The Role of Stroma in Ovarian Cancer

Silva, Ana Carolinne da; Jammal, Millena Prata; Crispim, Paula Carolina Arvelos; Murta, Eddie Fernando Cândido; Nomelini, Rosekeila Simões

doi:10.1080/08820139.2019.1658770

Cited by 10 publications

(7 citation statements)

References 137 publications

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“…Ovarian cancer is one of the gynecological malignancies, which leads to thousands of deaths in women around the world [ 23 ]. In spite of great progress in early detection and systematic treatment in the past few years, the 5-year survival rate of patients with ovarian cancer is still very low [ 2 ].…”

Section: Discussionmentioning

confidence: 99%

WISP1 induces ovarian cancer via the IGF1/αvβ3/Wnt axis

Wang

Liu

et al. 2022

J Ovarian Res

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Background This study intended to clarify the mechanisms by which WISP1-mediated IGF1/αvβ3/Wnt axis might affect the progression of ovarian cancer. Methods Bioinformatics analysis was implemented for pinpointing expression of IGF1 and WISP1 which was verified through expression determination in clinical tissue samples and cells. Next, gain- or loss-of-function experimentations were implemented for testing CAOV4 and SKOV3 cell biological processes. The interaction between WISP1 and IGF1 was verified by co-immunoprecipitation and the molecular mechanism was analyzed. Finally, ovarian cancer nude mouse models were prepared to unveil the in vivo effects of WISP1/IGF1. Results IGF1 and WISP1 expression was elevated in ovarian cancer tissues and cells, which shared correlation with poor prognosis of ovarian cancer sufferers. Elevated IGF1 induced malignant properties of ovarian cancer cells through activation of PI3K-Akt and Wnt signaling pathway. WISP1 was positively correlated with IGF1. WISP1 could enhance the interaction between IGF1 and αvβ3 to induce epithelial-mesenchymal transition. In vivo experiments also confirmed that upregulated WISP1/IGF1 induced tumorigenesis and metastasis of ovarian cancer cells. Conclusion In conclusion, WISP1 can facilitate ovarian cancer by activating Wnt via the interaction between IGF1 and αvβ3.

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Section: Discussionmentioning

confidence: 99%

WISP1 induces ovarian cancer via the IGF1/αvβ3/Wnt axis

Wang

Liu

et al. 2022

J Ovarian Res

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“…EMCs comprise of inflammatory cytokines, chemokines, MMPs, integrins and exosomes (22) (Fig.2). Tumor cells interact with stromal cells to promote angiogenesis, infiltration and metastasis that cause the tumor to grow and invade other tissues (23). TNF-α is a pro-inflammatory cytokine that is secreted primarily by macrophages along with other cells of the stroma, which promotes tumor necrosis or apoptosis.…”

Section: Cell Signaling and Exosome-mediated Tumor Immune Microenviromentioning

confidence: 99%

Role of exosomes in the immune microenvironment of ovarian cancer (Review)

et al. 2021

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Exosomes are excretory vesicles that can deliver a variety of bioactive cargo molecules to the extracellular environment. Accumulating evidence demonstrates exosome participation in intercellular communication, immune response, inflammatory response and they even play an essential role in affecting the tumor immune microenvironment. The role of exosomes in the immune microenvironment of ovarian cancer is mainly divided into suppression and stimulation. On one hand exosomes can stimulate the innate and adaptive immune systems by activating dendritic cells (DCs), natural killer cells and T cells, allowing these immune cells exert an antitumorigenic effect. On the other hand, ovarian cancer-derived exosomes initiate cross-talk with immunosuppressive effector cells, which subsequently cause immune evasion; one of the hallmarks of cancer. Exosomes induce the polarization of macrophages in M2 phenotype and induce apoptosis of lymphocytes and DCs. Exosomes further activate additional immunosuppressive effector cells (myeloid-derived suppressor cells and regulatory T cells) that induce fibroblasts to differentiate into cancer-associated fibroblasts. Exosomes also induce the tumorigenicity of mesenchymal stem cells to exert additional immune suppression. Furthermore, besides mediating the intercellular communication, exosomes carry microRNAs (miRNAs), proteins and lipids to the tumor microenvironment, which collectively promotes ovarian cancer cells to proliferate, invade and tumors to metastasize. Studying proteins, lipids and miRNAs carried by exosomes could potentially be used as an early diagnostic marker of ovarian cancer for designing treatment strategies.

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“…In recent years, investigating the interaction between tumour parenchymal cells and stromal cells in tumour progression at the tumour microenvironment level has been a hotspot in cancer research [ 31 , 32 ]. The glioma microenvironment, mainly composed of GSCs, tumour cells derived from GSCs, MSCs, endothelial cells, macrophages, extracellular matrix, and metabolites, provides not only a shelter for various cells but also a place for the interaction and signal transduction between parenchymal cells and various stromal cells [ 33 , 34 ].…”

Section: Discussionmentioning

confidence: 99%

HOTAIRM1 Maintained the Malignant Phenotype of tMSCs Transformed by GSCs via E2F7 by Binding to FUS

Liu

Zhou

Dong

et al. 2022

Journal of Oncology

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Objective. Mesenchymal stromal/stem cells (MSCs) are an important part of the glioma microenvironment and are involved in the malignant progression of glioma. In our previous study, we showed that MSCs can be induced to a malignant phenotype (tMSCs) by glioma stem cells (GSCs) in the microenvironment. However, the potential mechanism by which tMSCs maintain their malignant phenotype after malignant transformation has not been fully clarified. Methods. The expression of HOTAIRM1, FUS, and E2F7 was detected by qRT-PCR. Clone formation, EdU, and Transwell assay were used to explore the role of HOTAIRM1, FUS, and E2F7 on the proliferation, migration, and invasion of tMSCs. Bioinformatics analysis and RNA immunoprecipitation were used to explore the relation among HOTAIRM1, FUS, and E2F7. Results. HOTAIRM1 was upregulated in tMSCs compared with MSCs. Loss- and gain-of-function assays showed that HOTAIRM1 promoted the proliferation, migration, and invasion of tMSCs. qRT-PCR and functional assays revealed that E2F7 might be the downstream target of HOTAIRM1. A further study of the mechanism showed that HOTAIRM1 could bind to FUS, an RNA-binding protein (RBP), and thus regulate E2F7, which could promote the malignant phenotype of tMSCs. Conclusion. Our study revealed that the HOTAIRM1/FUS/E2F7 axis is involved in the malignant progression of tMSCs transformed by GSCs in the glioma microenvironment and may function as a novel target for glioma therapy.

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The Role of Stroma in Ovarian Cancer

Cited by 10 publications

References 137 publications

WISP1 induces ovarian cancer via the IGF1/αvβ3/Wnt axis

WISP1 induces ovarian cancer via the IGF1/αvβ3/Wnt axis

Role of exosomes in the immune microenvironment of ovarian cancer (Review)

HOTAIRM1 Maintained the Malignant Phenotype of tMSCs Transformed by GSCs via E2F7 by Binding to FUS

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