Feedback activation of GATA1/miR-885-5p/PLIN3 pathway decreases sunitinib sensitivity in clear cell renal cell carcinoma

Yao, Dayong; Xia, Shunyao; Jin, Chengjun; Zhao, Weiming; Lan, Wenjia; Liu, Zan; Xiu, Youcheng

doi:10.1080/15384101.2020.1801189

Cited by 13 publications

(2 citation statements)

References 40 publications

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“…Noteworthy findings suggest a 200-fold elevation in plateletderived growth factor-C (PDGF-C) levels in tumor cells resistant to vascular endothelial growth factor receptor (VEGFR)targeted drugs compared to their sensitive counterparts, implicating tumor-associated fibroblasts (TAFs) in inducing resistance through heightened PDGF-C expression. [78,79] Diverse investigations have affirmed that metabolic irregularities, [80][81][82] the tumor microenvironment, [83] DNA methylation, [84][85][86][87][88][89] , and RNA expression levels [82,[90][91][92][93][94] collectively contribute to drug resistance in RCC. Notably, ATP-binding cassette subfamily G member 2/breast cancer resistance protein (ABCG2/BCRP) efflux pump proteins, key constituents of ABC transporter protein efflux pump proteins, emerge as pivotal factors in drug resistance, with data illustrating a significant increase in resistance to SN-38 and topotecan upon ABCG2 overexpression.…”

Section: Renal Cancermentioning

confidence: 99%

The Role of Tumor‐Derived Extracellular Vesicles in Drug Resistance in Urologic Cancers

Xiong,

Chen,

et al. 2024

Advanced Therapeutics

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In spite of the therapeutic progress achieved in the treatment of urologic tumors, the persistence and intricate nature of tumor resistance significantly impact patient prognoses. Extracellular vesicles (EVs), actively secreted by diverse cell types, assume a crucial role in facilitating intercellular communication. These EVs facilitate the transfer of functional molecules, encompassing RNA, proteins, and lipids, to recipient cells. While these molecules participate in normal physiological processes, they also play a pivotal role in the pathogenesis of various diseases. Notably in the context of cancer, numerous investigations have substantiated the involvement of tumor‐derived EVs in the development of drug resistance. This review comprehensively explores the mechanisms underlying drug resistance in urologic cancers, elucidates the contributions of tumor‐derived EVs to drug resistance in urologic tumors, discusses advancements in targeting EVs to mitigate drug resistance in urologic tumors, and assesses the utility of EVs as biomarkers for drug resistance in urologic tumors.

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Section: Renal Cancermentioning

confidence: 99%

The Role of Tumor‐Derived Extracellular Vesicles in Drug Resistance in Urologic Cancers

Xiong,

Chen,

et al. 2024

Advanced Therapeutics

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“…Angiogenesis has presently been reported as vital to the progression of malignant RCC. Consequently, various angiogenesis inhibitors have been applied in preclinical and clinical trials, and anti-angiogenesis use has become among the options of drug therapy for RCC [ 6 ].…”

Section: Introductionmentioning

confidence: 99%

Circular RNA Eps15-homology domain-containing protein 2 induce resistance of renal cell carcinoma to sunitinib via microRNA-4731-5p/ABCF2 axis

Cao

2022

Bioengineered

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Circular RNAs (circRNAs) are linked with the occurrence and progression of renal cell carcinoma (RCC). However, circRNAs’ mechanism in developing resistance to RCC has not been clarified. This research assessed the role and mechanism of circular RNA circ Eps15-homology domain-containing protein 2 (EHD2) in the resistance of sunitinib (SU) to RCC. ACHN, 786-O, 769P, and HEK-293 T cells and RCC tissue samples were used for the investigations. The circEHD2 expression in RCC cells and tissues was determined through RT-qPCR. Association of circEHD2 with RCC histological grade of RCC was done through Chi-square. MiR-4731-5p, ABCF2, and circEHD2 were transfected into RCC cell lines. A dual-luciferase reporter assay was used to determine the interaction between miR-4731-5p, circEHD2, and ABCF2. MTT assay was used to analyze cell viability, while apoptosis was studied using flow cytometry. Colony-formation and transwell experiments were used to assess migration and invasion. The ATP Binding Cassette Subfamily F Member 2 (ABCF2) expression was analyzed through western blot. The results showed increased circEHD2 in SU-resistant RCC tissues and cell lines and implicated in RCC histological grade and SU resistance. Knock-down of circEHD2 down-regulated the resistance of RCC to SU in vitro and vivo ; circEHD2 bound to miR-4731-5p to mediate ABCF2 in RCC; ABCF2 rescued the inhibitory effect of circEHD2 knock-down on SU resistance of RCC. In conclusion, circEHD2 enhances RCC resistance to SU via acting as a miR-4731-5p sponge to mediate ABCF2. MiR-4731-5p can target circEHD2 and ABCF2, thus providing a novel and effective therapeutic against renal cell carcinoma.

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Lipid droplets provide metabolic flexibility for cancer progression

Safi,

Menéndez,

Pol

2024

FEBS Letters

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A hallmark of cancer cells is their remarkable ability to efficiently adapt to favorable and hostile environments. Due to a unique metabolic flexibility, tumor cells can grow even in the absence of extracellular nutrients or in stressful scenarios. To achieve this, cancer cells need large amounts of lipids to build membranes, synthesize lipid‐derived molecules, and generate metabolic energy in the absence of other nutrients. Tumor cells potentiate strategies to obtain lipids from other cells, metabolic pathways to synthesize new lipids, and mechanisms for efficient storage, mobilization, and utilization of these lipids. Lipid droplets (LDs) are the organelles that collect and supply lipids in eukaryotes and it is increasingly recognized that the accumulation of LDs is a new hallmark of cancer cells. Furthermore, an active role of LD proteins in processes underlying tumorigenesis has been proposed. Here, by focusing on three major classes of LD‐resident proteins (perilipins, lipases, and acyl‐CoA synthetases), we provide an overview of the contribution of LDs to cancer progression and discuss the role of LD proteins during the proliferation, invasion, metastasis, apoptosis, and stemness of cancer cells.

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Feedback activation of GATA1/miR-885-5p/PLIN3 pathway decreases sunitinib sensitivity in clear cell renal cell carcinoma

Cited by 13 publications

References 40 publications

The Role of Tumor‐Derived Extracellular Vesicles in Drug Resistance in Urologic Cancers

The Role of Tumor‐Derived Extracellular Vesicles in Drug Resistance in Urologic Cancers

Circular RNA Eps15-homology domain-containing protein 2 induce resistance of renal cell carcinoma to sunitinib via microRNA-4731-5p/ABCF2 axis

Lipid droplets provide metabolic flexibility for cancer progression

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