The role of circCNIH4 in the adipocyte's effects on metastasis of breast cancer cells.

2020 ◽  
Vol 38 (15_suppl) ◽  
pp. e13086-e13086
Author(s):  
Xiu Chen ◽  
Jinhai Tang
Keyword(s):  
Breast Cancer ◽  
Wound Healing ◽  
Cell Invasion ◽  
Invasion And Migration ◽  
Non Invasive ◽  
In Vivo Experiments ◽  
And Migration ◽  
Mcf 7

e13086 Background: Obesity is associated with the risk of breast cancer(BCa) incidence and development. However, biological changes in obesity BCa individuals are still uncertain. Nowadays, circCNIH4, one of novel non-coding RNAs, was found to be a non-invasive biomarker in cancers. Methods: We verified the cancer-promoting role of obesity in BCa patients by comparing BMI indexes of 33 BCa and 44 benign tumor patients. Then we cocultured viscera adipose cells(HPA-v) and BCa cells(MCF-7/H and MDA-MB-231/H) to confirm the function of adipocytes on metastasis of BCa cells through wound healing, transwell assays. In vivo experiments were also performed. We analyzed the expression level of circCNIH4 in MCF-7/H, MDA-MB-231/H and different subtypes of BCa cells by quantitative polymerase chain reaction. Simultaneously, we identified inhibited effects of circCNIH4 on metastasis of BCa cells by wound healing, transwell assays and verified the location of circCNIH4 by FISH. Luciferase Assay was used to detect harbored miRNA. Rescue experiments were then applied. Results: We found the BMI of BCa patients(24.37±2.51) was much higher than benign patients(22.97±2.91). Metastasis of BCa cells were obviously promoted after in vitro and in vivo experiments. Then we found the expression of circCNIH4 in MCF-7/H and MDA-MB-231/H were down-regulated 0.71 and 0.52 than that in MCF-7 and MDA-MB-231. Also, circCNIH4 was positively correlated with less aggressive types of BCa cells. Overexpression of circCNIH4 in MDA-MB-231 could suppress cell invasion and migration, while silencing of it in MCF-7 promoted cell invasion and migration. The FISH assay demonstrated that circCNIH4 mainly located in the cytoplasm and might function as a “sponge” for miRNA. MiR-135b functioned as a tumor promoter gene from data of 93 BCa patients (HR = 2.27; 1.01 − 5.12), and it could be captured by circCNIH4 via luciferase and rescued assays. Conclusions: In this study, we revealed that BMI or viscera adipocytes could deteriorate prognosis of BCa and circCNIH4 could be a novel biomarker for non-invasive BCa. In details, circCNIH4 mainly suppressed the adipocyte's pro-metastasis effects on BCa by capturing miR-135b.

scholarly journals MiR-125b-5p Inhibited The Progression of Hepatoblastoma As A Shared miRNA of The lncRNA NEAT1 and YES1

2020 ◽  
Author(s):  
Zhu Jin ◽  
Yutong Chen ◽  
Yuchen Mao ◽  
Mingjuan Gao ◽  
Zebing Zheng ◽  
...  
Keyword(s):  
Clinicopathological Characteristics ◽  
Luciferase Reporter ◽  
Tumor Growth Inhibition ◽  
Invasion And Migration ◽  
In Vivo Experiments ◽  
Reporter Assays ◽  
And Migration ◽  
Relationship Of

Abstract Background: microRNAs have been studied widely in hepatoblastoma. However, the role of miR-125b-5p and its relationship with the lncRNA sNEAT1 and YES1 in hepatoblastoma have not been reported previously. We aimed to reveal the role of NEAT1/miR-125b-5p/YES1 in the progression of hepatoblastoma.Methods: We collected tumor tissues and their adjacent tissues from 12 hepatoblastoma patients. qRT-PCR was applied to detect the expression of miR-125b-5p, and the relationship of miR-125b-5p with clinicopathological characteristics was analyzed. Dual luciferase reporter assays and RNA pull down assays were used to identify the relationships among NEAT1, miR-125b-5p and YES1. CCK8, Transwell assays and wound healing assays were used to examine cell viability, invasion and migration. In vivo experiments were also applied to detect the effect of miR-125b-5p on hepatoblastoma.Results: miR-125b-5p was significantly downregulated in hepatoblastoma tissue and cells. The higher the PRETEXT grade, the lower the miR-125b-5p level. NEAT1 could bind to miR-125b-5p and inhibit its expression. miR-125b-5p could target YES1 and inhibit its expression. Overexpression of miR-125b-5p decreased the proliferation, invasion, and migratory ability of hepatoblastoma cells. YES1 could rescue the above effects. At the same time, overexpression of miR-125b-5p resulted in decreased YES1 and tumor growth inhibition in vivo.Conclusion: miR-125b-5p acted as a shared miRNA of NEAT1 and YES1 in hepatoblastoma. Overexpression of miR-125b-5p could target YES1 and inhibit its expression, therefore inhibiting the progression of hepatoblastoma.

scholarly journals refMiR 142 5p inhibits cell invasion and migration by targeting DNMT1 in breast cancer

2021 ◽  
Author(s):  
Hui Li ◽  
Han-Han Li ◽  
Qian Chen ◽  
Yu-Yang Wang ◽  
Chang Chang Fan ◽  
...  
Keyword(s):  
Breast Cancer ◽  
Cancer Diagnosis ◽  
Cell Invasion ◽  
Feedback Loop ◽  
Regulatory Element ◽  
Breast Cancer Diagnosis ◽  
Invasion And Migration ◽  
And Migration ◽  
Abnormal Cell Proliferation

Abnormal cell proliferation caused by abnormal transcription regulation mechanismseems to be one of the reasons for the progression of breast cancer and also thepathological basis. MicroRNA 142 5p (miR 142 5p) is a low expressed miRNA inbreast cancer. T he role of MKL1's regulation of DNMT1 in breast cancer cellproliferation and migration is still unclear. MKL 1 (myocardi n related transcriptionfactor A) can bind to the conserved cis regulatory element CC (A/T) 6GG (called CarGbox) in the promoter to re gulate the transcription of miR 142 5p. The expression ofmiR 142 5p and MKL 1 are positively correlated. In addition, it has been proved thatDNMT1 is the target of miR 142 5p, which inhibits the expression of DNMT1 bytargeting the 3'UTR of DNMT1, thereby forming a feedback loop and inhibiting themigration and proliferation of breast cancer. Our data provide important and novelinsights into the MKL 1/miR 142 5p/DNMT1/maspin signaling pathway, and maybecome a new idea for breast cancer diagnosis, treatment and prognosis.

scholarly journals MicroRNA-197 Promotes Metastasis of Hepatocellular Carcinoma by Activating Wnt/β-Catenin Signaling

2018 ◽  
Vol 51 (1) ◽  
pp. 470-486 ◽  
Author(s):  
Zhaoxia Hu ◽  
Peipei Wang ◽  
Jiaxin Lin ◽  
Xingrong Zheng ◽  
Fangji Yang ◽  
...  
Keyword(s):  
Hepatocellular Carcinoma ◽  
Cell Lines ◽  
Cell Invasion ◽  
Invasion And Migration ◽  
Report System ◽  
And Migration ◽  
Signaling Activation

Background/Aims: MicroRNA-197 (miR-197) has been shown to play roles in epithelialmesenchymal transition (EMT) and metastasis. The Wnt/β-catenin pathway is associated with EMT, but whether miR-197 regulatesWnt/β-catenin remains unclear. This study was to demonstrate the role of miR-197 on the Wnt/β-catenin pathway in hepatocellular carcinoma (HCC). Methods: Quantitative reverse transcription polymerase chain reaction (qRT-PCR) was used to detect the expression of miR-197 in 105 HCC specimens and 15 HCC cell lines. We tested the predicted target gene of miR-197 using a genetic report system. The role of miR-197 in HCC cell invasion and migration (wound healingand cell invasion and migrationby Transwell assays) and in an HCC xenograft modelwas analyzed. Results: Using a miRNA microarray analysis of HCC specimens and compared with non-metastatic HCC, miR-197 was identified as one of the most upregulated miRNAs in metastatic HCC. miR-197 expression was positively associated with the invasiveness of HCC cell lines. Metastatic HCC cells with high miR-197 expression had Wnt/β-catenin signaling activation. High levels of miR-197 expression also promoted EMT and invasionHCC cells in vitro and in vivo. miR-197 directly targeted Axin-2, Naked cuticle 1 (NKD1), and Dickkopf-related protein 2 (DKK2), leading to inhibition of Wnt/β-catenin signaling. High miR-197 expression was found in HCC specimens from patients with portal vein metastasis;high miR-197 expression correlated to the expression of Axin2, NKD1, and DKK2. Conclusion: miR-197 promotes HCC invasion and metastasis by activating Wnt/β-catenin signaling. miR-197 could possibly be used as a prognostic marker and therapeutic target for HCC.

miR-3614-3p suppresses cell aggressiveness of human breast cancer by targeting AKT3 and HDAC1 expression

2021 ◽  
Vol 2 (3) ◽  
Author(s):  
Zhenzhen Wang ◽  
◽  
Xintao Jing ◽  
Zhenghao Zhao ◽  
Fang Li ◽  
...  
Keyword(s):  
Breast Cancer ◽  
Luciferase Reporter ◽  
Migration And Invasion ◽  
Transwell Migration Assay ◽  
Migration Assay ◽  
Invasion And Migration ◽  
Protein Levels ◽  
And Migration ◽  
Mcf 7

Purpose: MicroRNAs (miRNA) have been reported in the regulation of various pathobiological progression in cancer. Our recent study has reported that miR-3614-3p significantly suppressed the proliferation of Breast Cancer (BC) cells through the downregulation its host gene TRIM25. However, the other functional role of miR3614-3p migration and invasion in BC and its mechanism have not been investigated thoroughly. Materials and methods: The MDA-MB-231 and MCF-7 BC cell lines were purchased. The cell line expression levels of miR-3614- 3p and AKT3/HDAC1 were determined by quantitative real-time PCR (qPCR). The wound healing assay and transwell migration assay were determined. We next measured protein levels of AKT3/HDAC1 by Western blot. Finally, we investigated the role of AKT3/HDAC1 using siRNA; and confirmed the targeting of 3’UTR of AKT3 and HDAC1 through miR-3614-3p using a luciferase reporter assay. Results: In the present research, we studied that overexpression of miR-3614-3p markedly suppressed tumor cell invasion and migration independent TRIM25, whereas through regulated another targets AKT3 and HDAC1 expression. Notably, TRIM25 is also a target gene of miR-3614 which bind to pri-miR-3614 caused TRIM25 silence. Conclusion: miR-3614-3p is an anti-oncogene that can suppress breast cancer cell aggressiveness by targeting AKT3 and HDAC1, which reveals the potential values of miR-3614-3p for suppression of metastasis of BC. Keywords: Breast cancer; miR-3614; AKT3; HDAC1.

scholarly journals The Prompting Effects of MT1-MMP on EMT in Breast Cancer

2021 ◽  
Author(s):  
weiwei cao ◽  
Jianwei HE ◽  
Hongmei Zhang ◽  
Licui Zhang ◽  
Inayat Azeem
Keyword(s):  
Breast Cancer ◽  
Wound Healing ◽  
Cancer Tissue ◽  
Mesenchymal Transition ◽  
Cancer Resection ◽  
Expression Levels ◽  
Invasion And Migration ◽  
Associated Proteins ◽  
And Migration ◽  
Mcf 7

Abstract ObjectiveEpithelial to mesenchymal transition (EMT) was the initial process of invasion and metastasis leading to a relapse of breast cancer following resection and chemo-radiotherapy. Membrane type-1 Matrix Metalloproteinase (MT1-MMP) was confirmed to play an important role in EMT in various cancers. However, the MT1-MMP effects on EMT in breast cancer had not yet been studied. Here,We investigated the MT1-MMP effects on breast cancer EMTonset, invasion, and migration abilities in MCF-7 cells. MethodsExpressions of MT1-MMP and EMT-associated proteins including E-cadherin, N-cadherin, and Vimentin were detected by immunohistochemistry in 71 breast cancer resection samples. The relationships of MT1-MMP with clinic- pathological parameters were statistically analyzed, as well as EMT-associated proteins. Western blot tests were performed to test MT1-MMP and EMT-associated proteins expression levels in MCF-7 cells transfected by MT1-MMP plasmid. Wound-healing and transwell experiments were used to estimate MT1-MMP-induced invasion and migration. ResultsOverexpression of MT1-MMP was verified in 71 breast cancer patients. MT1-MMP levels were observed to be correlated with the breast cancer clinical TNM stage, lymph node metastasis, and tumor size. The EMT-associated proteins including N-cadherin and Vimentin expression levels were higher both in MT1-MMP strong positive breast cancer resection samples and MCF-7 cells transfected with MT1-MMP plasmid. Furthermore, MCF-7 cells also acquired more ability to migrate and invade according to the results of the wound-healing assays and transwell experiments.ConclusionMT1-MMP was overexpressed in breast cancer tissue, and MT1-MMP promoted breast cancer EMT incidence, which was closely associated with breast cancer invasion and migration.

A Review on Phytopharmaceutical shaving Concomitant Experimental Anti-Diabetic and Anti-Cancer Effects as Potential Sources for Targeted Therapies Against Insulin Mediated Breast Cancer Cell Invasion and Migration

2020 ◽  
Vol 16 ◽  
Author(s):  
Vibhavana Singh ◽  
Rakesh Reddy ◽  
Antarip Sinha ◽  
Venkatesh Marturi ◽  
Shravani Sripathi Panditharadyula ◽  
...  
Keyword(s):  
Breast Cancer ◽  
Medicinal Plants ◽  
Cancer Cell ◽  
Breast Cancer Cell ◽  
Cell Invasion ◽  
Breast Tumor ◽  
Cancer Cell Invasion ◽  
Invasion And Migration ◽  
Anti Cancer ◽  
And Migration

: Diabetes and breast cancer are pathophysiologically similar and clinically established diseases that co-exist with a wider complex similar molecular signalling and having similar set of risk factors. Insulin plays a pivotal role for invasion and migration of breast cancer cells. Several ethnopharmacological evidences light the concomitant anti-diabetic and anti-cancer activity of medicinal plant and phytochemicals against breast tumor of patients with diabetes. This present article reviewed the findings on medicinal plants and phytochemicals with concomitant anti-diabetic and anti-cancer effects reported in scientific literature to facilitate the development of dual-acting therapies against diabetes and breast cancer. The schematic tabular form of published literatures on medicinal plants (63 plants belongs to 45 families) concluded the dynamics of phytochemicals against diabetes and breast tumor that could be explored further for the discovery of therapies for controlling of breast cancer cell invasion and migration in patient with diabetes.

lncRNA SNHG14 promotes the proliferation, migration, and invasion of thyroid tumour cells by regulating miR-93-5p

Zygote ◽  
2021 ◽  
pp. 1-11
Author(s):  
Fang Tian ◽  
Huimin Ying ◽  
Shuaiju Liao ◽  
Yuanyuan Wang ◽  
Quansheng Wang
Keyword(s):  
Wound Healing ◽  
Xenograft Model ◽  
Tumour Cells ◽  
Luciferase Reporter ◽  
Migration And Invasion ◽  
Thyroid Tumour ◽  
Invasion And Migration ◽  
Vital Functions ◽  
And Migration

Summary Long non-coding RNAs (lncRNAs) exert vital functions in the occurrence and development of various tumours. The aim of this study was to examine the regulatory effect and underlying molecular mechanism of lncRNA small nucleolar RNA host gene 14 (SNHG14) on the proliferation, invasion and migration of thyroid tumour cells. The expression of SNHG14 in thyroid tumour cell lines was determined using qRT-PCR. CCK-8 and western blot were used to detect the effects of SNHG14 on proliferation and apoptosis of thyroid tumour cells. The effect of SNHG14 on the migration and invasion of thyroid tumour cells was analyzed using immunofluorescence, wound-healing and transwell assays. A targeting relationship between SNHG14 and miR-93-5p was determined using bioinformatics software and luciferase reporter assays. In addition, CCK-8, immunofluorescence, wound-healing and transwell assays were applied to demonstrate that SNHG14 promoted the proliferation, migration and invasion of thyroid tumour cells by targeting miR-93-5p. The biological function of SNHG14 in vivo was explored through a xenograft model and immunohistochemistry. SNHG14 was upregulated in thyroid tumour cells compared with normal cells. Downregulation of SNHG14 effectively reduced the proliferation, migration and invasion of TPC-1 cells, and induced cell apoptosis. Moreover, SNHG14 directly targeted miR-93-5p and there was a negative correlation between them. Further functional experiments illustrated that miR-93-5p overexpression dramatically reversed the promoting role of SNHG14 in proliferation, migration and invasion of TPC-1 cells. Our results demonstrated that SNHG14 promotes the proliferation, invasion and migration of thyroid tumour cells by downregulating miR-93-5p.

Impact of protamine I on colon cancer proliferation, invasion, migration, diagnosis and prognosis

2018 ◽  
Vol 399 (3) ◽  
pp. 265-275 ◽  
Author(s):  
Zhi Chen ◽  
Chunyu Shi ◽  
Shuohui Gao ◽  
Defeng Song ◽  
Ye Feng
Keyword(s):  
Colon Cancer ◽  
Cell Invasion ◽  
Cell Apoptosis ◽  
Xenograft Model ◽  
Enzyme Linked Immunosorbent Assay ◽  
Invasion And Migration ◽  
Diagnosis And Prognosis ◽  
And Migration ◽  
Cancer Tissues

AbstractThis paper investigates protamine I (PRM1) expression and its effects on proliferation, invasion and migration of colon cancer cells as well as its function in clinical diagnosis and prognosis. Gene chips were used to screen differentially expressed genes. PRM1 expression was detected by Western blotting and quantitative real time-polymerase chain reaction (qRT-PCR). Hematoxylin and eosin (HE) staining and immunohistochemistry were utilized to compare the expression of PRM1 from multiple differentiation levels of colon cancer tissues. Cell viability, cell apoptosis and cell cycle were tested using the MTT assay and flow cytometry. Cell invasion and migration capability were tested using the Transwell assay and wound healing.In vivoeffects of PRM1 on colon cancer were explored using a xenograft model.PRM1expression in serum was detected by enzyme-linked immunosorbent assay (ELISA). The expression level of PRM1 was significantly higher in colon cancer tissues and the staining degree of PRM1 in poorly-differentiated was stronger. pcDNA3.1-PRM1 decreased cell apoptosis while it increased the proliferation, cell invasion and migration. The si-PRM1 group displayed an opposite tendency. The serum PRM1 level was significantly higher and could serve as a diagnostic biomarker for colon cancer.

TIPE1 suppresses the invasion and migration of breast cancer cells and inhibits epithelial-to-mesenchymal transition primarily via the ERK signaling pathway

2019 ◽  
Vol 51 (10) ◽  
pp. 1008-1015 ◽  
Author(s):  
Shusheng Qiu ◽  
Wei Hu ◽  
Qiuhong Ma ◽  
Yi Zhao ◽  
Liang Li ◽  
...  
Keyword(s):  
Breast Cancer ◽  
Western Blot ◽  
Cancer Cells ◽  
Blot Analysis ◽  
Western Blot Analysis ◽  
Breast Cancer Cells ◽  
Mesenchymal Transition ◽  
Invasion And Migration ◽  
And Migration

Abstract Tumor necrosis factor α-induced protein 8-like-1 (TIPE1) functions as an activator or a repressor in a tumor cell type-specific manner. However, the role of TIPE1 in breast cancer, especially regarding metastasis, is unknown. In this study, we aimed to investigate the TIPE1 expression in breast cancer tissues, the biological functions, and the underlying mechanisms of TIPE1 regarding the metastatic properties of breast cancer cells. The results of immunohistochemical staining and western blot analysis indicated that TIPE1 expression was associated with tumor size and lymph node metastasis, and the expression of TIPE1 was downregulated in the tissues of patients with lymph node metastasis. Transwell and wound healing assay results showed that TIPE1 inhibited the invasive and migratory capacities of breast cancer cells. Moreover, the epithelial-mesenchymal transition (EMT) was suppressed in TIPE1-overexpressing cells, as demonstrated by western blot analysis. In addition, western blot analysis also showed that TIPE1 reduced the expression levels of MMP2 and MMP9 and decreased the phosphorylation level of ERK. These results suggested that TIPE1 might suppress the invasion and migration of breast cancer cells and inhibit EMT primarily via the ERK signaling pathway. Our findings revealed the anti-tumor metastasis role of TIPE1 in breast cancer and TIPE1 might be a new candidate prognostic indicator and a potential molecular target for the treatment of breast cancer.

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