Hypoxia-induced Rab11-family interacting proteinï¿½4ï¿½expression promotes migration and invasion of colon cancer and correlates with poor prognosis

Wang, Jian‐Zhang; Yang, Shou‐Xing; Ye, Fangpeng; Xia, Xuanping; Shao, Xiao-xiao; Xia, Shenglong; Zheng, Bo; Xu, Chunyan

doi:10.3892/mmr.2017.8283

Cited by 9 publications

(6 citation statements)

References 30 publications

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“…This suggests that Rab GTPase binding to PI4KIIIβ is not highly isoform selective and may be context dependent. It is noteworthy that Rab11 (126)(127)(128)(129), PI4KIIIβ (53) and ACBD3 (130) have all separately been reported to be upregulated in a range of cancers and this may imply that the entire PI4KIIIβ interactome at the Golgi is potentially oncogenic. These proteins can also mediate intracellular signalling; PI4KIIIβ and Rab11 co-operate to stimulate the activity of AKT in breast cancer cells although this occurs on endosomes rather than at the Golgi complex (53).…”

Section: Variety Of Pi4kiiiβ Roles and Binding Partners With Relevancmentioning

confidence: 99%

The Great Escape: how phosphatidylinositol 4-kinases and PI4P promote vesicle exit from the Golgi (and drive cancer)

Waugh

2019

Biochemical Journal

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Phosphatidylinositol 4-phosphate (PI4P) is a membrane glycerophospholipid and a major regulator of the characteristic appearance of the Golgi complex as well as its vesicular trafficking, signalling and metabolic functions. Phosphatidylinositol 4-kinases, and in particular the PI4KIIIβ isoform, act in concert with PI4P to recruit macromolecular complexes to initiate the biogenesis of trafficking vesicles for several Golgi exit routes. Dysregulation of Golgi PI4P metabolism and the PI4P protein interactome features in many cancers and is often associated with tumour progression and a poor prognosis. Increased expression of PI4P-binding proteins, such as GOLPH3 or PITPNC1, induces a malignant secretory phenotype and the release of proteins that can remodel the extracellular matrix, promote angiogenesis and enhance cell motility. Aberrant Golgi PI4P metabolism can also result in the impaired post-translational modification of proteins required for focal adhesion formation and cell–matrix interactions, thereby potentiating the development of aggressive metastatic and invasive tumours. Altered expression of the Golgi-targeted PI 4-kinases, PI4KIIIβ, PI4KIIα and PI4KIIβ, or the PI4P phosphate Sac1, can also modulate oncogenic signalling through effects on TGN-endosomal trafficking. A Golgi trafficking role for a PIP 5-kinase has been recently described, which indicates that PI4P is not the only functionally important phosphoinositide at this subcellular location. This review charts new developments in our understanding of phosphatidylinositol 4-kinase function at the Golgi and how PI4P-dependent trafficking can be deregulated in malignant disease.

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Section: Variety Of Pi4kiiiβ Roles and Binding Partners With Relevancmentioning

confidence: 99%

The Great Escape: how phosphatidylinositol 4-kinases and PI4P promote vesicle exit from the Golgi (and drive cancer)

Waugh

2019

Biochemical Journal

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“…Some studies reported that Rab11-family interacting proteins (Rab11-FIPs) are associated with progression and poor survival in various tumors. Overexpression of Rab11-FIP4 was detected in colorectal cancer and pancreatic cancer tissues, it may predict poor survival of patients, and is also correlated with tumor progression [ 20 , 21 ]. Xu et al reported that Rab11-FIP2 upregulation enhanced invasion and migration in colorectal cells via regulation of matrix metalloproteinase 7 (MMP7) [ 22 ].…”

Section: Discussionmentioning

confidence: 99%

Rab11 Functions as an Oncoprotein via Nuclear Factor kappa B (NF-κB) Signaling Pathway in Human Bladder Carcinoma

et al. 2018

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BackgroundElevated expression of Rab11 has been reported in different human cancers, including human bladder carcinoma. This study, we investigated the biological effects and mechanism of Rab11 overexpression in human bladder carcinoma for the first time.Material/MethodsRab11 expression in bladder cancer tissues was detected using immunohistochemistry and Western blot analysis. Then, Rab11 expression was inhibited in T24 cells and it was overexpressed in BIU-87 cells. The effects of Rab11 perturbations on cell growth rate and invasion were analyzed by CCK8, cell cycle assay, and matrix gel invasion assay. MMP-9, cyclin E, and cyclin D1 levels were studied using Western blot and qPCR. NF-κB activity was studied by luciferase assay.ResultsHigh expression of Rab11 was detected in 41.5% (66/159) of tumor specimens. We found a significant correlation between high Rab11 expression and depth of tumor invasion (P=0.004). Rab11 overexpression was observed to promote the growth rate and invasiveness of cancer cells through upregulation of MMP9, cyclin E, and cyclin D1 levels. Rab11 overexpression further elevated NF-κB reporter activity and enhanced p-IκB expression. Use of BAY 11-7082, a noted NF-κB inhibitor, partially abolished overexpression of MMP9 and cyclin D1 by Rab11.ConclusionsOur research proved that high Rab11 expression enhances cellular multiplication and invasiveness of bladder cancer, possibly by regulating the NF-κB signaling pathway.

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“…In the model organism zebrafish, RAB11FIP4 is expressed in neural tissues and is involved in the proliferation and differentiation of retinal tissues in the zebrafish retinal development process (19,20). RAB11FIP4 has also been shown to be perturbed in a variety of cancers, including pancreatic cancer, colon cancer and hepatocellular cancer (21)(22)(23).…”

Section: Ofmentioning

confidence: 99%

Differential expression of RAB11FIP2 and RAB11FIP4 in glioblastoma tumors.

Mamoor¹

2020

Preprint

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Glioblastoma multiforme is the most common brain cancer in adults, and it offers a median overall survival of 15 months to those diagnosed with it (1, 2). The development of novel and targeted therapies to extend the survival of those diagnosed with glioblastoma requires a basic understanding of the transcriptional behavior of these tumors compared to the tissue from which it arises - the brain. In this study I compared the transcriptomes of 17 glioblastoma tumors to that of brain tissues from 8 non-affected individuals using a published dataset (3). I found that two genes encoding proteins involved in the cellular transport of endocytic vesicles, RAB11FIP2 and RAB11FIP4 were differentially expressed in the tumors of patients with glioblastoma. Both genes were expressed at significantly lower levels in glioblastoma tumors when compared to non-affected brain tissues. These molecules should be studied in greater depth to understand the cargoes that they transport and whether targeting of these molecules could represent a viable approach for the development of novel targeted therapeutics aimed at extending median survival in glioblastoma.

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Hypoxia-induced Rab11-family interacting proteinï¿½4ï¿½expression promotes migration and invasion of colon cancer and correlates with poor prognosis

Cited by 9 publications

References 30 publications

The Great Escape: how phosphatidylinositol 4-kinases and PI4P promote vesicle exit from the Golgi (and drive cancer)

The Great Escape: how phosphatidylinositol 4-kinases and PI4P promote vesicle exit from the Golgi (and drive cancer)

Rab11 Functions as an Oncoprotein via Nuclear Factor kappa B (NF-κB) Signaling Pathway in Human Bladder Carcinoma

Differential expression of RAB11FIP2 and RAB11FIP4 in glioblastoma tumors.

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