Integrin β3/Akt signaling contributes to platelet-induced hemangioendothelioma growth

Gu, Rui; Sun, Xin; Chi, Yijie; Zhou, Qishuang; Xiang, Hongkai; Bosco, Dale B.; Lai, Xin‐He; Qin, Caixia; So, Kwok-Fai; Ren, Yi; Chen, Xiaoming

doi:10.1038/s41598-017-06927-0

Cited by 7 publications

(5 citation statements)

References 53 publications

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“…To generate hemangioendothelioma, the injection of MS1 cells in mice was performed as previously described with minor modifications . Briefly, MS1 cells were collected, resuspended in DMEM medium (4.5 × 10 5 cells in 200 μL) and subjected to dorsally subcutaneous injection in nude mice.…”

Section: Methodsmentioning

confidence: 99%

MicroRNA let‐7a regulates angiogenesis by targeting TGFBR3 mRNA

Shao

Zhou

et al. 2018

J Cellular Molecular Medi

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Angiogenesis has a great impact on human health, owing to its participation in development, wound healing and the pathogenesis of several diseases. It has been reported that let‐7a is a tumour suppressor, but whether it plays a role in angiogenesis is unclear. Here we showed that let‐7a, a microRNA conserved in vertebrates, regulated angiogenesis by concomitantly down‐regulating TGFBR3. Overexpression of let‐7a or knockdown of TGFBR3 in cell culture inhibited the tube formation and reduced migration rate. Moreover, xenograft experiments showed that overexpression of let‐7a or knockdown of TGFBR3 had smaller tumour size. Downstream genes, such as VEGFC and MMP9, were also down‐regulated in let‐7a overexpression or TGFBR3 knockdown groups. Therefore, our results revealed a novel mechanism that let‐7a regulate angiogenesis through post‐transcriptional regulation of TGFBR3.

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Section: Methodsmentioning

confidence: 99%

MicroRNA let‐7a regulates angiogenesis by targeting TGFBR3 mRNA

Shao

Zhou

et al. 2018

J Cellular Molecular Medi

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“…P-selectin, a C-type lectin expressed on the surface of platelets, interacts with P-selectin ligand 1 (PSGL-1) and other mucins on cancer cells, while another mucinous glycoprotein, podoplanin (PDPN), which is upregulated in various types of cancer, can bind to the CLEC-2 receptor on platelets and induce TCIPA [11] . Furthermore, direct contact via platelet membrane molecules CLEC-2 or integrin β3 also promotes tumor growth in vitro and in vivo [ 19 , 20 ]. By providing pro-coagulant surface, releasing bioactive molecules, and interacting with leukocytes, CEPs contribute to TME and cancer-associated immunothrombosis, which further supports cancer progression [21] .…”

Section: Direct Contact Between Platelets and Tumor Cell-induced Plat...mentioning

confidence: 99%

Revealing profile of cancer-educated platelets and their factors to foster immunotherapy development

Trivanović,

Mojsilović,

Bogosavljević

et al. 2024

Translational Oncology

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“…TGFβ1 can reduce the expression of E-cadherin (E-cad) and induce epithelial-mesenchymal transition (EMT) (19,20). The integrin β3 (ITGβ3)/AKT signaling pathway can promote the growth of platelet-induced hemangioendothelioma (21). Ni et al determined that the mechanism of CBX7 underlying its inhibitory effect on cell growth may involve the AKT signaling pathway (11).…”

Section: Introductionmentioning

confidence: 99%

CBX7 is involved in the progression of cervical cancer through the ITGβ3/TGFβ1/AKT pathway

Tian,

Deng,

et al. 2023

Oncol Lett

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The chromobox protein homolog 7 (CBX7) serves a tumor-suppressive role in human malignant neoplasias. The downregulation of CBX7 is associated with the poor prognosis and aggressiveness of various human cancers. However, the biological functions and underlying mechanisms of CBX7 in cervical cancer remain unclear. The present study investigated the role and mechanism of CBX7 in cervical cancer. Lentivirus and siRNA were used to construct cervical cancer cells with stable CBX7 knockdown and SiHa xenograft models. The cell growth, migration, invasion and apoptosis were observed through in vivo and in vitro experiments. The expression levels of CBX7, integrin β3 (ITGβ3), transforming growth factor β1 (TGFβ1), phosphatidylinositol-3-kinase (PI3K), AKT, E-cadherin (E-cad) and vimentin (VIM) were detected by western blot analysis and reverse transcription-quantitative PCR. The correlation between CBX7 and these genes was analyzed. TGFβ1 was also silenced through shRNA in cells with stable CBX7 knockdown to detect its effect on cell growth, invasion and apoptosis, and on pathway-related gene expression. It was revealed that knockdown of CBX7 promoted the proliferation, migration, and invasion of cervical cancer cells, and inhibited apoptosis. In addition, CBX7 knockdown promoted tumor growth in vivo. Correlation analysis demonstrated that CBX7 was negatively correlated with ITGβ3, TGFβ1, PI3K, AKT, phosphorylated AKT and VIM, but positively correlated with E-cad. Moreover, the knockdown of TGFβ1 reversed the promotion of cell proliferation and inhibition of apoptosis induced by CBX7 knockdown and attenuated the increase of ITGβ3, TGFβ1, PI3K, AKT and VIM caused by CBX7 knockdown. In conclusion, the findings of the present study indicated that the downregulation of CBX7 enhances cell migration and invasion while inhibiting cell apoptosis in cervical cancer by modulating the ITGβ3/TGFβ1/AKT signaling pathways.

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Integrin β3/Akt signaling contributes to platelet-induced hemangioendothelioma growth

Cited by 7 publications

References 53 publications

MicroRNA let‐7a regulates angiogenesis by targeting TGFBR3 mRNA

MicroRNA let‐7a regulates angiogenesis by targeting TGFBR3 mRNA

Revealing profile of cancer-educated platelets and their factors to foster immunotherapy development

CBX7 is involved in the progression of cervical cancer through the ITGβ3/TGFβ1/AKT pathway

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