Vascular mimicry: A potential therapeutic target in breast cancer

Chavoshi, Hadi; Poormolaie, Neda; Vahedian, Vahid; Kazemzadeh, Hamid; Mir, Amirabbas; Nejabati, Hamid Reza; Behroozi, Javad; Isazadeh, Alireza; Hajezimian, Saba; Nouri, Mohammad; Maroufi, Nazila Fathi

doi:10.1016/j.prp.2022.153922

Cited by 12 publications

(8 citation statements)

References 98 publications

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“…Leptin is involved in the proliferation, survival, angiogenesis, and metastasis of breast cancer cells and plays an important role in the development of breast cancer in obese postmenopausal women [17][18][19]. VM implies poor prognosis and the presence or absence of VM is an important indicator for the diagnosis and treatment of patients with breast cancer [35]. The relationship between leptin and VM has not been studied extensively [29].…”

Section: Discussionmentioning

confidence: 99%

Leptin Promotes Vasculogenic Mimicry in Breast Cancer Cells by Regulating Aquaporin-1

Han,

Lee

2024

IJMS

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Leptin is an obesity-related hormone that plays an important role in breast cancer progression. Vasculogenic mimicry (VM) refers to the formation of vascular channels lined by tumor cells. This study aimed to investigate the relationship between leptin and VM in human breast cancer cells. VM was measured by a 3D culture assay. Signal transducers and activators of transcription 3 (STAT3) signaling, aquaporin-1 (AQP1), and the expression of VM-related proteins, including vascular endothelial cadherin (VE-cadherin), twist, matrix metalloproteinase-2 (MMP-2), and laminin subunit 5 gamma-2 (LAMC2), were examined by Western blot. AQP1 mRNA was analyzed by a reverse transcriptase-polymerase chain reaction (RT-PCR). Leptin increased VM and upregulated phospho-STAT3, VE-cadherin, twist, MMP-2, and LAMC2. These effects were inhibited by the leptin receptor-blocking peptide, Ob-R BP, and the STAT3 inhibitor, AG490. A positive correlation between leptin and AQP1 mRNA was observed and was confirmed by RT-PCR. Leptin upregulated AQP1 expression, which was blocked by Ob-R BP and AG490. AQP1 overexpression increased VM and the expression of VM-related proteins. AQP1 silencing inhibited leptin-induced VM and the expression of VM-related proteins. Thus, these results showed that leptin facilitates VM in breast cancer cells via the Ob-R/STAT3 pathway and that AQP1 is a key mediator in leptin-induced VM.

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Section: Discussionmentioning

confidence: 99%

Leptin Promotes Vasculogenic Mimicry in Breast Cancer Cells by Regulating Aquaporin-1

Han,

Lee

2024

IJMS

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“…Metastasis remains as one of the more devastating cancer hallmarks, which account for most of cancer-related deaths. Notably, VM has been established a s a novel marker of poor prognosis in breast cancer patients, as it promotes resistance to therapy [ [20] , [21] ], and tumor progression [22] . Although the molecular mechanisms for VM development have been the objective of intense research, little is known about its regulation by ncRNAs.…”

Section: Discussionmentioning

confidence: 99%

Metastatic breast tumors downregulate miR-145 regulating the hypoxia-induced vasculogenic mimicry

Contreras-Sanzón¹,

Carlos‐Reyes²,

Sierra-Martínez³

et al. 2023

Translational Oncology

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“…However, the presence of angiogenic mimicry in all highly aggressive tumors has yet to be confirmed, and the means to target angiogenic mimicry to treat tumors have yet to reach a mature stage of development (16,17). Angiogenic mimicry and tumor types are listed in Table I (12,(18)(19)(20)(21)(22)(23)(24)(25).…”

Section: Vasculogenic Mimicry (Vm)mentioning

confidence: 99%

“…The special neovascular structure was first discovered under an optical microscope in 1941 and was observed through techniques such as Periodic acid-Schiff staining in 1999, when the concept of VM was first proposed ( 11 ). VM predominantly exists in malignant tumors that have the characteristics of high recurrence, high metastasis, poor prognosis for the patient and low survival rate ( 12 ). Over a continuous period of development, the status of research has gradually advanced towards the identification of pathological structures, the establishment of in vivo animal models, identification of the associated signaling pathways and prospective treatments with targeted drugs ( Fig.…”

Section: Vasculogenic Mimicry (Vm)mentioning

confidence: 99%

Advance in vasculogenic mimicry in ovarian cancer (Review)

Tian,

Si,

Liu

et al. 2023

Oncol Lett

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Ovarian cancer (OC) is a common and highly prevalent malignant tumor in women, associated with a high mortality rate, easy recurrence and easy metastasis, which is predominantly at an advanced stage when detected in patients. This renders the cancer more difficult to treat, and consequently it is also associated with a low survival rate, being the malignancy with the highest mortality rate among the various gynecological tumors. As an important factor affecting the development and metastasis of OC, understanding the underlying mechanism(s) through which it is formed and developed is crucial in terms of its treatment. At present, the therapeutic methods of angiogenic mimicry for OC remain in the preliminary stages of exploration and have not been applied in actual clinical practice. In the present review, various signaling pathways and factors affecting angiogenic mimicry in OC were described, and the chemical synthetic drugs, natural compound extracts, small-molecule protein antibodies and their associated targets, and so on, that target angiogenic mimicry in the treatment of OC, were discussed. The purpose of this review was to provide new research ideas and potential theoretical support for the discovery of novel therapeutic targets for OC that may be applied in the clinic, with the aim of effectively reducing its metastasis and recurrence rates. Contents1. Introduction 2. Ovarian cancer 3. Vasculogenic mimicry (VM) 4. Signaling pathways associated with angiogenic mimicry in OC 5. OC angiogenesis mimetic-associated inhibitors 6.

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Vascular mimicry: A potential therapeutic target in breast cancer

Cited by 12 publications

References 98 publications

Leptin Promotes Vasculogenic Mimicry in Breast Cancer Cells by Regulating Aquaporin-1

Leptin Promotes Vasculogenic Mimicry in Breast Cancer Cells by Regulating Aquaporin-1

Metastatic breast tumors downregulate miR-145 regulating the hypoxia-induced vasculogenic mimicry

Advance in vasculogenic mimicry in ovarian cancer (Review)

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