Overexpression of ARF1 is associated with cell proliferation and migration through PI3K signal pathway in ovarian cancer

Gu, Gui-Fang; Chen, Yannan; Duan, Chengwei; Zhou, Linsen; Chen, Caiwen; Chen, Jie; Cheng, Jialin; Shi, Nannan; Jin, Yajie; Xi, Qinghua; Zhong, Jun

doi:10.3892/or.2017.5388

Cited by 25 publications

(24 citation statements)

References 28 publications

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“…26 On the other hand, ARF1 has been proved to accelerate prostate tumorigenesis through activating the mitogen-activated protein kinase pathway. For example, ARF1 overexpression would promote the proliferation and migration of ovarian cancer cells.…”

Section: Discussionmentioning

confidence: 99%

LncRNA TP73‐AS1 is a novel regulator in cervical cancer via miR‐329‐3p/ARF1 axis

Zhang

2019

J of Cellular Biochemistry

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Cervical cancer holds one of the highest morbidity and mortality in various types of cancers. It even leads to the most number of cancer‐related deaths of women. A lot of research has indicated that the anomalous expression of long noncoding RNAs (lncRNAs) would induce carcinogenesis and is associated with poor prognosis of patients with cancer. However, the function and mechanism of many lncRNAs still call for further research. Tumor Protein P73 Antisense RNA 1 (TP73‐AS1) is no exception. LncRNA TP73‐AS1 has been found to promote cancer progressions in various cancers. It is upregulated in cervical cancer cells. The proliferation and migration ability of cervical cancer cells can also be boosted by TP73‐AS1 in return. Meanwhile, miRNA‐329‐3p is downregulated in cervical cancer cells and could bind with both TP73‐AS1 and ADP Ribosylation Factor 1 (ARF1). TP73‐AS1 inhibited miR‐329‐3p expression while miR‐329‐3p inhibited ARF1 expression. More importantly, TP73‐AS1 can positively regulate ARF1 expression. Based on all these experiments, TP73‐AS1 regulates ARF1 expression by competitively binding with miR‐329‐3p, thus regulating cervical cancer progression. Further rescue assays confirmed TP73‐AS1 regulates cervical cell proliferation and migration via miR‐329‐3p/ARF1. TP73‐AS1 might serve as a novel regulator in cervical cancer.

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Section: Discussionmentioning

confidence: 99%

LncRNA TP73‐AS1 is a novel regulator in cervical cancer via miR‐329‐3p/ARF1 axis

Zhang

2019

J of Cellular Biochemistry

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“…ARF1 plays a central role in maintaining the structure and function of the Golgi apparatus and is highly expressed in breast, prostate and ovarian cancers (Schlienger et al, 2015;Davis et al, 2016;Gu et al, 2017). In the context of cancer, ARF1 has an important function in inter-and intracellular signaling, cell cycle regulation and DNA repair, as well as necrosis and apoptosis (D'Souza-Schorey and Chavrier, 2006;Gu et al, 2017). Moreover, ARF1 regulates breast cancer cell adhesion and proliferation, being essential for EGF-mediated phosphorylation of Focal Adhesion Kinase (FAK) and Src (Schlienger et al, 2015).…”

Section: Arf1mentioning

confidence: 99%

“…In myeloma cells, ARF1 expression promotes cell proliferation and inhibits cell adhesion, controlling proliferation-and cell adhesion-mediated drug resistance (Xu et al, 2017). Finally, ARF1 is upregulated in ovarian tumors, when compared with adjacent non-cancerous tissues and its overexpression is associated with ovarian cancer cell proliferation and migration through the PhosphoInositide 3-Kinase (PI3K) pathway (Gu et al, 2017).…”

Section: Arf1mentioning

confidence: 99%

“…Moreover, ARF3 overexpression promotes breast cancer cell proliferation by regulating the cellcycle G1/S transition, through inhibition of FOXO1 transcription factor activity . Additionally, ARF3 was found to be a candidate gene involved in the progression of Olstad et al, 2003;Ma et al, 2005;Kannangai et al, 2007;Tsai et al, 2012;Schlienger et al, 2015;Davis et al, 2016;Gu et al, Woo et al, 2009;Bidkhori et al, 2013;Howley et al, 2018;Wu Q. et al, 2018ARF6 ↑ Breast, Gastric, Glioma, Liver, Lung, Melanoma, Pancreatic, Prostate, Renal Cell Carcinoma Hashimoto et al, 2004Hu et al, 2009;Knizhnik et al, 2011;Oka et al, 2014;Morgan et al, 2015;Zhang et al, 2015;Hashimoto et al, 2016;Liang et al, 2017; Fujii et al, 2014;Guo et al, 2015;Fujii et al, 2016;Hu et al, 2018;Chen et al, 2019;Harada et al, 2019;Isono et al, Calin et al, 2005;Petrocca et al, 2006;Yendamuri et al, 2008;Siltanen et al, pregnancy-associated breast cancer, based on integrated analysis of microarray profile datasets (Zhang et al, 2019).…”

Section: Arf3mentioning

confidence: 99%

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The Role of ARF Family Proteins and Their Regulators and Effectors in Cancer Progression: A Therapeutic Perspective

Casalou

Ferreira

Barral

2020

Front. Cell Dev. Biol.

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The Adenosine diphosphate-Ribosylation Factor (ARF) family belongs to the RAS superfamily of small GTPases and is involved in a wide variety of physiological processes, such as cell proliferation, motility and differentiation by regulating membrane traffic and associating with the cytoskeleton. Like other members of the RAS superfamily, ARF family proteins are activated by Guanine nucleotide Exchange Factors (GEFs) and inactivated by GTPase-Activating Proteins (GAPs). When active, they bind effectors, which mediate downstream functions. Several studies have reported that cancer cells are able to subvert membrane traffic regulators to enhance migration and invasion. Indeed, members of the ARF family, including ARF-Like (ARL) proteins have been implicated in tumorigenesis and progression of several types of cancer. Here, we review the role of ARF family members, their GEFs/GAPs and effectors in tumorigenesis and cancer progression, highlighting the ones that can have a pro-oncogenic behavior or function as tumor suppressors. Moreover, we propose possible mechanisms and approaches to target these proteins, toward the development of novel therapeutic strategies to impair tumor progression.

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“…18,19 Furthermore, high expression of ARF1 in EOC cells can promote cell proliferation and migration. 20 Among selected molecules (from PITA and miRmap databases), ARF1 (ADPribosylation factor 1) is rarely reported in EOC, and its function is closely related to the research phenotype. Nevertheless, it is not clear whether miRNA-744-5p could target ARF1 and participate in the EOC process.…”

Section: Introductionmentioning

confidence: 99%

miR‐744‐5p inhibits cellular proliferation and invasion via targeting ARF1 in epithelial ovarian cancer

Zhao

Wang

Jin

et al. 2020

The Kaohsiung J of Med Scie

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miR-744-5p has been demonstrated to play an important role in cancer progression. However, the functions of miR-744-5p in epithelial ovarian cancer (EOC) are not well clarified. In this study, our aim was to investigate the role of miR-744-5p and its underlying molecular mechanism in cell progression of EOC. EOC clinical tissues and matched adjacent ovarian epithelial tissues were collected from 18 patients. Tissues and cell lines were analyzed by qPCR or Western blot to investigate the expression of miR-744-5p and ARF1 in EOC. Cell proliferative capacity was assessed by CCK8 and colony formation assays. Wound healing and transwell assays were performed to evaluate cell migration and invasion. The potential binding relation between miR-744-5p and IRF1 was demonstrated by dual luciferase report assay. The results showed that expression of miR-744-5p was low in EOC clinical tissues and cells. Overexpression of miR-744-5p inhibited proliferation, migration, and invasion of EOC cells. Further mechanistic study identified that ARF1 is a target of miR-744-5p, which is negatively correlated with the expression of miR-744-5p, and overexpression of ARF1 could reverse the inhibition of miR-744-5p on the proliferation, migration, and invasion of EOC cells. Taken together, our results indicated that miR-744-5p attenuated EOC progression via targeting IRF1, providing potential guidance for the clinical treatment of ovarian cancer.

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Overexpression of ARF1 is associated with cell proliferation and migration through PI3K signal pathway in ovarian cancer

Cited by 25 publications

References 28 publications

LncRNA TP73‐AS1 is a novel regulator in cervical cancer via miR‐329‐3p/ARF1 axis

LncRNA TP73‐AS1 is a novel regulator in cervical cancer via miR‐329‐3p/ARF1 axis

The Role of ARF Family Proteins and Their Regulators and Effectors in Cancer Progression: A Therapeutic Perspective

miR‐744‐5p inhibits cellular proliferation and invasion via targeting ARF1 in epithelial ovarian cancer

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