SAC-1 ensures epithelial endocytic recycling by restricting ARF-6 activity

Chen, Dan; Yang, Chao; Li, Sha; Hang, Weijian; Wang, Xianghong; Chen, Juan; Shi, Anbing

doi:10.1083/jcb.201711065

Cited by 16 publications

(15 citation statements)

References 101 publications

(191 reference statements)

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“…Through confocal stack imaging of intestinal epithelial cells from intact living animals ( Fig 1B), we found that, in both sid-3 mutants, the number and size of hTAC-GFP-labeled intracellular structures increased significantly (~9-fold increase in total area) ( Fig 1C-1C''). This phenotype is typical of basolateral recycling mutants [5,12,[28][29][30]. We further assayed the accumulation of FGT-1, the worm homolog of another clathrin-independent recycling cargo, GLUT1 [8], and observed that SID-3 deficiency led to substantial intracellular aggregation of FGT-1-positive structures (~7.8-fold increase in total area) (S1A and S1A ' Fig).…”

Section: Loss Of Sid-3 Causes Endocytic Recycling Defectsmentioning

confidence: 82%

An EHBP-1-SID-3-DYN-1 axis promotes membranous tubule fission during endocytic recycling

et al. 2020

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The ACK family tyrosine kinase SID-3 is involved in the endocytic uptake of double-stranded RNA. Here we identified SID-3 as a previously unappreciated recycling regulator in the Caenorhabditis elegans intestine. The RAB-10 effector EHBP-1 is required for the endosomal localization of SID-3. Accordingly, animals with loss of SID-3 phenocopied the recycling defects observed in ehbp-1 and rab-10 single mutants. Moreover, we detected sequential protein interactions between EHBP-1, SID-3, NCK-1, and DYN-1. In the absence of SID-3, DYN-1 failed to localize at tubular recycling endosomes, and membrane tubules breaking away from endosomes were mostly absent, suggesting that SID-3 acts synergistically with the downstream DYN-1 to promote endosomal tubule fission. In agreement with these observations, overexpression of DYN-1 significantly increased recycling transport in SID-3deficient cells. Finally, we noticed that loss of RAB-10 or EHBP-1 compromised feeding RNAi efficiency in multiple tissues, implicating basolateral recycling in the transport of RNA silencing signals. Taken together, our study demonstrated that in C. elegans intestinal epithelia, SID-3 acts downstream of EHBP-1 to direct fission of recycling endosomal tubules in concert with NCK-1 and DYN-1.

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Section: Loss Of Sid-3 Causes Endocytic Recycling Defectsmentioning

confidence: 82%

An EHBP-1-SID-3-DYN-1 axis promotes membranous tubule fission during endocytic recycling

et al. 2020

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“…Previous studies reported that CD147 is internalized through Rab5-associated CIE, recycled via Rab22-dependent endosomes, and by-passed merging with the EEA1-positive endosomes in cervical cancer cells [13–15]. Arf6 (ADP-ribosylation factor 6) is another GTPase that regulates the endocytic recycling process in concert with different Rab GTPases [2, 16–22]. Arf6 activation can further promote CD147 trafficking, especially to accelerate it entering in the fast recycling pathway [15, 23].…”

Section: Introductionmentioning

confidence: 99%

Arf6-driven endocytic recycling of CD147 determines HCC malignant phenotypes

et al. 2019

J Exp Clin Cancer Res

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BackgroundAdhesion molecules distributed on the cell-surface depends upon their dynamic trafficking that plays an important role during cancer progression. ADP-ribosylation factor 6 (Arf6) is a master regulator of membrane trafficking. CD147, a tumor-related adhesive protein, can promote the invasion of liver cancer. However, the role of Arf6 in CD147 trafficking and its contribution to liver cancer progression remain unclear.MethodsStable liver cancer cell lines with Arf6 silencing and over-expression were established. Confocal imaging, flow cytometry, biotinylation and endomembrane isolation were used to detect CD147 uptake and recycling. GST-pull down, gelatin zymography, immunofluorescence, cell adhesion, aggregation and tight junction formation, Transwell migration, and invasion assays were used to examine the cellular phenotypes. GEPIA bioinformatics, patient’s specimens and electronic records collection, and immunohistochemistry were performed to obtain the clinical relevance for Arf6-CD147 signaling.ResultsWe found that the endocytic recycling of CD147 in liver cancer cells was controlled by Arf6 through concurrent Rab5 and Rab22 activation. Disruption of Arf6-mediated CD147 trafficking reduced the cell-matrix and cell-cell adhesion, weakened cell aggregation and junction stability, attenuated MMPs secretion and cytoskeleton reorganization, impaired HGF-stimulated Rac1 activation, and markedly decreased the migration and invasion of liver cancer cells. Moreover, high-expression of the Arf6-CD147 signaling components in HCC (hepatocellular carcinoma) was closely correlated with poor clinical outcome of patients.ConclusionsOur results revealed that Arf6-mediated CD147 endocytic recycling is required for the malignant phenotypes of liver cancer. The Arf6-driven signaling machinery provides excellent biomarkers or therapeutic targets for the prevention of liver cancer.

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“…, 2016 ). Intriguingly, in Caenorhabditis elegans, Sac1 inhibits Arf6 by sequestering the Arf6-GEF Bris-1 ( Chen et al. , 2018 ).…”

Section: Discussionmentioning

confidence: 99%