scholarly journals sFlt-1 Gene Therapy of Follicular Thyroid Carcinoma

Endocrinology ◽  
2004 ◽  
Vol 145 (2) ◽  
pp. 817-822 ◽  
Author(s):  
Caisheng Ye ◽  
Chong Feng ◽  
Shenming Wang ◽  
Kent Z. Q. Wang ◽  
Nancy Huang ◽  
...  
Keyword(s):  
Gene Therapy ◽  
Thyroid Carcinoma ◽  
Tumor Growth ◽  
Tumor Progression ◽  
Tumor Angiogenesis ◽  
Follicular Thyroid Carcinoma ◽  
Umbilical Vein ◽  
Control Treatment ◽  
Vegf Receptor ◽  
Antitumor Effects

Abstract Tumor progression largely depends on blood supply and neovessel formation, and angiogenesis is emerging as a promising target for cancer therapy. Vascular endothelial growth factor (VEGF), a major proangiogenic molecule, stimulates angiogenesis via promoting endothelial proliferation, survival and migration. VEGF has been found to be up-regulated in various types of tumors and to be associated with tumor progression and poor prognosis. Inhibition of VEGF or its signaling pathway has been shown to suppress tumor angiogenesis and tumor growth. In the present study, we tested the antiangiogenic and antitumor effects of soluble VEGF receptor-1 [soluble Flt (sFlt)-1] on the growth of follicular thyroid carcinoma (FTC). We constructed a 293 embryonic kidney cell line (293-Flt1–3d) that expresses sFlt-1, which is composed of the first three extracellular domains of Flt-1. The 293-Flt1–3d cells inhibited the in vitro growth of human umbilical vein endothelial cells in a paracrine manner. The in vivo antitumor and antiangiogenic activities of the 293-Flt1–3d cells were tested. When 293-Flt1–3d cells were inoculated at a site remote to the FTC-133 tumor transplant, the growth of FTC-133 tumors were inhibited by 70.37%, as compared with the control treatment with 293 cells expressing control gene LacZ. Immunohistochemical analysis of microvessel densities in treated tumors demonstrated that 293-Flt1–3d cells robustly suppressed intratumoral angiogenesis. Our data suggest that a mammalian cell-mediated approach could effectively deliver sFlt-1 gene therapy and inhibit tumor angiogenesis and tumor growth.

scholarly journals miR-23a-3p is a Key Regulator of IL-17C-Induced Tumor Angiogenesis in Colorectal Cancer

Cells ◽  
2020 ◽  
Vol 9 (6) ◽  
pp. 1363 ◽  
Author(s):  
Yunna Lee ◽  
Su Jin Kim ◽  
Jieun Choo ◽  
Gwangbeom Heo ◽  
Jin-Wook Yoo ◽  
...  
Keyword(s):  
Colorectal Cancer ◽  
Tumor Growth ◽  
Tumor Angiogenesis ◽  
Ex Vivo ◽  
Underlying Mechanism ◽  
Vegf Receptor ◽  
Invasion And Migration ◽  
Novel Target ◽  
And Migration

MicroRNAs (miRNAs) have emerged as key players in tumor angiogenesis. Interleukin-17C (IL-17C) was identified to promote colorectal cancer (CRC) progression. Therefore, we aimed to investigate the effect of IL-17C on tumor angiogenesis, the involvement of miR-23a-3p in IL-17C signaling, and the direct target gene of miR-23a-3p in CRC. In vitro and ex vivo angiogenesis, a mouse xenograft experiment, and immunostaining were performed to test the effect of IL-17C on tumor angiogenesis. ELISA, quantitative real time PCR, and gene silencing were used to uncover the underlying mechanism. IL-17C induced angiogenesis of intestinal endothelial cells, subsequently enhancing cell invasion and migration of DLD-1 cells. IL-17C-stimulated DLD-1 cells produced vascular endothelial growth factor (VEGF) to enhance angiogenesis. Moreover, IL-17C markedly accelerated xenograft tumor growth, which was manifested by substantially reduced tumor growth when treated with the VEGF receptor 2 inhibitor Ki8751. Accordingly, Ki8751 suppressed the expression of IL-17C-stimulated PECAM and VE-cadherin in xenografts. Furthermore, IL-17C activated STAT3 to increase the expression of miR-23a-3p that suppressed semaphorin 6D (SEMA6D) expression, thereby permitting VEGF production. Taken together, our study demonstrates that IL-17C promotes tumor angiogenesis through VEGF production via a STAT3/miR-23a-3p/SEMA6D axis, suggesting its potential as a novel target for anti-CRC therapy.

scholarly journals New Insights Into the Regulatory Roles of Extracellular Vesicles in Tumor Angiogenesis and Their Clinical Implications

2021 ◽  
Vol 9 ◽  
Author(s):  
Maohua Huang ◽  
Yuhe Lei ◽  
Yinqin Zhong ◽  
Chiwing Chung ◽  
Mei Wang ◽  
...  
Keyword(s):  
Tumor Growth ◽  
Tumor Progression ◽  
Cancer Patients ◽  
Extracellular Vesicles ◽  
Tumor Angiogenesis ◽  
Growth And Development ◽  
Noncoding Rnas ◽  
Clinical Implications ◽  
Biological Processes ◽  
Bodily Fluids

Angiogenesis is required for tumor growth and development. Extracellular vesicles (EVs) are important signaling entities that mediate communication between diverse types of cells and regulate various cell biological processes, including angiogenesis. Recently, emerging evidence has suggested that tumor-derived EVs play essential roles in tumor progression by regulating angiogenesis. Thousands of molecules are carried by EVs, and the two major types of biomolecules, noncoding RNAs (ncRNAs) and proteins, are transported between cells and regulate physiological and pathological functions in recipient cells. Understanding the regulation of EVs and their cargoes in tumor angiogenesis has become increasingly important. In this review, we summarize the effects of tumor-derived EVs and their cargoes, especially ncRNAs and proteins, on tumor angiogenesis and their mechanisms, and we highlight the clinical implications of EVs in bodily fluids as biomarkers and as diagnostic, prognostic, and therapeutic targets in cancer patients.

scholarly journals Increased FSHD region gene1 expression reduces in vitro cell migration, invasion, and angiogenesis, ex vivo supported by reduced expression in tumors

2017 ◽  
Vol 37 (5) ◽  
Author(s):  
Ankit Tiwari ◽  
Niharika Pattnaik ◽  
Archita  Mohanty Jaiswal ◽  
Manjusha Dixit
Keyword(s):  
Cell Proliferation ◽  
Cell Migration ◽  
Tumor Progression ◽  
Tumor Angiogenesis ◽  
Umbilical Vein ◽  
Ectopic Expression ◽  
Migration And Invasion ◽  
Rt Pcr ◽  
Cell Functions

Facioscapulohumeral muscular dystrophy (FSHD) region gene 1 (FRG1) is a candidate gene for FSHD. FRG1 regulates various muscle-related functions, but studies have proposed its role in development and angiogenesis also, where it is involved with tumor-associated molecules. Therefore, we decided to look into its role in tumor progression, tumor angiogenesis, and its impact on cellular properties. Cell proliferation, migration, invasion and in vitro angiogenesis assays were performed to decipher the effect of FRG1 on endothelial and epithelial cell functions. Q-RT PCR was done for human embyonic kidney (HEK293T) cells with altered FRG1 levels to identify associated molecules. Further, immunohistochemistry was done to identify FRG1 expression levels in various cancers and its association with tumor angiogenesis. Subsequently, inference was drawn from Oncomine and Kaplan–Meier plotter analysis, for FRG1 expression in different cancers. Ectopic expression of FRG1 affected cell migration and invasion in both HEK293T and human umbilical vein endothelial cells (HUVECs). In HUVECs, FRG1 overexpression led to reduced angiogenesis in vitro. No effect was observed in cell proliferation in both the cell types. Q-RT PCR data revealed reduction in granulocyte-colony stimulating factor (G-CSF) expression with FRG1 overexpression and increased expression of matrix metalloproteinase 10 (MMP10) with FRG1 knockdown. Immunohistochemistry analysis showed reduced FRG1 levels in tumors which were supported by in silico analysis data. These findings suggest that reduction in FRG1 expression in gastric, colon and oral cavity tumor might have a role in tumor progression, by regulating cell migration and invasiveness. To elucidate a better understanding of molecular signaling involving FRG1 in angiogenesis regulation, further study is required.

scholarly journals Antiangiogenic and Antitumor Effects of Endostatin on Follicular Thyroid Carcinoma

Endocrinology ◽  
2002 ◽  
Vol 143 (9) ◽  
pp. 3522-3528 ◽  
Author(s):  
Caisheng Ye ◽  
Chong Feng ◽  
Shenming Wang ◽  
Xiaoning Liu ◽  
Yongjie Lin ◽  
...  
Keyword(s):  
Thyroid Carcinoma ◽  
Follicular Thyroid Carcinoma ◽  
Antitumor Effects

scholarly journals Conjugation of VEGFR1/R2-targeting peptide with gold nanoparticles to enhance antiangiogenic and antitumoral activity

2022 ◽  
Vol 20 (1) ◽  
Author(s):  
Pegah Zanjanchi ◽  
S. Mohsen Asghari ◽  
Hassan Mohabatkar ◽  
Mostafa Shourian ◽  
Mehdi Shafiee Ardestani
Keyword(s):  
Gold Nanoparticles ◽  
Adverse Effects ◽  
Tumor Growth ◽  
Mammary Carcinoma ◽  
Inductively Coupled Plasma ◽  
Umbilical Vein ◽  
Clinical Translation ◽  
Antitumoral Activity ◽  
Antitumor Effects ◽  
Mesenchymal Transition

Abstract Background Inhibition of tumor angiogenesis through simultaneous targeting of vascular endothelial growth factor receptor (VEGFR)-1 and -2 is highly efficacious. An antagonist peptide of VEGFA/VEGFB, referred to as VGB3, can recognize and neutralize both VEGFR1 and VEGFR2 on the endothelial and tumoral cells, thereby inhibits angiogenesis and tumor growth. However, improved efficacy and extending injection intervals is required for its clinical translation. Given that gold nanoparticles (GNPs) can enhance the efficacy of biotherapeutics, we conjugated VGB3 to GNPs to enhance its efficacy and extends the intervals between treatments without adverse effects. Results GNP–VGB3 bound to VEGFR1 and VEGFR2 in human umbilical vein endothelial (HUVE) and 4T1 mammary carcinoma cells. GNP–VGB3 induced cell cycle arrest, ROS overproduction and apoptosis and inhibited proliferation and migration of endothelial and tumor cells more effectively than unconjugated VGB3 or GNP. In a murine 4T1 mammary carcinoma tumor model, GNP–VGB3 more strongly than VGB3 and GNP inhibited tumor growth and metastasis, and increased animal survival without causing weight loss. The superior antitumor effects were associated with durable targeting of VEGFR1 and VEGFR2, thereby inhibiting signaling pathways of proliferation, migration, differentiation, epithelial-to-mesenchymal transition, and survival in tumor tissues. MicroCT imaging and inductively coupled plasma mass spectrometry showed that GNP–VGB3 specifically target tumors and exhibit greater accumulation within tumors than the free GNPs. Conclusion Conjugation to GNPs not only improved the efficacy of VGB3 peptide but also extended the intervals between treatments without adverse effects. These results suggest that GNP–VGB3 is a promising candidate for clinical translation. Graphical Abstract

scholarly journals Anti-Angiogenic Effects of Phytochemicals on miRNA Regulating Breast Cancer Progression

Biomolecules ◽  
2020 ◽  
Vol 10 (2) ◽  
pp. 191 ◽  
Author(s):  
Elizabeth Varghese ◽  
Alena Liskova ◽  
Peter Kubatka ◽  
Samson Mathews Samuel ◽  
Dietrich Büsselberg
Keyword(s):  
Breast Cancer ◽  
Tumor Growth ◽  
Tumor Progression ◽  
Cancer Progression ◽  
Tumor Angiogenesis ◽  
Expression Profiles ◽  
Metabolic Reprogramming ◽  
Breast Cancers ◽  
Oncogenic Signaling ◽  
Metabolic Switch

Several phytochemicals have been identified for their role in modifying miRNA regulating tumor progression. miRNAs modulate the expression of several oncogenes and tumor suppressor genes including the genes that regulate tumor angiogenesis. Hypoxia inducible factor-1 alpha (HIF-1α) signaling is a central axis that activates oncogenic signaling and acts as a metabolic switch in endothelial cell (EC) driven tumor angiogenesis. Tumor angiogenesis driven by metabolic reprogramming of EC is crucial for tumor progression and metastasis in many different cancers, including breast cancers, and has been linked to aberrant miRNA expression profiles. In the current article, we identify different miRNAs that regulate tumor angiogenesis in the context of oncogenic signaling and metabolic reprogramming in ECs and review how selected phytochemicals could modulate miRNA levels to induce an anti-angiogenic action in breast cancer. Studies involving genistein, epigallocatechin gallate (EGCG) and resveratrol demonstrate the regulation of miRNA-21, miRNA-221/222 and miRNA-27, which are prognostic markers in triple negative breast cancers (TNBCs). Modulating the metabolic pathway is a novel strategy for controlling tumor angiogenesis and tumor growth. Cardamonin, curcumin and resveratrol exhibit their anti-angiogenic property by targeting the miRNAs that regulate EC metabolism. Here we suggest that using phytochemicals to target miRNAs, which in turn suppresses tumor angiogenesis, should have the potential to inhibit tumor growth, progression, invasion and metastasis and may be developed into an effective therapeutic strategy for the treatment of many different cancers where tumor angiogenesis plays a significant role in tumor growth and progression.

scholarly journals HIF1α/PD-L1 axis mediates hypoxia-induced cell apoptosis and tumor progression in follicular thyroid carcinoma

2019 ◽  
Vol Volume 12 ◽  
pp. 6461-6470 ◽  
Author(s):  
Lingyan Zhou ◽  
Guofen Cha ◽  
Liyu Chen ◽  
Chen Yang ◽  
Dong Xu ◽  
...  
Keyword(s):  
Thyroid Carcinoma ◽  
Tumor Progression ◽  
Cell Apoptosis ◽  
Follicular Thyroid Carcinoma
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