RAB5A promotes the formation of filopodia in pancreatic cancer cells via the activation of cdc42 and β1-integrin

Yuan, Zhengrong; Wei, Wei

doi:10.1016/j.bbrc.2020.12.022

Cited by 13 publications

(9 citation statements)

References 26 publications

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“…It is reported that knockdown of RAB10 arrests the growth cycle and colony formation, as well as promotes cell apoptosis in hepatocellular carcinoma cells; in addition, high RAB10 expression correlates with poor prognosis of the patients 13 . And over-expression of RAB5A promotes filopodia formation and migration in pancreatic cancer cells, while down-regulation of RAB5A plays an opposite role 14 . Besides, deletion of RAB13 inhibits gastric cancer cell proliferation and promotes apoptosis 15 .…”

Section: Introductionmentioning

confidence: 97%

RAB27A promotes the proliferation and invasion of colorectal cancer cells

Zhao

Dong

et al. 2022

Sci Rep

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Colorectal cancer (CRC) is one of the most commonly diagnosed cancer types worldwide. Despite significant advances in prevention and diagnosis, CRC is still one of the leading causes of cancer-related mortality globally. RAB27A, the member of RAB27 family of small GTPases, is the critical protein for intracellular secretion and has been reported to promote tumor progression. However, it is controversial for the role of RAB27A in CRC progression, so we explored the exact function of RAB27A in CRC development in this study. Based on the stable colon cancer cell lines of RAB27A knockdown and ectopic expression, we found that RAB27A knockdown inhibited proliferation and clone formation of SW480 colon cancer cells, whereas ectopic expression of RAB27A in RKO colon cancer cells facilitated cell proliferation and clone formation, indicating that RAB27A is critical for colon cancer cell growth. In addition, our data demonstrated that the migration and invasion of colon cancer cells were suppressed by RAB27A knockdown, but promoted by RAB27A ectopic expression. Therefore, RAB27A is identified as an onco-protein in mediating CRC development, which may be a valuable prognostic indicator and potential therapeutic target for CRC.

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Section: Introductionmentioning

confidence: 97%

RAB27A promotes the proliferation and invasion of colorectal cancer cells

Zhao

Dong

et al. 2022

Sci Rep

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“…Rab5 is encoded as three isoforms, Rab5A, Rab5B, and Rab5C in human genomes. It is reported that Rab5B is overexpressed in BC, and Rab5A is overexpressed in pancreatic, glioma, and ovarian cancers compared with normal tissues (Heng et al, 2020; Liu et al, 2019; Wu et al, 2021; Yuan & Wei, 2021; Z. Zhao et al, 2010). However, there are no results available regarding the Rab5C expression and function in BC.…”

Section: Discussionmentioning

confidence: 99%

RAB5C, a new mRNA binding target of HuR, regulates breast cancer cell proliferation

Wang

Zhang

et al. 2022

Cell Biology International

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The posttranscriptional control of gene expression mediated by RNA‐binding proteins (RBPs) is essential to determine tumor cell fate. HuR is an RBP with increased expression in various cancer types. This study aimed to clarify the regulatory mechanism of HuR's contribution to breast cancer (BC) cell proliferation by inducing RAB5C expression. First, we analyzed the expression level of HuR and RAB5C in BC tissues and cell lines by immunohistochemistry, qRT‐PCR, and western blot. Next, to further investigate the effect of HuR on RAB5C expression, we used short hairpin RNAs (shRNAs) to silence endogenous HuR expression in BC cell lines MCF7 and MDA‐MB‐231. The binding site of RAB5C mRNA and HuR was confirmed by RNA immunoprecipitation. Finally, the function of RAB5C was investigated using flow cytometry, colony formation, and MTT assays. We found that the expression of HuR and RAB5C was significantly upregulated in BC tissues and MCF‐7 and MDA‐MB231 cell lines. Importantly, RAB5C mRNA stability was increased through binding of HuR to its 3′UTR. Inhibition of HuR expression using shRNA decreased RAB5C mRNA, suggesting that HuR plays a role in regulating RAB5C expression level. In addition, suppression of RAB5C expression reduced BC cell growth. These results suggest RAB5C functions as an oncogene in BC cells, HuR promoted BC cell survival by facilitating RAB5C expression. Our findings suggest that HuR and RAB5C play important roles in BC cell survival.

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“…For example, the inflammatory cytokine IL-6, known to be present and potent in PDAC, can promote Cdc42-mediated filopodia formation through the scaffolding protein IQGAP1 [ 140 ]. The GTPase Rab5A, which regulates vesicular trafficking, supports filopodia formation and migration in PDAC cell lines by promoting the activity of Cdc42 and the activation of β1-integrin [ 141 ]. As RhoGTPases, including Rac and Cdc42, are activated by GEFs, overexpression or hyperactivation of GEFs in PDAC can activate migration via promoting lamellipodial and filopodial-based migration.…”

Section: Tumor Cell Migration Via Lamellipodia and Focal Adhesionsmentioning

confidence: 99%

The Cell Biology of Metastatic Invasion in Pancreatic Cancer: Updates and Mechanistic Insights

Joshi

Ruiz

Razidlo

2023

Cancers

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Pancreatic ductal adenocarcinoma (PDAC) is one of the leading causes of cancer-related mortality worldwide. This is largely due to the lack of routine screening protocols, an absence of symptoms in early-stage disease leading to late detection, and a paucity of effective treatment options. Critically, the majority of patients either present with metastatic disease or rapidly develop metastatic disease. Thus, there is an urgent need to deepen our understanding of metastasis in PDAC. During metastasis, tumor cells escape from the primary tumor, enter the circulation, and travel to a distant site to form a secondary tumor. In order to accomplish this relatively rare event, tumor cells develop an enhanced ability to detach from the primary tumor, migrate into the surrounding matrix, and invade across the basement membrane. In addition, cancer cells interact with the various cell types and matrix proteins that comprise the tumor microenvironment, with some of these factors working to promote metastasis and others working to suppress it. In PDAC, many of these processes are not well understood. The purpose of this review is to highlight recent advances in the cell biology of the early steps of the metastatic cascade in pancreatic cancer. Specifically, we will examine the regulation of epithelial-to-mesenchymal transition (EMT) in PDAC and its requirement for metastasis, summarize our understanding of how PDAC cells invade and degrade the surrounding matrix, and discuss how migration and adhesion dynamics are regulated in PDAC to optimize cancer cell motility. In addition, the role of the tumor microenvironment in PDAC will also be discussed for each of these invasive processes.

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RAB5A promotes the formation of filopodia in pancreatic cancer cells via the activation of cdc42 and β1-integrin

Cited by 13 publications

References 26 publications

RAB27A promotes the proliferation and invasion of colorectal cancer cells

RAB27A promotes the proliferation and invasion of colorectal cancer cells

RAB5C, a new mRNA binding target of HuR, regulates breast cancer cell proliferation

The Cell Biology of Metastatic Invasion in Pancreatic Cancer: Updates and Mechanistic Insights

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