Cancer stem cells contribute to angiogenesis and lymphangiogenesis in serous adenocarcinoma of the ovary

Krishnapriya, Syama; Sidhanth, Chirukandath; Manasa, P; Sneha, Smarakan; Bindhya, S.; Nagare, Rohit P.; Ramachandran, Balaji; Vishwanathan, Pushpa; Murhekar, Kanchan; Sundersingh, Shirley; Ganesan, Trivadi S.

doi:10.1007/s10456-019-09669-x

Cited by 21 publications

(20 citation statements)

References 44 publications

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“…It is well known that cancer cells stimulate endothelial cell proliferation by releasing a vascular endothelial growth factor (VEGF) or other growth factors. − Consistent with previous findings, by using our microfluidic system, we confirmed that tumor cells promoted endothelial cell proliferation. The tumor vasculature demonstrates abnormal features, which are characterized by dilated, excessively curved, and disorganized vessels, as compared to normal blood vessels.…”

Section: Discussionsupporting

confidence: 90%

A Three-Dimensional Microfluidic Device for Monitoring Cancer and Chemotherapy-Associated Platelet Activation

Hao

Tan

et al. 2021

ACS Omega

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Platelet activation and the risk of thrombosis are increased in cancer patients, especially after chemotherapy. Our previous studies indicated that chemotherapy-induced platelet activation is largely due to endothelial cell damage. Thus, simple in vitro tests, such as aggregometry, are not desirable tests to predict platelet responsiveness to different chemotherapeutic agents because other contributory factors, such as tumor cells, endothelial cells, and the flow rate of platelets, also contribute to the formation of cancer-associated thrombosis. Therefore, developing a platelet detection system, which includes all possible risk parameters, is necessary. In the present study, we described a microengineered microfluidic system that contained a drug concentration generator, cancer cell culture chip, and three-dimensional (3D) circular microvascular model covered with a confluent endothelial layer and perfused with human platelets at a stable flow rate. Doxorubicin was injected through two injection sites. Endothelial cell injury was evaluated by counting, cell cytoskeleton observation, and the level of IACM1 and ET-1 in endothelial cells or a culture medium. Prestained platelets were perfused into the artificial blood vessel, and plateletendothelial cell adhesion was measured. We found that (i) MCF7 cell-released factors had a cytotoxicity effect on both endothelial cells and platelets. (ii) We confirmed that doxorubicin-induced platelet activation was endothelial cell-dependent. (iii) A lower dosage of doxorubicin (0−2.0 μM) induced platelet activation, while a higher dosage of doxorubicin (2.0−4.0 μM) led to platelet death. Our findings indicated that platelet-endothelial cell adhesion could be used as a diagnostic marker of platelet activation, providing a simple and rapid detective way to predict platelet responsiveness before or during chemotherapy.

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Section: Discussionsupporting

confidence: 90%

A Three-Dimensional Microfluidic Device for Monitoring Cancer and Chemotherapy-Associated Platelet Activation

Hao

Tan

et al. 2021

ACS Omega

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“…Therefore, we hypothesized that NOP14 could function as a metastasis suppressor in melanoma CSCs. A close relationship between CSCs and angiogenesis was previously suggested [ 26 , 27 ]. CSCs may differentiate into endothelial cells to participate in angiogenesis or the regulation of angiogenesis by secreting pro-angiogenic, matrix-derived, and hypoxia-inducible factors.…”

Section: Discussionmentioning

confidence: 77%

The NOP14 nucleolar protein suppresses the function and stemness of melanoma stem-like cells through Wnt/beta-catenin signaling inactivation

Fang

et al. 2022

Bioengineered

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Cancer stem cells (CSCs) are closely related to tumor occurrence, development, metastasis, drug resistance, and recurrence. The role of CSCs in melanoma is poorly understood. Our previous studies suggested that the NOP14 nucleolar protein (NOP14) is involved in melanoma pathogenesis regulation. Importantly, NOP14 overexpression inhibits the Wnt/beta (β)-catenin signaling pathway, an important mechanism regulating CSCs stemness. Therefore, in this study, we aimed to explore the role of NOP14 in the stemness and function of CSCs in melanoma in vitro . CD133, a stem cell marker, was used to identify melanoma stem-like cells (SLCs). NOP14 overexpression subsequently decreased the proportion of CD133 + SLCs, impaired the colony-forming capabilities, and downregulated the expression of Nanog, SOX2, and OCT4 stem cell markers in A375 and A875 cells, suggesting that NOP14 suppresses the stemness of melanoma SLCs. NOP14 overexpression suppressed the migration, invasion, and angiogenesis-inducing ability of A375-SLCs and A875-SLCs. NOP14 overexpression also inactivated Wnt/β-catenin signaling in melanoma CD133 + SLCs. The Wnt signaling activator BML-284 alleviated the effect of NOP14 overexpression on the stemness and function of melanoma CSCs. In conclusion, NOP14 suppresses the stemness and function of melanoma SLCs by inactivating Wnt/β-catenin signaling. Thus, NOP14 is a novel target for CSC treatment in melanoma. Abbreviations : CSCs, cancer stem cells; SLCs, stem-like cells; NOP14, NOP14 nucleolar protein; SCID, severe combined immunodeficiency; β-catenin, beta-catenin; lv-NOP14, lentivirals expressing NOP14; PBS, phosphate buffer saline; HUVECs, human umbilical vein endothelial cells.

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“…Its function was either dependent or independent of the vascular endothelial growth factor receptor (VEGFR). Vascular endothelial growth factors (VEGFs) have the function of receptor tyrosine kinases activity to promote angiogenesis and increase vascular permeability by binding with VEGFR, and are involved in maintaining the stem cell characteristics of CSCs in many tumors [28,35]. While the co-receptor NRP2 can form a complex with VEGFR to enhance its a nity with VEGF and enhance tumor-promoting effect of VEGF [46].…”

Section: Discussionmentioning

confidence: 99%

Integrated analysis of cancer stem cells-associated lncRNA-miRNA-mRNA network for ovarian cancer via microarray and Gene Expression Omnibus database

Li¹,

Wang²,

Zhou³

2020

Preprint

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Background: Cancer stem cells (CSCs) are associated with the recurrence, metastasis and chemoresistance of epithelial ovarian cancer. Competing endogenous RNAs (CeRNAs) play an important role in maintenance of ovarian cancer stem cell-like cells (OCSCs) characteristics. To construct a ceRNA regulatory network for OCSCs, microarray technology and Gene Expression Omnibus (GEO) database had been used. Human serous epithelial ovarian carcinoma cell line COC1 cells were treated with cisplatin and paclitaxel then maintained in stem cell conditions for 6 days to obtain CD117+/CD133+ cells (OCSCs). We identified the differentially expressed miRNAs (DEMs), lncRNA (DELs) and mRNA (DEGs) between OCSCs and COC1 by microarray and combined them with representative microarray profiles in GEO Database. Results: According to the combination, 28 DEMs were identified at first, and 452 DEGs were obtained combining with the predicted targets of these miRNAs and our mRNA microarray results. Up-regulated DEGs of them were significantly enriched in ‘p53 signaling pathway’, ‘FoxO signaling pathway’ and ‘MicroRNAs in cancer’, whereas down-regulated DEGs were significantly enriched in ‘Adherens junction’ and ‘Hepatitis C’ pathway. 29 transcripts of 17 lncRNAs should be the ceRNAs of 10 of these miRNAs according to bioinformatics predicted results and lncRNA microarray. Finally, we obtained ceRNA network with 10 DEMs, 21 DEGs, and 25 transcripts of 13 DELs which should play an important role in maintenance of OCSCs characteristics. LINC00665-miR-146a-5p-NRP2 should be one of ceRNA pathways of the network. The qPCR results indicated that the expression of miR-146a-5p in OCSCs was lower than that in COC1, and LINC00665 shows the opposite trend. These results were consistent with the results of microarray partially. When LINC00665 expression was up-regulated in COC1, the cell proliferation ability enhanced, apoptosis rate reduced, and the percentage of G2/M phase cells increased. Conclusions: The ceRNA network we constructed may be involved in the stem cell characteristics maintenance of OCSCs and provide directions for further OCSCs research in the future, so as to assist the development and treatment of ovarian cancer.

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Cancer stem cells contribute to angiogenesis and lymphangiogenesis in serous adenocarcinoma of the ovary

Cited by 21 publications

References 44 publications

A Three-Dimensional Microfluidic Device for Monitoring Cancer and Chemotherapy-Associated Platelet Activation

A Three-Dimensional Microfluidic Device for Monitoring Cancer and Chemotherapy-Associated Platelet Activation

The NOP14 nucleolar protein suppresses the function and stemness of melanoma stem-like cells through Wnt/beta-catenin signaling inactivation

Integrated analysis of cancer stem cells-associated lncRNA-miRNA-mRNA network for ovarian cancer via microarray and Gene Expression Omnibus database

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