Breast cancer cells-derived Von Willebrand Factor promotes VEGF-A-related angiogenesis through PI3K/Akt-miR-205-5p signaling pathway

Tao, Qianying; Qi, Yanfei; Gu, Jiayi; Yu, Die; Lu, Yuxin; Liu, Jianwen; Liang, Xin

doi:10.1016/j.taap.2022.115927

Cited by 19 publications

(15 citation statements)

References 31 publications

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“…RNA-Seq- or qRT-PCR-based quantification of prognostically significant transcripts (e.g., VWF or MRTG.153013.3) in MCL tumor tissues during routine clinical evaluations can potentially be used to improve prognostication of MCL cases during diagnosis. Consistent with the association of high VWF expression and shortened MCL survival, high expression of VWF may promote metastatic dissemination of the MCL tumor cells, as it was reported to promote metastasis in gastric adenocarcinoma [ 55 ] and breast cancer [ 93 ]. Many of the top overexpressed (e.g., FSTL1, TNS1, DDR2, or VWF) or underexpressed genes were suggested to promote invasion and/or metastasis in different cancer types.…”

Section: Discussionmentioning

confidence: 60%

Whole Transcriptome Sequencing Reveals Cancer-Related, Prognostically Significant Transcripts and Tumor-Infiltrating Immunocytes in Mantle Cell Lymphoma

Sönmez

Hatipoğlu

Kurşun

et al. 2022

Cells

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Mantle cell lymphoma (MCL) is an aggressive B-cell non-Hodgkin lymphoma (NHL) subtype characterized by overexpression of CCND1 and SOX11 genes. It is generally associated with clinically poor outcomes despite recent improvements in therapeutic approaches. The genes associated with the development and prognosis of MCL are still largely unknown. Through whole transcriptome sequencing, we identified mRNAs, lncRNAs, and alternative transcripts differentially expressed in MCL cases compared with reactive tonsil B-cell subsets. CCND1, VCAM1, and VWF mRNAs, as well as MIR100HG and ROR1-AS1 lncRNAs, were among the top 10 most significantly overexpressed, oncogenesis-related transcripts. Survival analyses with each of the top upregulated transcripts showed that MCL cases with high expression of VWF mRNA and low expression of FTX lncRNA were associated with poor overall survival. Similarly, high expression of MSTRG.153013.3, an overexpressed alternative transcript, was associated with shortened MCL survival. Known tumor suppressor candidates (e.g., PI3KIP1, UBXN) were significantly downregulated in MCL cases. Top differentially expressed protein-coding genes were enriched in signaling pathways related to invasion and metastasis. Survival analyses based on the abundance of tumor-infiltrating immunocytes estimated with CIBERSORTx showed that high ratios of CD8+ T-cells or resting NK cells and low ratios of eosinophils are associated with poor overall survival in diagnostic MCL cases. Integrative analysis of tumor-infiltrating CD8+ T-cell abundance and overexpressed oncogene candidates showed that MCL cases with high ratio CD8+ T-cells and low expression of FTX or PCA3 can potentially predict high-risk MCL patients. WTS results were cross-validated with qRT-PCR of selected transcripts as well as linear correlation analyses. In conclusion, expression levels of oncogenesis-associated transcripts and/or the ratios of microenvironmental immunocytes in MCL tumors may be used to improve prognostication, thereby leading to better patient management and outcomes.

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Section: Discussionmentioning

confidence: 60%

Whole Transcriptome Sequencing Reveals Cancer-Related, Prognostically Significant Transcripts and Tumor-Infiltrating Immunocytes in Mantle Cell Lymphoma

Sönmez

Hatipoğlu

Kurşun

et al. 2022

Cells

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“…reported that vWF derived from tumor cells promotes angiogenesis in breast cancer. [ 32 ] It is postulated that vWF + sEVs determine the angiogenic activity after left ventricular assist device (LVAD) implantation. [ 33 ]…”

Section: Discussionmentioning

confidence: 99%

Small Extracellular Vesicle‐Derived vWF Induces a Positive Feedback Loop between Tumor and Endothelial Cells to Promote Angiogenesis and Metastasis in Hepatocellular Carcinoma

et al. 2023

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Hepatocellular carcinoma (HCC) is a hypervascular malignancy by which its growth and dissemination are largely driven by the modulation of tumor‐derived small extracellular vesicles (sEVs). Proteomic profiling of circulating sEVs of control individuals and HCC patients identifies von Willibrand factor (vWF) to be upregulated progressively along HCC stages. Elevated sEV–vWF levels are found in a larger cohort of HCC–sEV samples and metastatic HCC cell lines compared to their respective normal counterparts. Circulating sEVs of late‐stage HCC patients markedly augment angiogenesis, tumor–endothelial adhesion, pulmonary vascular leakiness, and metastasis, which are significantly compromised by anti‐vWF antibody. The role of vWF is further corroborated by the enhanced promoting effect of sEVs collected from vWF‐overexpressing cells. sEV–vWF modulates endothelial cells through an elevated level of vascular endothelial growth factor A (VEGF‐A) and fibroblast growth factor 2 (FGF2). Mechanistically, secreted FGF2 elicits a positive feedback response in HCC via the FGFR4/ERK1 signaling pathway. The co‐administration of anti‐vWF antibody or FGFR inhibitor significantly improves the treatment outcome of sorafenib in a patient‐derived xenograft mouse model. This study reveals mutual stimulation between HCC and endothelial cells by tumor‐derived sEVs and endothelial angiogenic factors, facilitating angiogenesis and metastasis. It also provides insights into a new therapeutic strategy involving blocking tumor–endothelial intercellular communication.

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“…For example, the carcinogenic function of IGF2BP2 in pancreatic cancer is achieved through the activation of the PI3K/AKT signaling pathway to accelerate tumor proliferation 36 ; microRNA functions in the growth, and metastasis of breast cancer cells by targeting the PI3K/AKT carcinogenic signaling pathway. 37 Emerging evidence suggests that the PI3K/AKT signaling pathway participates in ovarian cancer progression. Ediriweera et al confirmed the importance of the PI3K/AKT signaling pathway in ovarian cancer progression and comprehensively analyze the clinical application of the PI3K/AKT signaling pathway inhibitors in ovarian cancer 38 ; Deng et al expounded that inactivating the PI3K/AKT signaling pathway reduces ovarian cancer chemoresistance by decreasing the cancer stem cell markers levels, 39 implying that repressing the abnormal activation of the PI3K/AKT signaling pathway slowed down the occurrence and development of ovarian cancer.…”

Section: Discussionmentioning

confidence: 99%

Ropivacaine represses the ovarian cancer cell stemness and facilitates cell ferroptosis through inactivating the PI3K/AKT signaling pathway

Lü

Mao

et al. 2022

Hum Exp Toxicol

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Purpose Ovarian cancer is a malignant tumor in women all over the world. Ropivacaine is identified as a potential drug for the treatment of malignant tumors, but the role and mechanism of ropivacaine in ovarian cancer remains unknown. Materials and methods Ovarian cancer cells were treated with different doses of ropivacaine. The function of ropivacaine in ovarian cancer was assessed using Cell Counting Kit-8 assay, flow cytometry, sphere-formation assay, Western blot, Fe2+ level analysis, and immunofluorescence. Meanwhile, the mechanism of ropivacaine in ovarian cancer was investigated by multiple molecular experiments. The protective function of ropivacaine in ovarian cancer was further confirmed by in vivo assay. Results The functional research data indicated that the growth and stemness of ovarian cancer cells were restrained after ropivacaine treatment, while the ferroptosis in ovarian cancer cells was facilitated. The mechanism results confirmed that ropivacaine inactivated the PI3K/AKT signaling pathway in ovarian cancer cells. Furthermore, in vivo assay demonstrated that ropivacaine repressed the proliferation of ovarian cancer cells in vivo and had a protective function in ovarian cancer. Conclusion Ropivacaine restrained ovarian cancer cell stemness and accelerated cell ferroptosis by inactivating PI3K/AKT signaling pathway.

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Breast cancer cells-derived Von Willebrand Factor promotes VEGF-A-related angiogenesis through PI3K/Akt-miR-205-5p signaling pathway

Cited by 19 publications

References 31 publications

Whole Transcriptome Sequencing Reveals Cancer-Related, Prognostically Significant Transcripts and Tumor-Infiltrating Immunocytes in Mantle Cell Lymphoma

Whole Transcriptome Sequencing Reveals Cancer-Related, Prognostically Significant Transcripts and Tumor-Infiltrating Immunocytes in Mantle Cell Lymphoma

Small Extracellular Vesicle‐Derived vWF Induces a Positive Feedback Loop between Tumor and Endothelial Cells to Promote Angiogenesis and Metastasis in Hepatocellular Carcinoma

Ropivacaine represses the ovarian cancer cell stemness and facilitates cell ferroptosis through inactivating the PI3K/AKT signaling pathway

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