MicroRNA-126 modulates the tumor microenvironment by targeting calmodulin-regulated spectrin-associated protein 1 (Camsap1)

Sun, Xin; Wang, Zhiming; Song, Yan; Tai, Xuhui; Ji, Wenyue; Gu, Hui

doi:10.3892/ijo.2014.2321

Cited by 31 publications

(22 citation statements)

References 23 publications

Supporting

Mentioning

Contrasting

Order By: Relevance

“…CAMSAP1 is overexpressed in laryngeal squamous cell carcinoma and its expression was shown to be inhibited by miRNA-126. Although no correlation between the plasma levels of miRNA-126 and lymph node metastasis was found, its inhibitory action on CAMSAP1 may explain the expected dysregulation of microtubule dynamics and why loss of miRNA-126 is frequently associated with tumor metastasis [312]. Furthermore, deletion of CAMSAP3 in human lung carcinoma-derived cells promotes EMT by a mechanism implicating tubulin acetylation and the subsequent activation of the Akt pathway [313].…”

Section: Targeting Calmodulin-dependent Systems To Inhibit Tumor Cellmentioning

confidence: 96%

The Role of Calmodulin in Tumor Cell Migration, Invasiveness, and Metastasis

Villalobo

Berchtold

2020

IJMS

View full text Add to dashboard Cite

Calmodulin (CaM) is the principal Ca2+ sensor protein in all eukaryotic cells, that upon binding to target proteins transduces signals encoded by global or subcellular-specific changes of Ca2+ concentration within the cell. The Ca2+/CaM complex as well as Ca2+-free CaM modulate the activity of a vast number of enzymes, channels, signaling, adaptor and structural proteins, and hence the functionality of implicated signaling pathways, which control multiple cellular functions. A basic and important cellular function controlled by CaM in various ways is cell motility. Here we discuss the role of CaM-dependent systems involved in cell migration, tumor cell invasiveness, and metastasis development. Emphasis is given to phosphorylation/dephosphorylation events catalyzed by myosin light-chain kinase, CaM-dependent kinase-II, as well as other CaM-dependent kinases, and the CaM-dependent phosphatase calcineurin. In addition, the role of the CaM-regulated small GTPases Rac1 and Cdc42 (cell division cycle protein 42) as well as CaM-binding adaptor/scaffold proteins such as Grb7 (growth factor receptor bound protein 7), IQGAP (IQ motif containing GTPase activating protein) and AKAP12 (A kinase anchoring protein 12) will be reviewed. CaM-regulated mechanisms in cancer cells responsible for their greater migratory capacity compared to non-malignant cells, invasion of adjacent normal tissues and their systemic dissemination will be discussed, including closely linked processes such as the epithelial–mesenchymal transition and the activation of metalloproteases. This review covers as well the role of CaM in establishing metastatic foci in distant organs. Finally, the use of CaM antagonists and other blocking techniques to downregulate CaM-dependent systems aimed at preventing cancer cell invasiveness and metastasis development will be outlined.

show abstract

Section: Targeting Calmodulin-dependent Systems To Inhibit Tumor Cellmentioning

confidence: 96%

The Role of Calmodulin in Tumor Cell Migration, Invasiveness, and Metastasis

Villalobo

Berchtold

2020

IJMS

View full text Add to dashboard Cite

show abstract

“…RT‐qPCR followed by miR‐126 up‐ and downregulation demonstrated that, among the five selected genes, only CAMSAP1 was differentially regulated by miR‐126. Interestingly, it was reported that CAMSAP1 is a direct target of miR‐126 in larynx carcinoma cells [Sun et al, ]. The authors suggest that miR‐126‐mediated decrease in CAMSAP1 levels is deleterious for survival and metastatic behavior of larynx cell carcinoma cells.…”

Section: Discussionmentioning

confidence: 99%

Calmodulin Regulated Spectrin Associated Protein 1 mRNA is Directly Regulated by miR‐126 in Primary Human Osteoblasts

Strassburg

Nabar

Lampert

et al. 2017

J of Cellular Biochemistry

View full text Add to dashboard Cite

Vascularization is essential for bone development, fracture healing, and bone tissue engineering. We have previously described that coculture of primary human osteoblasts (hOBs) and human umbilical vein endothelial cells (HUVECs) improves differentiation of both cell types. Investigating the role of microRNAs (miRNAs) in this system, we found that miR-126 is highly upregulated in hOBs following coculturing with HUVECs. In this study we performed miR-126 gain-of-function and loss-of-function experiments in hOBs followed by microarray analysis in order to identify targets of miR-126. The transcript cluster IDs were sieved by applying cut-off criteria and by selecting transcripts which were upregulated following miR-126 downregulation and vice versa. The calmodulin regulated spectrin associated protein 1 (CAMSAP1) mRNA was confirmed to be differentially regulated by miR-126. Using the luciferase reporter assay it was demonstrated that CAMSAP1 is directly targeted by miR-126. In this study, we show that miR-126 and CAMSAP1 directly interact in hOBs. This finding has potential implications for tissue engineering applications. J. Cell. Biochem. 118: 1756-1763, 2017. © 2016 Wiley Periodicals, Inc.

show abstract

“…IRS1 is not only a metabolic and growth-promoting protein via regulation of the insulin receptor (IR) and insulin-like growth factor I receptor (IGF-IR), but also contributes to neoplastic transformation [99]. Typically, endothelial cells (ECs) express and release miR-126 at a high level in the TME [100,101]. Notably, the level of exosome-associated miR-126 is elevated during glucose deprivation and oxidative stress [98,102,103].…”

Section: Singing Together: Pca Cell-cell Interaction Via Exosomal Sigmentioning

confidence: 99%

Exosomes are the Driving Force in Preparing the Soil for the Metastatic Seeds: Lessons from the Prostate Cancer

Saber

Ali

Gaballa

et al. 2020

Cells

View full text Add to dashboard Cite

Exosomes are nano-membrane vesicles that various cell types secrete during physiological and pathophysiological conditions. By shuttling bioactive molecules such as nucleic acids, proteins, and lipids to target cells, exosomes serve as key regulators for multiple cellular processes, including cancer metastasis. Recently, microvesicles have emerged as a challenge in the treatment of prostate cancer (PCa), encountered either when the number of vesicles increases or when the vesicles move into circulation, potentially with an ability to induce drug resistance, angiogenesis, and metastasis. Notably, the exosomal cargo can induce the desmoplastic response of PCa-associated cells in a tumor microenvironment (TME) to promote PCa metastasis. However, the crosstalk between PCa-derived exosomes and the TME remains only partially understood. In this review, we provide new insights into the metabolic and molecular signatures of PCa-associated exosomes in reprogramming the TME, and the subsequent promotion of aggressive phenotypes of PCa cells. Elucidating the molecular mechanisms of TME reprogramming by exosomes draws more practical and universal conclusions for the development of new therapeutic interventions when considering TME in the treatment of PCa patients.

show abstract

MicroRNA-126 modulates the tumor microenvironment by targeting calmodulin-regulated spectrin-associated protein 1 (Camsap1)

Cited by 31 publications

References 23 publications

The Role of Calmodulin in Tumor Cell Migration, Invasiveness, and Metastasis

The Role of Calmodulin in Tumor Cell Migration, Invasiveness, and Metastasis

Calmodulin Regulated Spectrin Associated Protein 1 mRNA is Directly Regulated by miR‐126 in Primary Human Osteoblasts

Exosomes are the Driving Force in Preparing the Soil for the Metastatic Seeds: Lessons from the Prostate Cancer

Contact Info

Product

Resources

About