  
Cancer Cell ◽  
Translocator Protein ◽  
Human Thyroid ◽  
Thyroid Cancer Cell ◽  
Thyroid Cancer Cell Lines

The translocator protein (TSPO), formerly known as a peripheral benzodiazepine receptor, exerts pro-apoptotic function via regulation of mitochondrial membrane potential. We examined TSPO expression in human thyroid tumors (25 follicular adenomas (FA), 15 follicular cancers (FC), and 70 papillary cancers (PC)). The role of TSPO in the regulation of cell growth, migration, and apoptosis was examined in thyroid cancer cell lines after TSPO knockdown with siRNA and after treatment with TSPO antagonist (PK11195). Compared with normal thyroid, the level of TSPO expression was increased in FA, FC, and PC in 24, 26.6, and 55.7% of cases respectively. Thyroid cancer cell lines demonstrated variable levels of TSPO expression, without specific association with thyroid oncogene mutations. Treatment with inhibitors of PI3K/AKT or MEK/ERK signaling was not associated with changes in TSPO expression. Treatment with histone deacetylase inhibitor (valproic acid) increased TSPO expression in TSPO-deficient cell lines (FTC236 cells). TSPO gene silencing or treatment with PK11195 did not affect thyroid cancer cell growth and migration but prevented depolarization of mitochondrial membranes induced by oxidative stress. Induction of TSPO expression by valproic acid was associated with increased sensitivity of FTC236 to oxidative stress-inducible apoptosis. Overall, we showed that TSPO expression is frequently increased in PC. In vitro data suggested the role of epigenetic mechanism(s) in the regulation of TSPO in thyroid cells. Implication of TSPO in the thyroid cancer cell response to oxidative stress suggested its potential role in the regulation of thyroid cancer cell response to treatment with radioiodine and warrants further investigation.

scholarly journals miR-142-5p promotes cervical cancer progression by targeting LMX1A through Wnt/β-catenin pathway

Open Medicine ◽  
2021 ◽  
Vol 16 (1) ◽  
pp. 224-236
Author(s):  
Lijuan Ke ◽  
Yanping Chen ◽  
Yiying Li ◽  
Zheng Chen ◽  
Yihui He ◽  
...  
Keyword(s):  
Cervical Cancer ◽  
Cancer Progression ◽  
Hela Cells ◽  
Luciferase Reporter ◽  
Carcinogenic Effect ◽  
Expression Levels ◽  
Normal Tissues ◽  
Homeobox Transcription Factor ◽  
Reporter Assays ◽  
Cancer Tissues

Abstract Background Previous work has shown that miR-142-5p in cervical cancer tissues increased significantly compared with adjacent normal tissues. However, the function and the mechanism of miR-142-5p in cervical cancer have not been reported. Methods Quantitative reverse transcription-polymerase chain reaction (qRT-PCR) was used to determine the gene expression levels. MTT, flow cytometry, and transwell assays were performed to explore the functions of miR-142-5p in HeLa cells. The potential target gene of miR-142-5p was investigated via luciferase reporter assays. The protein expression levels were analyzed by Western blotting. Results We found that miR-142-5p expression was elevated but LIM homeobox transcription factor 1 alpha (LMX1A) was decreased in cervical cancer tissues and cells. Overexpression of miR-142-5p or knockdown of LMX1A inhibited cell apoptosis, promoted cell proliferation, migration, invasion abilities, and activated the Wnt/β-catenin pathway. However, knockdown of miR-142-5p or overexpression of LMX1A showed opposite results. LMX1A was identified as a direct target of miR-142-5p by luciferase reporter assays. Finally, rescue experiments demonstrated that LMX1A overexpression attenuated the carcinogenic effect of miR-142-5p mimic on HeLa cells. Conclusions These findings suggested that miR-142-5p might be a cervical cancer oncogene and could serve as a potential therapeutic target for the treatment of cervical cancer.

scholarly journals Long non-coding RNA LINC01194 promotes the proliferation, migration and invasion of lung adenocarcinoma cells by targeting miR-641/SETD7 axis

2020 ◽  
Vol 20 (1) ◽  
Author(s):  
Fanmei Meng ◽  
Yijing Zhou ◽  
Baohua Dong ◽  
Aiqin Dong ◽  
Jingtao Zhang
Keyword(s):  
Cell Proliferation ◽  
Lung Adenocarcinoma ◽  
Luciferase Reporter ◽  
Migration And Invasion ◽  
Non Coding Rna ◽  
Adenocarcinoma Cells ◽  
Reporter Assays ◽  
Cancer Types ◽  
Long Non Coding Rna

Abstract Background It is increasingly evidenced that long non-coding RNAs (lncRNAs) play an important role in various diseases. LncRNA LINC01194 acts as an oncogene in several cancer types. Nevertheless, the role of LINC01194 in lung adenocarcinoma (LUAD) has not yet been revealed. Methods qRT-PCR was used to detect the expression of LINC01194, miR-641 and SETD7 mRNA, while western blot was exploited to examine SETD7 protein level. Cell proliferation was detected by colony formation and EdU assays. Transwell assays detected cell migration and invasion. TUNEL assay and flow cytometry analysis were used to detect cell apoptosis. RIP, RNA pull down and luciferase reporter assays detected the binding among LINC01194, miR-641 and SETD7. Results LINC01194 was significantly upregulated in LUAD tissues and cell lines. Knockdown of LINC01194 resulted in decreased cell proliferation, migration and invasion, and increased apoptosis. Mechanistic experiments unveiled that LINC01194 augmented SETD7 expression in LUAD cells by competitively interacting with miR-641. Rescue experiments showed that miR-641 inhibition and SETD7 overexpression rescued the repressing impacts on LUAD cell proliferation, migration and invasion caused by LINC01194 knockdown. Conclusion LINC01194 promotes the progression of LUAD by enhancing miR-641-targeted SETD7. The LINC01194/miR-641/SETD7 axis might provide new molecular targets for treating LUAD.

THYROID PROTEINS AND HORMONE SYNTHESIS IN HUMAN THYROID CANCER

1974 ◽  
Vol 76 (3) ◽  
pp. 651-669 ◽  
Author(s):  
Colette Thomas-Morvan ◽  
Berthe Nataf ◽  
Maurice Tubiana
Keyword(s):  
Thyroid Cancer ◽  
Organ Culture ◽  
Human Thyroid ◽  
Coupling Reactions ◽  
Variable Effect ◽  
Hormone Synthesis ◽  
Normal Tissues ◽  
Cancer Tissues ◽  
Stable Iodine

ABSTRACT Thyroid iodoproteins and hormone synthesis have been studied in vivo and in organ culture in 44 cases of thyroid cancer. In a few cases, Tg1) (17–19 S) is virtually absent; a portion of the light fractions (3–8 S), which seems to represent some precursors of Tg, incorporated in culture the 14C-amino acids. In most of the cases, the solubility profiles, sedimentation patterns as well as electrophoretic migration of proteins were normal. The content of Tg and the concentration of stable iodine (127I) in Tg are less than that of "normal" tissues, and the deficiency in iodination appears to be more pronounced than the depression of the Tg synthesis. Most frequently the radioiodine uptake is very low and most of the iodine remains in the gland as iodide and MIT. In those tissues which organify radioiodine, it is incorporated into tyrosine molecules and is metabolized to the stage of iodothyronines (T4 + T3); there must then be little or no defect in coupling reactions. There is a linear relation between the concentration of stable iodine in Tg and the level of hormone synthesis, as we have found in "normal" gland and benign thyroid diseases. These results suggest that the overall disorder seen in thyroid cancer tissues appears to involve one of the initial steps of hormone synthesis. The very low mean iodination of Tg in these tissues suggests a great heterogeneity in the functional activity throughout the tumour. TSH has a very variable effect on thyroid cancer tissues maintained in organ culture: in 46 % of the cases the hormone has no effect. In some instances TSH may significantly increase the incorporation of radioiodine into soluble iodoproteins, Tg as well as the albumin fraction.

scholarly journals miRNA-6715-5p Inhibits Cellular Proliferation and Invasion in Colorectal Cancer by Directly Targeting CST4

2021 ◽  
Vol 2021 ◽  
pp. 1-12
Author(s):  
Ding Shi ◽  
Zheng Zhou ◽  
Shun Zhang
Keyword(s):  
Colorectal Cancer ◽  
Cellular Proliferation ◽  
Quantitative Polymerase Chain Reaction ◽  
Normal Tissues ◽  
Reporter Assays ◽  
Proliferation And Metastasis ◽  
Cancer Tissues ◽  
The Relationship ◽  
Proliferation And Invasion ◽  
Hct116 Cells

Background. Data on the correlation between CST4 and colorectal cancer (CRC) metastasis are scarce. The aim of this study was to analyze CST4 expression and investigate its biological roles and related microRNA- (miRNA-) mediated regulation in CRC. Methods. The expression of CST4 was examined in cancer tissues and their corresponding adjacent normal tissues from 40 gastric adenocarcinoma patients. The expression level of CST4 in specimens (cancer and normal tissues) was assessed through immunohistochemistry and/or quantitative polymerase chain reaction. miRNAs targeting CST4 in CRC were predicted by bioinformatics software. CST4 was knocked down in HCT116 cells and candidate miRNAs were transfected into HCT116 cells, and the effects of CST4 knockdown and miRNA transfection on cell proliferation and invasion were examined using CCK8, cell colony formation, and Transwell migration assays. Luciferase double-reporter assays were performed to verify the relationship between miRNA and CST4. Results. The expression of CST4 in CRC tissues was significantly higher than that in normal paracancerous tissues, but the results for miRNA-6715-5p were opposite. Regardless of CST4 knockdown or miRNA-6715-5p overexpression, the proliferation and invasion ability of HCT116 cells decreased significantly. Luciferase double-reporter assays showed that the upregulation of miR-6715-5p significantly reduced the luciferase activities of the CST4 3′-UTR plasmid in HCT116 cells. Conclusion. CST4 may be involved in CRC proliferation and metastasis. miRNA-6715-5p directly targets CST4 and negatively regulates its expression.

scholarly journals Fentanyl Exerts an Antitumor Effect on Papillary Thyroid Cancer by Regulating the miR-204/KLF5 Axis

2021 ◽  
Vol 2021 ◽  
pp. 1-8
Author(s):  
Dahao Lu ◽  
Lulu Jiang ◽  
Chen Dai ◽  
Keshi Yan ◽  
Ju Gao
Keyword(s):  
Thyroid Cancer ◽  
Papillary Thyroid Cancer ◽  
Tumor Development ◽  
Cell Counting ◽  
Luciferase Reporter ◽  
Papillary Thyroid ◽  
Antitumor Effects ◽  
Reporter Assays ◽  
Potential Antitumor

Fentanyl is a strong anesthetic analgesic drug that plays important roles in many types of cancers. However, the role of fentanyl in papillary thyroid cancer (PTC) tumor development remains ambiguous. In this study, we aimed to investigate the potential antitumor effects of fentanyl on PTC cell viability and invasion. Results of cell counting kit-8 and Transwell assays demonstrated that fentanyl treatment (5 ng/ml) reduced the viability and invasion of two PTC cells, TCP-1 and BCPAP. Our data subsequently showed that fentanyl induced antitumor effects by increasing miR-204 expressions. Furthermore, the results of luciferase reporter assays identified that miR-204 directly targets Krüppel-like transcription factor 5 (KLF5), which serves as tumor-promoting genes in many cancers. Further mechanistic analyses revealed that fentanyl performs its tumor-suppressive functions by regulating the miR-204/KLF5 axis in PTC cells. These results contribute to understanding the important role of fentanyl in treating PTC.

scholarly journals MiR-489-3p Reduced Pancreatic Cancer Proliferation and Metastasis By Targeting PKM2 and LDHA Involving Glycolysis

2021 ◽  
Vol 11 ◽  
Author(s):  
Dan Zhang ◽  
Zhiwei He ◽  
Yiyi Shen ◽  
Jie Wang ◽  
Tao Liu ◽  
...  
Keyword(s):  
Pancreatic Cancer ◽  
Glucose Metabolism ◽  
Cell Lines ◽  
Stress Responses ◽  
Hot Spot ◽  
Luciferase Reporter ◽  
Proliferation And Metastasis ◽  
Cancer Tissues

IntroductionMalignant proliferation and metastasis are some of the causes of high mortality in pancreatic cancer. MicroRNAs have been a hot spot in cancer research and are involved in tumor formation and metabolic stress responses. However, the biology function and underlying mechanism of miRNA regulating pancreatic cancer progress is remained uncleared.MethodsRNA-seq analysis the glycolysis associated miRNAs and verified miRNA-489-3p was involving in glycolysis. We used RNA in situ hybridization (ISH) and qRT-PCR to analyze the differential expression of miR-489-3p in pancreatic cancer tissues and adjacent tissues and cell lines. Then the function assay of in vivo and in vitro were used to evaluated the role of miR-489-3p in the proliferation, metastasis and glucose metabolism of pancreatic cancer. Furthermore, dual luciferase reporter and rescue experiments were performed to explore the mechanism underlying in the role of miRNA-489-3p.ResultsWe determined that glycolysis associated miRNA miR-489-3p was downregulated in pancreatic cancer tissues and cell lines. The gain and loos of function experiments confirmed that miR-489-3p could inhibit the proliferation, metastasis and glucose metabolism of pancreatic cancer. Further, we found that miR-489-3p could target regulating LDHA and PKM through the luciferase report experiment. Finally, in vivo experiment confirmed that highly expressed miR-489-3p inhibited the growth of pancreatic cancer.ConclusionIn short, this study identified miR-489-3p as a novel therapy target for pancreatic cancer which was involving in the proliferation, metastasis and glycolysis, but its diagnostic value deserves further study.

scholarly journals miR-103 promotes the progression of non-Hodgkins lymphoma by inhibiting OTUD7B expression

2020 ◽  
Author(s):  
Chong Wang ◽  
Yating Wu ◽  
Mengya Li ◽  
Shujuan Wang ◽  
Yanfang Liu
Keyword(s):  
Western Blot ◽  
Luciferase Reporter ◽  
Migration And Invasion ◽  
Normal Tissues ◽  
Qrt Pcr ◽  
Non Hodgkin Lymphoma ◽  
Reporter Assays ◽  
Non Hodgkins Lymphoma ◽  
Polymerase Chain

Abstract Background MicroRNAs (miRNAs) are vital for regulating the malignant phenotypes of tumor cells. The purpose of this work is to investigate the function and downstream mechanism of miR-103 in the progression of non-Hodgkin lymphoma (NHL). Methods and Materials Quantitative real-time polymerase chain reaction (qRT-PCR) was employed to detect miR-103 and OTU deubiquitinase 7B (OTUD7B) mRNA expressions in NHL tissues and cells. Immunohistochemistry and Western blot were used to detect the expression of OTUD7B in NHL tissues and cells. CCK-8 experiment, flow cytometry analysis, and Transwell experiment were used to detect the role of NHL cell proliferation, apoptosis, migration and invasion. Bioinformatics, qRT-PCR, Western blot and dual-luciferase reporter assays were used to validate the targeting relationship between miR-103 and OTUD7B. NF-κB p65 luciferase reporter assay and Western blot were applied to determine NF-κB activity and the expression of NF-κB targeted genes. Results Compared to normal tissues and cells, miR-103 expression levels were remarkably up-regulated in NHL tissues and cell lines. The up-regulation of miR-103 dramatically promoted the proliferation, migration and invasion of NHL cells and inhibited apoptosis. Conversely, down-regulating miR-103 significantly inhibited malignant phenotypes of the NHL cells. Additionally, OTUD7B was identified as a target gene of miR-103, and miR-103 increased NF-κB activity indirectly via repressing OTUD7B. Conclusion The miR-103/OTUD7B/NF-κB axis is involved in NHL progression.

scholarly journals MiR-105-3p acts as an oncogene to promote the proliferation and metastasis of breast cancer cells by targeting GOLIM4

BMC Cancer ◽  
2021 ◽  
Vol 21 (1) ◽  
Author(s):  
Bo Lin ◽  
Chunhua Liu ◽  
Enyi Shi ◽  
Qiu Jin ◽  
Wenhui Zhao ◽  
...  
Keyword(s):  
Breast Cancer ◽  
Cancer Cells ◽  
Breast Cancer Cells ◽  
Molecular Mechanisms ◽  
Quantitative Polymerase Chain Reaction ◽  
Luciferase Reporter ◽  
Reporter Assays ◽  
Proliferation And Metastasis ◽  
Cancer Tissues ◽  
Mcf 7

Abstract Background Dysregulated miRNAs are involved in carcinogenesis of the breast and may be used as prognostic biomarkers and therapeutic targets during the cancer process. The purpose of this study was to explore the effect of miR-105-3p on the tumourigenicity of breast cancer and its underlying molecular mechanisms. Methods Reverse transcription-quantitative polymerase chain reaction (RT-qPCR) was applied to detect the expression of miR-105-3p in breast cancer tissues and cell lines. The impacts of miR-105-3p on the proliferation, migration, invasion and apoptosis of human breast cancer cells (MCF-7 and ZR-75-30) were evaluated by CCK-8 assays, Transwell chamber assays, TUNEL assays and western blot analyses. In addition, bioinformatics and luciferase reporter assays were used to determine the target genes of miR-105-3p. Results The expression of miR-105-3p was elevated in breast cancer tissues and increased with tumour severity. Downregulation of miR-105-3p could inhibit cell proliferation, suppress cell migration/invasion, and promote cell apoptosis in MCF-7 and ZR-75-30 cells. Furthermore, Golgi integral membrane protein 4 (GOLIM4) was identified as the direct target gene of miR-105-3p by bioinformatics and luciferase reporter assays. In addition, silencing GOLIM4 restored the anti-breast cancer effects induced by miR-105-3p downregulation. Conclusions MiR-105-3p acts as an oncogene to promote the proliferation and metastasis of breast cancer cells by targeting GOLIM4, which provides a new target for the prevention and treatment of breast cancer.

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