Redox-responsive microbeads containing thiolated pectin-doxorubicin conjugate inhibit tumor growth and metastasis: An in vitro and in vivo study

Gastric cancer (GC) is one of the most common cancers in the world and remains a heavy burden of health worldwide. Adenylate cyclase 3 ( ADCY3) is a widely expressed membrane-associated protein in human tissues and has been identified to be a new molecular target of GC. Long noncoding RNAs have a substantial influence on tumorigenesis and progression of tumors by binding to microRNAs. Therefore, this study is to clarify the mechanism by which LINC00319 sponges micro RNA-335–5p ( miR-335–5p) to influence the development of GC. Initially, microarray analysis identified GC-related differentially expressed LINC00319 and ADCY3 for this study. The interaction was confirmed that LINC00319 interacted with miR-335–5p to regulate ADCY3. Next, SGC-7901 cells presenting with the lowest LINC00319 expression and the highest miR-335–5p expression were transfected with LINC00319, miR-335–5p inhibitor, or ADCY3 vector to examine their roles in growth and metastasis of GC cells, which was further ascertained by in vivo experiments. LINC00319 was upregulated and miR-335–5p was downregulated in GC cells. LINC00319 overexpression, miR-335–5p inhibitor, or ADCY3 overexpression was shown to significantly elevate the expression of cyclin-dependent kinase 4 and metastasis associated 1, decrease that of growth arrest-specific 1, and promote tumor growth and metastasis by increasing proliferation and migration and reducing cell apoptosis. Importantly, it was found that overexpressed miR-335–5p exerted its tumor suppressive role in GC through downregulating ADCY3. Collectively, LINC00319 expedited growth and metastasis of GC by upregulating miR-335–5p-mediated ADCY3. NEW & NOTEWORTHY This study is carried out based on in vivo and in vitro studies in mice and gastric cancer (GC) cells with the aim of clarifying the role of LINC00319 on GC growth and metastasis, which associated with micro RNA-335–5p-mediated adenylate cyclase 3. Altogether, we identified LINC00319 to be a potential therapy to treat GC.

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Kinesin Family Member 18A (KIF18A) Contributes to the Proliferation, Migration, and Invasion of Lung Adenocarcinoma Cells In Vitro and In Vivo

Disease Markers ◽

10.1155/2019/6383685 ◽

2019 ◽

Vol 2019 ◽

pp. 1-9 ◽

Cited By ~ 2

Author(s):

Fu-Tao Chen ◽

Fu-Kuan Zhong

Keyword(s):

Tumor Growth ◽

Lung Adenocarcinoma ◽

Clinical Stage ◽

Migration And Invasion ◽

Expression Levels ◽

Adenocarcinoma Cells ◽

Lung Adenocarcinoma Cells ◽

Tumor Growth And Metastasis

Objective. To determine the expression levels of KIF18A in lung adenocarcinoma and its relationship with the clinicopathologic features of patients undergoing radical colectomy and explore the potential role in the progression of lung adenocarcinoma. Methods. Immunohistochemical assays were performed to explore the expression levels of KIF18A in 82 samples of lung adenocarcinoma and corresponding normal tissues. According to the levels of KIF18A expression in lung adenocarcinoma tissue samples, patients were classified into the KIF18A high expression group and low expression group. Clinical data related to the perioperative clinical features (age, gender, smoking, tumor size, differentiation, clinical stage, and lymph node metastasis), the potential correlation between KIF18A expression levels, and clinical features were analyzed, and the effects of KIF18A on lung adenocarcinoma cell proliferation, migration, and invasion were measured by colony formation assay, MTT assay, wound healing assay, and transwell assays. The possible effects of KIF18A on tumor growth and metastasis were measured in mice through tumor growth and tumor metastasis assays in vivo. Results. KIF18A in lung adenocarcinoma tissues. Further, KIF18A was significantly associated to clinical characteristic features including the tumor size (P=0.033) and clinical stage (P=0.041) of patients with lung adenocarcinoma. Our data also investigated that KIF18A depletion dramatically impairs the proliferation, migration, and invasion capacity of lung adenocarcinoma cells in vitro and inhibits tumor growth and metastasis in mice. Conclusions. Our study reveals the involvement of KIF18A in the progression and metastasis of lung adenocarcinoma and provides a novel therapeutic target for the treatment of lung adenocarcinoma.

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Inhibition of tumor growth and metastasis in vitro and in vivo by targeting macrophage migration inhibitory factor in human neuroblastoma

Oncogene ◽

10.1038/sj.onc.1209395 ◽

2006 ◽

Vol 25 (25) ◽

pp. 3501-3508 ◽

Cited By ~ 47

Author(s):

Y Ren ◽

H M Chan ◽

J Fan ◽

Y Xie ◽

Y X Chen ◽

...

Keyword(s):

Tumor Growth ◽

Migration Inhibitory Factor ◽

Macrophage Migration Inhibitory Factor ◽

Inhibitory Factor ◽

Macrophage Migration ◽

Human Neuroblastoma ◽

Inhibition Of Tumor Growth ◽

Tumor Growth And Metastasis

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H3K4me3 and H3K27ac Activated lncRPL34-AS1 Acts as a Suppressor of Esophageal Squamous Cell Carcinoma via Targeting miR-575/ACAA2 Axis and Binding to ALOX12B and CAT

10.21203/rs.3.rs-103657/v1 ◽

2020 ◽

Author(s):

Hu Zhang ◽

Enchun Pan ◽

Ying Zhang ◽

Chao Zhao ◽

Qiwei Liu ◽

...

Keyword(s):

Squamous Cell Carcinoma ◽

Esophageal Squamous Cell Carcinoma ◽

Tumor Growth ◽

Cell Carcinoma ◽

Squamous Cell ◽

Chromatin Immunoprecipitation ◽

Tumor Growth And Metastasis ◽

Rip Assay

Abstract Background: Long noncoding RNAs (lncRNAs) are abnormally expressed in a broad type of cancers and play significant roles that regulate tumor development and metastasis. However, the pathological roles of lncRNAs in esophageal squamous cell carcinoma (ESCC) remain largely unknown. Here we aimed to investigate the role and regulatory mechanism of the novel lncRPL34-AS1 in the development and progression of ESCC. Methods: The expression level of lncRPL34-AS1 in ESCC tissues and different cell lines was determined by quantitative real-time PCR (RT-qPCR). Chromatin immunoprecipitation (ChIP) assay was used to evaluate the regulatory effect of histone modification on lncRPL34-AS1. Then, functional experiments in vitro and in vivo were employed to explore the effects of lncRPL34-AS1 on tumor growth and metastasis in ESCC. Mechanistically, fluorescence in situ hybridization (FISH), bioinformatics analyses, luciferase reporter assay, RNA immunoprecipitation (RIP) assay and western blot assays were used to detect the regulatory relationship between lncRPL34-AS1, miR-575 and ACAA2. In addition, comprehensive identification of RNA binding proteins (ChIRP), mass spectrometry, and RIP assay were used to identify lncRPL34-AS1-interacting proteins.Results: LncRPL34-AS1 was significantly down-regulated in ESCC tissues and cells, which was negatively correlated with overall survival in ESCC patients. The chromatin immunoprecipitation (ChIP) assays indicated that gain of H3K4me3 and H3K27 acetylation-activated lncRPL34-AS1 was down-regulated in ESCC. Functionally, upregulation of lncRPL34-AS1 dramatically suppressed ESCC cell proliferation, colony formation, cell cycle progression and induced apoptosis in vitro, whereas knockdown of lncRPL34-AS1 elicited the opposite function. Consistently, overexpression of lncRPL34-AS1 inhibited tumor growth and metastasis in vivo. Mechanistically, lncRPL34-AS1 acted as competing endogenous RNA (ceRNA) of miR-575 to relieve the repressive effect of miR-575 on its target ACAA2, then suppressed the tumorigenesis of ESCC. In addition, protein ALOX12B and CAT resulted direct binding targets of lncRPL34‐AS1 and affected biological process in ESCC. Conclusions: Together, our results reveal a role for lncRPL34-AS1 in ESCC tumorigenesis and may provide a strategy for using lncRPL34-AS1 as a potential biomarker and a therapeutic target for patients with ESCC.

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Zn‐doped CuO nanocomposites inhibit tumor growth in vitro and in vivo : Involvement of reactive oxygen species‐dependent autophagy and apoptosis cross‐linked by NF‐kappaB pathway

The FASEB Journal ◽

10.1096/fasebj.2019.33.1_supplement.811.7 ◽

2019 ◽

Vol 33 (S1) ◽

Author(s):

Huanli Xu ◽

Ru Yuan ◽

Xiaohui Liu ◽

Aharon Gedanken ◽

Xiukun Lin

Keyword(s):

Reactive Oxygen Species ◽

Tumor Growth ◽

Reactive Oxygen ◽

Oxygen Species ◽

Inhibit Tumor Growth ◽

Nf Kappab

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Deoxyelephantopin exhibits potent effects against breast tumor growth and metastasis in vitro and in vivo

Planta Medica ◽

10.1055/s-2007-987360 ◽

2007 ◽

Vol 73 (09) ◽

Author(s):

CC Huang ◽

CP Lo ◽

CY Chiu ◽

MC Hsieh ◽

LF Shyur

Keyword(s):

Tumor Growth ◽

Breast Tumor ◽

Tumor Growth And Metastasis

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Neuronal Repressor REST Controls Ewing Sarcoma Growth and Metastasis by Affecting Vascular Pericyte Coverage and Vessel Perfusion

Cancers ◽

10.3390/cancers12061405 ◽

2020 ◽

Vol 12 (6) ◽

pp. 1405

Author(s):

Zhichao Zhou ◽

Yuanzheng Yang ◽

Fei Wang ◽

Eugenie S. Kleinerman

Keyword(s):

Tumor Growth ◽

Ewing Sarcoma ◽

Vascular Function ◽

Fusion Gene ◽

Critical Role ◽

Survival Rates ◽

Tumor Vasculature ◽

Tumor Growth And Metastasis

Survival rates for Ewing sarcoma (ES) patients with metastatic disease have not improved in over 20 years. Tumor growth and metastasis are dependent on tumor vasculature expansion; therefore, identifying the regulators that control this process in ES may provide new therapeutic opportunities. ES expresses high levels of repressor element 1 silencing transcription factor (REST), which is regulated by the EWS-FLI-1 fusion gene. However, the role of REST in ES growth and the regulation of the tumor vasculature have not been elucidated. To study this role, we established REST-knockout human TC71 ES cell lines through CRISPR/Cas9 recombination. While knockout of REST did not alter tumor cell proliferation in vitro, REST knockout reduced tumor growth and metastasis to the lung in vivo and altered tumor vascular morphology and function. Tumor vessels in the REST-knockout tumors had a punctate appearance with significantly decreased tumor vascular pericytes, decreased perfusion, and increased permeability. REST-knockout tumors also showed increased apoptosis and hypoxia. These results indicate that REST plays a critical role in ES vascular function, which in turn impacts the ability of ES tumors to grow and metastasize. These findings therefore provide a basis for the targeting of REST as a novel therapeutic approach in ES.

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