Melittin Inhibits Hypoxia-Induced Vasculogenic Mimicry Formation and Epithelial-Mesenchymal Transition through Suppression of HIF-1<mml:math xmlns:mml="http://www.w3.org/1998/Math/MathML" id="M1"><mml:mrow><mml:mtext mathvariant="bold">α</mml:mtext></mml:mrow></mml:math>/Akt Pathway in Liver Cancer

Chen, Qun-wei; Lin, Wanfu; Yin, Zifei; Zou, Yong; Liang, Shufang; Ruan, Shanming; Chen, Peifeng; Li, Shu; Shu, Qijin; Cheng, Baohua; Ling, Changquan

doi:10.1155/2019/9602935

Cited by 19 publications

(17 citation statements)

References 42 publications

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“…Melittin has been confirmed as an inhibitor in the process of tumor angiogenesis and metastasis. In the study, melittin inhibits liver cancer through suppressing hypoxia-induced VM formation [118]. Both thalidomide and rapamycin target VEGF to inhibit tumor VM formation [119,120].…”

Section: Clinical Significance Of Vm In Cancermentioning

confidence: 99%

Vasculogenic mimicry in carcinogenesis and clinical applications

et al. 2020

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Distinct from classical tumor angiogenesis, vasculogenic mimicry (VM) provides a blood supply for tumor cells independent of endothelial cells. VM has two distinct types, namely tubular type and patterned matrix type. VM is associated with high tumor grade, tumor progression, invasion, metastasis, and poor prognosis in patients with malignant tumors. Herein, we discuss the recent studies on the role of VM in tumor progression and the diverse mechanisms and signaling pathways that regulate VM in tumors. Furthermore, we also summarize the latest findings of non-coding RNAs, such as lncRNAs and miRNAs in VM formation. In addition, we review application of molecular imaging technologies in detection of VM in malignant tumors. Increasing evidence suggests that VM is significantly associated with poor overall survival in patients with malignant tumors and could be a potential therapeutic target.

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Section: Clinical Significance Of Vm In Cancermentioning

confidence: 99%

Vasculogenic mimicry in carcinogenesis and clinical applications

et al. 2020

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“…The presence of such pathological pseudo blood vessels in tumor tissue indicates poor patient prognosis. Studies have reported that the expression of HIF‐1α was associated with VM channels, as well as with the growth and potential proliferation of tumor cells . When oxygen supply is far less than the demand, tumor cells enter an anoxic state and then form VM channels.…”

Section: Discussionmentioning

confidence: 99%

RPV‐modified epirubicin and dioscin co‐delivery liposomes suppress non‐small cell lung cancer growth by limiting nutrition supply

et al. 2020

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| 621 wileyonlinelibrary.com/journal/cas | INTRODUC TI ONLung cancer is one of the most common malignancies and a leading cause of cancer-related death worldwide. 1 Among all lung cancers, approximately 85% are non-small cell lung cancer (NSCLC), for which morbidity is significantly higher than for small cell lung cancer. 2 In the past decade, targeted therapy, immunotherapy, and similar approaches rapidly developed to become the new treatment modalities for NSCLC. Despite recent developments and improvements in diagnosis and treatment, prospects for patients with NSCLC are dismal and the 5-year overall survival rate is only 15%-18%. 3,4 Rapid growth and metastasis are basic biological characteristics of malignant tumors, including NSCLC. 5 It is well known that angiogenesis plays a key role in cancer growth and metastasis. Anti-angiogenesis treatment has evolved to achieve encouraging results, but despite the widespread application of anti-angiogenic drugs, they have not attained satisfactory efficacy. [6][7][8] This means that alternative nutrient supply channels support tumor growth.Vasculogenic mimicry (VM) is defined as formation of vascu- lar-like structures lined with tumor cells without the presenceThis is an open access article under the terms of the Creative Commons Attribution-NonCommercial-NoDerivs License, which permits use and distribution in any medium, provided the original work is properly cited, the use is non-commercial and no modifications or adaptations are made. AbstractChemotherapy for non-small cell lung cancer (NSCLC) is far from satisfactory, mainly due to poor targeting of antitumor drugs and self-adaptations of the tumors.Angiogenesis, vasculogenic mimicry (VM) channels, migration, and invasion are the main ways for tumors to obtain nutrition. Herein, RPV-modified epirubicin and dioscin co-delivery liposomes were successfully prepared. These liposomes showed ideal physicochemical properties, enhanced tumor targeting and accumulation in tumor sites, and inhibited VM channel formation, tumor angiogenesis, migration and invasion. The liposomes also downregulated VM-related and angiogenesis-related proteins in vitro. Furthermore, when tested in vivo, the targeted co-delivery liposomes increased selective accumulation of drugs in tumor sites and showed extended stability in blood circulation. In conclusion, RPV-modified epirubicin and dioscin co-delivery liposomes showed strong antitumor efficacy in vivo and could thus be considered a promising strategy for NSCLC treatment. K E Y W O R D Sangiogenesis, cell-penetrating peptide, co-delivery liposome, non-small cell lung cancer, vasculogenic mimicry

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“…The mechanism of CD133 + cells in maintaining the characteristics of stem cells as well as the regulatory mechanisms of EMT have been substantially discussed. 14,37 Many genes and related signal pathways are found involved in the gene expression profile of CD133 + subpopulation of various tumors, including the STAT3/PI3K/AKT pathway. 14,38 In addition, the STAT3/ PI3K/AKT pathway was also closely related to EZH2mediated EMT progression.…”

Section: Dovepressmentioning

confidence: 99%