ARLTS1, potential candidate gene in familial aggregation of hematological malignancies

Hamadou, Walid Sabri; Besbes, Sawsen; Mani, Rahma; Bourdon, Violaine; Youssef, Yosra Ben; Achour, B.; Regaïeg, H.; Eisinger, François; Mari, Véronique; Gesta, Paul; Dreyfus, Hélène; Bonadona, Valérie; Dugast, Catherine; Zattara, Hélène; Faivre, Laurence; Noguchi, T; Khélif, Abderrahim; Sobol, Hagay; Soua, Zohra

doi:10.1016/j.bulcan.2016.10.016

Cited by 8 publications

(4 citation statements)

References 30 publications

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“…The nonsense mutation Trp149Stop leads to the production of a truncated protein unable to bind GTP, which results in decreased apoptotic potential of the cell (Petrocca et al, 2006). Both variants were found to be associated with predisposition to familial breast cancer and, more recently to familial hematological malignancies (Calin et al, 2005;Frank et al, 2006b;Hamadou et al, 2017). Additionally, the Cys148Arg variant was associated with melanoma and both familial and sporadic colorectal cancers (Frank et al, 2006a,c;Castellví-Bel et al, 2007).…”

Section: Arl11mentioning

confidence: 99%

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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Section: Arl11mentioning

confidence: 99%

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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“…Downregulation of ARL4C can even suppress AKT signaling and decrease cell proliferation in lung adenocarcinoma cells [ 12 ], and ARL13B is conducive to the progression of gastric cancer in vitro and in vivo by modulating smoothened trafficking and activating Hedgehog signaling [ 13 ]. Finally, ARL11 is also implicated in a number of familial cancer types [ 14 – 16 ]. All of this indicates the promise of ARLs as therapeutic targets for tumors.…”

Section: Introductionmentioning

confidence: 99%

ARL11 correlates with the immunosuppression and poor prognosis in breast cancer: A comprehensive bioinformatics analysis of ARL family members

et al. 2022

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ADP-ribosylation factor-like protein (ARL) family members (ARLs) may regulate the malignant phenotypes of cancer cells. However, relevant studies on ARLs in breast cancer (BC) are limited. In this research, the expression profiles, genetic variations, and prognostic values of ARLs in BC have been systematically analyzed for the first time using various databases. We find that ARLs are significantly dysregulated in BC according to the TCGA database, which may result from DNA methylation and copy number alteration. Prognostic analysis suggests that ARL11 is the most significant prognostic indicator for BC, and higher ARL11 predicts worse clinical outcomes for BC patients. Further functional enrichment analysis demonstrates that ARL11 enhances the immunosuppression in BC, and dysregulation of ARL11 is significantly associated with immune infiltration in various types of cancer. Our results demonstrate the potential of ARL11 as an immune therapeutic target for BC.

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“…9 ARL11 is established as a tumor suppressor in a variety of solid tumors. [10][11][12] A recent study identifies ARL14 as a crucial prognostic factor of lung adenocarcinoma based on The Cancer Genome Atlas (TCGA) database. 13 Furthermore, they discover that downregulation of ARL14 inhibits cell proliferation, migration and invasion as well as attenuates radiation damage of lung adenocarcinoma cells.…”

Section: Introductionmentioning

confidence: 99%

MicroRNA-302s Might Regulate ARL4C-Mediated Gastric Cancer Progression via p53 Signaling: Bioinformatics Analysis and Experiments Validation

Xie¹,

Pan²,

Wu³

et al. 2021

OTT

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Background Our previous studies demonstrate that ARL4C is the most critical clinical biomarker for gastric cancer (GC) patients among ARL family members (ARLs) and functions as an oncogene in GC. However, its underlying mechanisms in GC need to be further illustrated. In this study, we aim to explore the upstream and downstream molecular mechanisms of ARL4C in GC cells. Methods The genetic alteration of ARL4C in GC is analyzed by cBioPortal database. Potential ARL4C-targeted microRNAs (miRs) are predicted by three databases. The high-throughput RNA sequencing is performed to explore the underlying mechanisms of ARL4C in GC cells. The effects of predicted microRNAs on ARL4C, the RNA-sequencing results validation and the biological functions of ARL4C in GC cells are illustrated by in vitro experiments. Results Genetic analyses indicate that ARL4C is significantly upregulated in GC, which is not caused by gene amplification. MicroRNAs prediction shows the high relevance between ARL4C and miR-302 members. Moreover, miR-302c or miR-302d transfection reduces ARL4C protein expression in GC cells. Based on the high-throughput RNA sequencing of ARL4C-knockdown cells, enrichment analyses demonstrate that ARL4C is closely related to cell growth and involved in p53 signaling. Moreover, there are strong gene–gene interactions between ARL4C and genes in p53 signaling, and ARL4C downregulation could inhibit the protein expression of MDM2, a critical gene in p53 pathway. Further functional experiments demonstrate that ARL4C silencing leads to cell cycle arrest and increased cell apoptosis in AGS and MKN45 cells. Conclusion Our data suggest that miR-302c and miR-302d may function as the upstream regulators of ARL4C. And, ARL4C might promote GC cell cycle progression via regulating p53 signaling. Our findings provide novel insights into the key role of ARL4C and the underlying mechanisms in GC progression, thus facilitating the development of ARL4C-targeted therapy.

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ARLTS1, potential candidate gene in familial aggregation of hematological malignancies

Cited by 8 publications

References 30 publications

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

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

ARL11 correlates with the immunosuppression and poor prognosis in breast cancer: A comprehensive bioinformatics analysis of ARL family members

MicroRNA-302s Might Regulate ARL4C-Mediated Gastric Cancer Progression via p53 Signaling: Bioinformatics Analysis and Experiments Validation

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