Platelets promote breast cancer cell MCF-7 metastasis by direct interaction: surface integrin α2β1-contacting-mediated activation of Wnt-β-catenin pathway

Zuo, Xianbo; Yang, Ya; Zhang, Yue; Zhang, Zhigang; Wang, Xiaofei; Shi, Yonggang

doi:10.1186/s12964-019-0464-x

Cited by 58 publications

(38 citation statements)

References 35 publications

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“…ITGB1 in several cancers (Wang et al, 2019;Zuo et al, 2019). Consistently, in this study, we found that through upregulating ITGB1 expression, ITGB1-DT activated Wnt/β-catenin pathway and further increased Wnt/β-catenin downstream target MYC expression.…”

Section: Discussionsupporting

confidence: 87%

ITGB1-DT Facilitates Lung Adenocarcinoma Progression via Forming a Positive Feedback Loop With ITGB1/Wnt/β-Catenin/MYC

Chang

Xiao

et al. 2021

Front. Cell Dev. Biol.

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Lung adenocarcinoma (LUAD) is the main histological type of lung cancer, which is the leading cause of cancer-related deaths. Long non-coding RNAs (lncRNAs) were recently revealed to be involved in various cancers. However, the clinical relevance and potential biological roles of most lncRNAs in LUAD remain unclear. Here, we identified a prognosis-related lncRNA ITGB1-DT in LUAD. ITGB1-DT was upregulated in LUAD and high expression of ITGB1-DT was correlated with advanced clinical stages and poor overall survival and disease-free survival. Enhanced expression of ITGB1-DT facilitated LUAD cellular proliferation, migration, and invasion, and also lung metastasis in vivo. Knockdown of ITGB1-DT repressed LUAD cellular proliferation, migration, and invasion. ITGB1-DT interacted with EZH2, repressed the binding of EZH2 to ITGB1 promoter, reduced H3K27me3 levels at ITGB1 promoter region, and therefore activated ITGB1 expression. Through upregulating ITGB1, ITGB1-DT activated Wnt/β-catenin pathway and its downstream target MYC in LUAD. The expressions of ITGB1-DT, ITGB1, and MYC were positively correlated with each other in LUAD tissues. Intriguingly, ITGB1-DT was found as a transcriptional target of MYC. MYC directly transcriptionally activated ITGB1-DT expression. Thus, ITGB1-DT formed a positive feedback loop with ITGB1/Wnt/β-catenin/MYC. The oncogenic roles of ITGB1-DT were reversed by depletion of ITGB1 or inhibition of Wnt/β-catenin pathway. In summary, these findings revealed ITGB1-DT as a prognosis-related and oncogenic lncRNA in LUAD via activating the ITGB1-DT/ITGB1/Wnt/β-catenin/MYC positive feedback loop. These results implicated ITGB1-DT as a potential prognostic biomarker and therapeutic target for LUAD.

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Section: Discussionsupporting

confidence: 87%

ITGB1-DT Facilitates Lung Adenocarcinoma Progression via Forming a Positive Feedback Loop With ITGB1/Wnt/β-Catenin/MYC

Chang

Xiao

et al. 2021

Front. Cell Dev. Biol.

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“…The same study provided evidence for a correlation between α2β1 integrin expression and estrogen positivity in breast cancer patients and that the decreased α2β1 integrin levels predict metastasis and decreased survival in prostate and breast cancer patients. Conversely, in another recent study of a xenograft model of MCF-7 cells interacting with platelets, α2 downregulation prevented breast cancer metastasis (313). In an experimental model of breast cancer metastasis, the MMP13 expression observed in MDA-MB-231 metastasizing cells to the bones was induced by collagen type I through integrin α1β1 and α2β1-mediated p38 MAPK pathway (314).…”

Section: Collagen-binding Integrins In Cancermentioning

confidence: 99%

Reciprocal Interplay Between Fibrillar Collagens and Collagen-Binding Integrins: Implications in Cancer Progression and Metastasis

et al. 2020

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Cancers are complex ecosystems composed of malignant cells embedded in an intricate microenvironment made of different non-transformed cell types and extracellular matrix (ECM) components. The tumor microenvironment is governed by constantly evolving cell-cell and cell-ECM interactions, which are now recognized as key actors in the genesis, progression and treatment of cancer lesions. The ECM is composed of a multitude of fibrous proteins, matricellular-associated proteins, and proteoglycans. This complex structure plays critical roles in cancer progression: it functions as the scaffold for tissues organization and provides biochemical and biomechanical signals that regulate key cancer hallmarks including cell growth, survival, migration, differentiation, angiogenesis, and immune response. Cells sense the biochemical and mechanical properties of the ECM through specialized transmembrane receptors that include integrins, discoidin domain receptors, and syndecans. Advanced stages of several carcinomas are characterized by a desmoplastic reaction characterized by an extensive deposition of fibrillar collagens in the microenvironment. This compact network of fibrillar collagens promotes cancer progression and metastasis, and is associated with low survival rates for cancer patients. In this review, we highlight how fibrillar collagens and their corresponding integrin receptors are modulated during cancer progression. We describe how the deposition and alignment of collagen fibers influence the tumor microenvironment and how fibrillar collagen-binding integrins expressed by cancer and stromal cells critically contribute in cancer hallmarks.

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“…EMT and invasion in MCF-7 cells was also promoted by physical interactions between platelets and tumor cells via direct contacting of surface integrin α2β1. This integrin activated the Wnt/β-catenin and TGF-β1/Smad3 pathways via aTGF-β1 production, which together promoted the expression of EMT proteins [ 60 ]. In HCC, sphingosine-1-phosphate (S1P) induced EMT via activation of PI3K/AKT signaling, which triggered heparanase, leading to increased expression and activity of MMP-7 and shedding and suppression of SDC1.…”

Section: Autocrine Tgf-β In the Regulation Of Specific Proteinsmentioning

confidence: 99%

Autocrine TGF-β in Cancer: Review of the Literature and Caveats in Experimental Analysis

Ungefroren

2021

IJMS

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Autocrine signaling is defined as the production and secretion of an extracellular mediator by a cell followed by the binding of that mediator to receptors on the same cell to initiate signaling. Autocrine stimulation often operates in autocrine loops, a type of interaction, in which a cell produces a mediator, for which it has receptors, that upon activation promotes expression of the same mediator, allowing the cell to repeatedly autostimulate itself (positive feedback) or balance its expression via regulation of a second factor that provides negative feedback. Autocrine signaling loops with positive or negative feedback are an important feature in cancer, where they enable context-dependent cell signaling in the regulation of growth, survival, and cell motility. A growth factor that is intimately involved in tumor development and progression and often produced by the cancer cells in an autocrine manner is transforming growth factor-β (TGF-β). This review surveys the many observations of autocrine TGF-β signaling in tumor biology, including data from cell culture and animal models as well as from patients. We also provide the reader with a critical discussion on the various experimental approaches employed to identify and prove the involvement of autocrine TGF-β in a given cellular response.

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Platelets promote breast cancer cell MCF-7 metastasis by direct interaction: surface integrin α2β1-contacting-mediated activation of Wnt-β-catenin pathway

Cited by 58 publications

References 35 publications

ITGB1-DT Facilitates Lung Adenocarcinoma Progression via Forming a Positive Feedback Loop With ITGB1/Wnt/β-Catenin/MYC

ITGB1-DT Facilitates Lung Adenocarcinoma Progression via Forming a Positive Feedback Loop With ITGB1/Wnt/β-Catenin/MYC

Reciprocal Interplay Between Fibrillar Collagens and Collagen-Binding Integrins: Implications in Cancer Progression and Metastasis

Autocrine TGF-β in Cancer: Review of the Literature and Caveats in Experimental Analysis

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