Caveolin-1 and Flotillin-1 Differential Expression in Clinical Samples of Renal Cell Carcinoma

Raimondo, Francesca; Valerio, Davide Ticozzi; Magni, Fulvio; Perego, R; Bianchi, Cristina; Sarto, Cecilia; Casellato, Stefano; Fasoli, Ester; Ferrero, Stefano; Cifola, Ingrid; Rocco, Francesco; Kienle, Marzia Galli; Mocarelli, Paolo; Brambilla, Paolo; Pitto, Marina

doi:10.2174/1875039700801010087

Cited by 8 publications

(4 citation statements)

References 43 publications

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“…Regarding RCC, Raimondo’s membrane proteomic study suggested that FLOT1 was up-regulated in human RCC tissues compared to para-cancer kidney tissues [ 47 ]. However, until now, the function of FLOT1 in RCC has not been reported.…”

Section: Discussionmentioning

confidence: 99%

Downregulation of microRNA-182-5p contributes to renal cell carcinoma proliferation via activating the AKT/FOXO3a signaling pathway

et al. 2014

Mol Cancer

102

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BackgroundEmerging evidence has suggested that dysregulation of miR-182-5p may contribute to tumor development and progression in several types of human cancers. However, its role in renal cell carcinoma (RCC) is still unknown.MethodsQuantitative RT-PCR was used to quantify miR-182-5p expression in RCC clinical tissues. Bisulfite sequencing PCR was used for DNA methylation analysis. The CCK-8, colony formation, flow cytometry, and a xenograft model were performed. Immunohistochemistry was conducted using the peroxidase and DAB methods. A miR-182-5p target was determined by luciferase reporter assays, quantitative RT-PCR, and Western blotting.ResultsmiR-182-5p is frequently down-regulated in human RCC tissues. Epigenetic modulation may be involved in the regulation of miR-182-5p expression. Enforced expression of miR-182-5p in RCC cells significantly inhibited the proliferation and tumorigenicity in vitro and in vivo. Additionally, overexpression of miR-182-5p induced G1-phase arrest via inhibition of AKT/FOXO3a signaling. Moreover, FLOT1 was confirmed as a target of miR-182-5p. Silencing FLOT1 by small interfering RNAs phenocopied the effects of miR-182-5p overexpression, whereas restoration of FLOT1 in miR-182-5p -overexpressed RCC cells partly reversed the suppressive effects of miR-182-5p.ConclusionsThese findings highlight an important role for miR-182-5p in the pathogenesis of RCC, and restoration of miR-182-5p could be considered as a potential therapeutic strategy for RCC therapy.

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Section: Discussionmentioning

confidence: 99%

Downregulation of microRNA-182-5p contributes to renal cell carcinoma proliferation via activating the AKT/FOXO3a signaling pathway

et al. 2014

Mol Cancer

102

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“…For one-dimensional electrophoresis (1-DE) Western blotting, 30 g of protein lysates, obtained from primary cell cultures and from renal tissue homogenate as described, 5,16 quantified with a Bio-Rad microassay (Hercules, CA), were separated on 10% SDS-PAGE and on NuPage 4 to 12% Bis-Tris pre-cast gels using MOPS SDS running buffer (Invitrogen), with described conditions. 5 For two-dimensional electrophoresis (2-DE) Western blotting, 50 g of proteins were loaded onto 7-cm 3-10 NL IPG-strips (GE Health care, Uppsala, Sweden) and then separated on NuPage 4% to 12% pre-cast gels.…”

Section: One-and Two-dimensional Electrophoresis and Western Blottingmentioning

confidence: 99%

Primary Cell Cultures from Human Renal Cortex and Renal-Cell Carcinoma Evidence a Differential Expression of Two Spliced Isoforms of Annexin A3

Bianchi

Bombelli

Raimondo

et al. 2010

The American Journal of Pathology

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“…Moreover, flotillin-1 functions as a regulatory signaling molecule that coordinates a variety of signal transduction processes. 14,15,21 Recent studies have revealed that flotillin-1 has important roles in the progression of several tumor types, including hepatocellular carcinoma, 22 neuroblastoma, 23 breast cancer, [24][25][26] tongue squamous cell cancer, 27 esophageal squamous cell carcinoma, [28][29][30] prostate cancer, 19 NSCLC, 5,31,32,33 renal cell carcinoma 34 and bladder transitional cell carcinoma. 35 Zhang SH et al have reported that a high level of flotillin-1 expression is associated with disease progression and poor prognosis in patients with hepatocellular carcinoma.…”

Section: Introductionmentioning

confidence: 99%

Flotilin-1 promotes the tumorigenicity and progression of malignant phenotype in human lung adenocarcinoma

Guo

Liu

et al. 2017

Cancer Biology & Therapy

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Lung adenocarcinoma (LUAD) accounts for the most common histological subtype of lung cancer which remains the leading cause of cancer death worldwide. The discovery of more sensitive and specific novel target biomarkers for predicting the development and progression of LUAD is imperative. Flotillin-1 (Flot-1) has been reported to have important roles in the progression of several tumor types but not been reported in the progression of LUAD. Here, we demonstrated that the expression of flotillin-1 was upregulated in 5 LUAD cells. Moreover, multiple approaches were used to explore the tumorigenicity of flotillin-1 in LUAD cell lines. The expression levels of flotillin-1 were analyzed by immunoblotting after overexpression and siRNA-based knockdown. Cell proliferation, scratch wound healing, transwell migration and matrigel invasion and xenograft tumor growth assays were used to determine the role of flotillin-1 in LUAD progression. Downregulation of flotillin-1 reversed, whereas upregulation of flotillin-1 enhanced, the malignant phenotype of LUAD cells in vitro. Consistently, cells with flotillin-1 knockdown formed smaller tumors in nude mice than cells transfected with the empty vector. Furthermore, the control group demonstrated significantly more tumorigenic effects compared to the flotillin-1-silenced group in the xenograft model of LUAD. In all, there draws a conclusion that flotillin-1 is a tumorigenic protein that plays an important role in promoting the proliferation and tumorigenicity of LUAD, suggesting that flotillin-1 may represent a novel the therapeutic target to LUAD.

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Caveolin-1 and Flotillin-1 Differential Expression in Clinical Samples of Renal Cell Carcinoma

Cited by 8 publications

References 43 publications

Downregulation of microRNA-182-5p contributes to renal cell carcinoma proliferation via activating the AKT/FOXO3a signaling pathway

Downregulation of microRNA-182-5p contributes to renal cell carcinoma proliferation via activating the AKT/FOXO3a signaling pathway

Primary Cell Cultures from Human Renal Cortex and Renal-Cell Carcinoma Evidence a Differential Expression of Two Spliced Isoforms of Annexin A3

Flotilin-1 promotes the tumorigenicity and progression of malignant phenotype in human lung adenocarcinoma

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