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Article ; Online: Paradigms of vascularization in melanoma: Clinical significance and potential for therapeutic targeting.

Mabeta, Peace

Biomedicine & pharmacotherapy = Biomedecine & pharmacotherapie

2020 Volume 127, Page(s) 110135

Abstract: Melanoma is the most aggressive form of skin cancer. Malignant melanoma in particular has a poor prognosis and although treatment has improved, drug resistance continues to be a challenge. Angiogenesis, the formation of blood vessels from existing ... ...

Abstract	Melanoma is the most aggressive form of skin cancer. Malignant melanoma in particular has a poor prognosis and although treatment has improved, drug resistance continues to be a challenge. Angiogenesis, the formation of blood vessels from existing microvessels, precedes the progression of melanoma from a radial growth phase to a malignant phenotype. In addition, melanoma cells can form networks of vessel-like fluid conducting channels through vasculogenic mimicry (VM). Both angiogenesis and VM have been postulated to contribute to the development of resistance to treatment and to enable metastasis. Also, the metastatic spread of melanoma is highly dependent on lymphangiogenesis, the formation of lymphatic vessels from pre-existing vessels. Interestingly, the design and clinical testing of drugs that target VM and lymphangiogenesis lag behind that of angiogenesis inhibitors. Despite this, antiangiogenic drugs have not significantly improved the overall survival of melanoma patients, thus necessitating the targeting of alternative mechanisms. In this article, I review the roles of the three paradigms of tissue perfusion, namely, angiogenesis, VM and lymphangiogenesis, in promoting melanoma progression and metastasis. This article also explores the latest development and potential opportunities in the therapeutic targeting of these processes.
MeSH term(s)	Angiogenesis Inhibitors/therapeutic use ; Humans ; Lymphangiogenesis ; Melanoma/blood supply ; Melanoma/drug therapy ; Melanoma/secondary ; Neovascularization, Pathologic/etiology
Chemical Substances	Angiogenesis Inhibitors
Language	English
Publishing date	2020-04-22
Publishing country	France
Document type	Journal Article ; Review
ZDB-ID	392415-4
ISSN	1950-6007 ; 0753-3322 ; 0300-0893
ISSN (online)	1950-6007
ISSN	0753-3322 ; 0300-0893
DOI	10.1016/j.biopha.2020.110135
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Article ; Online: Angiogenesis and Pancreatic Cancer: Novel Approaches to Overcome Treatment Resistance.

Grobbelaar, Craig / Kgomo, Mpho / Mabeta, Peace

Current cancer drug targets

2024

Abstract: Pancreatic cancer (PCa) is acknowledged as a significant contributor to global cancer- related mortality and is widely recognized as one of the most challenging malignant diseases to treat. Pancreatic ductal adenocarcinoma (PDAC), which is the most ... ...

Abstract	Pancreatic cancer (PCa) is acknowledged as a significant contributor to global cancer- related mortality and is widely recognized as one of the most challenging malignant diseases to treat. Pancreatic ductal adenocarcinoma (PDAC), which is the most common type of PCa, is highly aggressive and is mostly incurable. The poor prognosis of this neoplasm is exacerbated by the prevalence of angiogenic molecules, which contribute to stromal stiffness and immune escape. PDAC overexpresses various proangiogenic proteins, including vascular endothelial growth factor (VEGF)-A, and the levels of these molecules correlate with poor prognosis and treatment resistance. Moreover, VEGF-targeting anti-angiogenesis treatments are associated with the onset of resistance due to the development of hypoxia, which in turn induces the production of angiogenic molecules. Furthermore, excessive angiogenesis is one of the hallmarks of the second most common form of PCa, namely, pancreatic neuroendocrine tumor (PNET). In this review, the role of angiogenesis regulators in promoting disease progression in PCa, and the impact of these molecules on resistance to gemcitabine and various therapies against PCa are discussed. Finally, the use of anti-angiogenic agents in combination with chemotherapy and other targeted therapeutic molecules is discussed as a novel solution to overcome current treatment limitations in PCa.
Language	English
Publishing date	2024-01-31
Publishing country	Netherlands
Document type	Journal Article
ZDB-ID	2064824-8
ISSN	1873-5576 ; 1568-0096
ISSN (online)	1873-5576
ISSN	1568-0096
DOI	10.2174/0115680096284588240105051402
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Article ; Online: The VEGF/VEGFR Axis Revisited: Implications for Cancer Therapy.

Mabeta, Peace / Steenkamp, Vanessa

International journal of molecular sciences

2022 Volume 23, Issue 24

Abstract: The vascular endothelial growth factor (VEGF)/vascular endothelial growth factor receptor (VEGFR) axis is indispensable in the process of angiogenesis and has been implicated as a key driver of tumor vascularization. Consequently, several strategies that ...

Abstract	The vascular endothelial growth factor (VEGF)/vascular endothelial growth factor receptor (VEGFR) axis is indispensable in the process of angiogenesis and has been implicated as a key driver of tumor vascularization. Consequently, several strategies that target VEGF and its cognate receptors, VEGFR-1 and VEGFR-2, have been designed to treat cancer. While therapies targeting full-length VEGF have resulted in an improvement in both overall survival and progression-free survival in various cancers, these benefits have been modest. In addition, the inhibition of VEGFRs is associated with undesirable off-target effects. Moreover, VEGF splice variants that modulate sprouting and non-sprouting angiogenesis have been identified in recent years. Cues within the tumor microenvironment determine the expression patterns of these variants. Noteworthy is that the mechanisms of action of these variants challenge the established norm of VEGF signaling. Furthermore, the aberrant expression of some of these variants has been observed in several cancers. Herein, developments in the understanding of the VEGF/VEGFR axis and the splice products of these molecules, as well as the environmental cues that regulate these variants are reviewed. Furthermore, strategies that incorporate the targeting of VEGF variants to enhance the effectiveness of antiangiogenic therapies in the clinical setting are discussed.
Language	English
Publishing date	2022-12-09
Publishing country	Switzerland
Document type	Journal Article ; Review
ZDB-ID	2019364-6
ISSN	1422-0067 ; 1422-0067 ; 1661-6596
ISSN (online)	1422-0067
ISSN	1422-0067 ; 1661-6596
DOI	10.3390/ijms232415585
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Article ; Online: Oncosuppressors and Oncogenes: Role in Haemangioma Genesis and Potential for Therapeutic Targeting.

Mabeta, Peace

International journal of molecular sciences

2018 Volume 19, Issue 4

Abstract: Genetic lesions in proto-oncogenes result in the perturbation of angiogenesis, the formation of neovessels from a pre-existing microvasculature. Similarly, the subversion of tumor suppressor genes promotes tumor vascularization. Excessive neovessel ... ...

Abstract	Genetic lesions in proto-oncogenes result in the perturbation of angiogenesis, the formation of neovessels from a pre-existing microvasculature. Similarly, the subversion of tumor suppressor genes promotes tumor vascularization. Excessive neovessel formation is associated with various neoplasms such as infantile hemangiomas (IH). Hemangiomas are the most common tumors in pediatric patients and at present have no definitive treatment. The pathogenesis of IH is not well understood; however, both vasculogenesis and angiogenesis are associated with hemangioma genesis. A number of factors that modulate angiogenesis and vasculogenesis have been shown to be dysregulated in IH. Several of the oncogenes and tumor suppressors linked to the promotion of angiogenesis are also altered in infantile hemangioma. In this review, the roles of oncogenes and tumor suppressor genes during neovascularization and hemangioma genesis are explored. In addition, the potential for targeting these genes in IH therapy is discussed.
MeSH term(s)	Angiogenesis Inhibitors/pharmacology ; Angiogenesis Inhibitors/therapeutic use ; Antineoplastic Agents/pharmacology ; Antineoplastic Agents/therapeutic use ; Child ; Clinical Trials as Topic ; Genetic Testing ; Hemangioma/drug therapy ; Hemangioma/genetics ; Humans ; Neovascularization, Pathologic/drug therapy ; Neovascularization, Pathologic/genetics ; Oncogene Proteins/genetics ; Signal Transduction/drug effects ; Tumor Suppressor Proteins/genetics
Chemical Substances	Angiogenesis Inhibitors ; Antineoplastic Agents ; Oncogene Proteins ; Tumor Suppressor Proteins
Language	English
Publishing date	2018-04-13
Publishing country	Switzerland
Document type	Journal Article ; Review
ZDB-ID	2019364-6
ISSN	1422-0067 ; 1422-0067 ; 1661-6596
ISSN (online)	1422-0067
ISSN	1422-0067 ; 1661-6596
DOI	10.3390/ijms19041192
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Article ; Online: Oncosuppressors and Oncogenes

Peace Mabeta

International Journal of Molecular Sciences, Vol 19, Iss 4, p

Role in Haemangioma Genesis and Potential for Therapeutic Targeting

2018 Volume 1192

Abstract	Genetic lesions in proto-oncogenes result in the perturbation of angiogenesis, the formation of neovessels from a pre-existing microvasculature. Similarly, the subversion of tumor suppressor genes promotes tumor vascularization. Excessive neovessel formation is associated with various neoplasms such as infantile hemangiomas (IH). Hemangiomas are the most common tumors in pediatric patients and at present have no definitive treatment. The pathogenesis of IH is not well understood; however, both vasculogenesis and angiogenesis are associated with hemangioma genesis. A number of factors that modulate angiogenesis and vasculogenesis have been shown to be dysregulated in IH. Several of the oncogenes and tumor suppressors linked to the promotion of angiogenesis are also altered in infantile hemangioma. In this review, the roles of oncogenes and tumor suppressor genes during neovascularization and hemangioma genesis are explored. In addition, the potential for targeting these genes in IH therapy is discussed.
Keywords	angiogenesis ; hemangioma ; oncogene ; oncosuppressor ; vascular endothelial growth factor ; Biology (General) ; QH301-705.5 ; Chemistry ; QD1-999
Subject code	610
Language	English
Publishing date	2018-04-01T00:00:00Z
Publisher	MDPI AG
Document type	Article ; Online
Database	BASE - Bielefeld Academic Search Engine (life sciences selection)

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Article ; Online: PF573,228 inhibits vascular tumor cell growth, migration as well as angiogenesis, induces apoptosis and abrogates PRAS40 and S6RP phosphorylation.

Mabeta, Peace

Acta pharmaceutica (Zagreb, Croatia)

2016 Volume 66, Issue 3, Page(s) 399–410

Abstract: PF573,228 is a compound that targets focal adhesion kinase (FAK), a non-receptor protein kinase, which is over-expressed in various tumors. The aim of this study was to evaluate the effects of PF573,228 on the cells derived from mouse vascular tumors, ... ...

Abstract	PF573,228 is a compound that targets focal adhesion kinase (FAK), a non-receptor protein kinase, which is over-expressed in various tumors. The aim of this study was to evaluate the effects of PF573,228 on the cells derived from mouse vascular tumors, namely, endothelioma cells. The treatment of endothelioma cells with PF573,228 reduced their growth with an IC50 of approximately 4.6 μmol L-1 and inhibited cell migration with an IC50 of about 0.01 μmol L-1. Microscopic studies revealed morphological attributes of apoptosis. These observations were confirmed by ELISA, which showed increased caspase-3 activity. PF573,228 also inhibited angiogenesis in a dose-dependent manner, with an IC50 of approximately 3.7 μmol L-1, and abrogated the phosphorylation of cell survival proteins, proline-rich Akt substrate (PRAS40) and S6 ribosomal protein (S6RP). Array data further revealed that PF573,228 induced caspase-3 activation, thus promoting apoptosis. Since all the processes inhibited by PF573,228 provide important support to tumor survival and progression, the drug may have a potential role in the treatment of vascular tumors.
MeSH term(s)	Animals ; Antineoplastic Agents/pharmacology ; Aorta/drug effects ; Aorta/metabolism ; Aorta/pathology ; Apoptosis/drug effects ; Cell Line, Tumor ; Cell Movement/drug effects ; Cell Proliferation/drug effects ; Cell Survival/drug effects ; Enzyme Inhibitors/pharmacology ; Focal Adhesion Protein-Tyrosine Kinases/antagonists & inhibitors ; Focal Adhesion Protein-Tyrosine Kinases/metabolism ; Hemangioendothelioma/drug therapy ; Hemangioendothelioma/metabolism ; Hemangioendothelioma/pathology ; Hemangioendothelioma/ultrastructure ; Male ; Mice ; Neoplasm Proteins/antagonists & inhibitors ; Neoplasm Proteins/metabolism ; Neovascularization, Pathologic/metabolism ; Neovascularization, Pathologic/pathology ; Neovascularization, Pathologic/prevention & control ; Phosphoproteins/metabolism ; Phosphorylation/drug effects ; Protein Processing, Post-Translational/drug effects ; Quinolones/pharmacology ; Rats, Sprague-Dawley ; Ribosomal Protein S6/metabolism ; Sulfones/pharmacology ; Tissue Culture Techniques
Chemical Substances	6-(4-(3-(methylsulfonyl)benzylamino)-5-(trifluoromethyl)pyrimidin-2-ylamino)-3,4-dihydroquinolin-2(1H)-one ; Antineoplastic Agents ; Enzyme Inhibitors ; Neoplasm Proteins ; Phosphoproteins ; Quinolones ; Ribosomal Protein S6 ; Sulfones ; proline-rich Akt substrate, 40 kDa protein, mouse ; ribosomal protein S6, mouse ; Focal Adhesion Protein-Tyrosine Kinases (EC 2.7.10.2)
Language	English
Publishing date	2016-09-01
Publishing country	Croatia
Document type	Journal Article
ZDB-ID	1111806-4
ISSN	1846-9558 ; 1330-0075
ISSN (online)	1846-9558
ISSN	1330-0075
DOI	10.1515/acph-2016-0031
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Article ; Online: LncRNAs and the Angiogenic Switch in Cancer: Clinical Significance and Therapeutic Opportunities.

Mabeta, Peace / Hull, Rodney / Dlamini, Zodwa

Genes

2022 Volume 13, Issue 1

Abstract: Angiogenesis is one of the hallmarks of cancer, and the establishment of new blood vessels is vital to allow for a tumour to grow beyond 1-2 mm in size. The angiogenic switch is the term given to the point where the number or activity of the pro- ... ...

Abstract	Angiogenesis is one of the hallmarks of cancer, and the establishment of new blood vessels is vital to allow for a tumour to grow beyond 1-2 mm in size. The angiogenic switch is the term given to the point where the number or activity of the pro-angiogenic factors exceeds that of the anti-angiogenic factors, resulting in the angiogenic process proceeding, giving rise to new blood vessels accompanied by increased tumour growth, metastasis, and potential drug resistance. Long noncoding ribonucleic acids (lncRNAs) have been found to play a role in the angiogenic switch by regulating gene expression, transcription, translation, and post translation modification. In this regard they play both anti-angiogenic and pro-angiogenic roles. The expression levels of the pro-angiogenic lncRNAs have been found to correlate with patient survival. These lncRNAs are also potential drug targets for the development of therapies that will inhibit or modify tumour angiogenesis. Here we review the roles of lncRNAs in regulating the angiogenic switch. We cover specific examples of both pro and anti-angiogenic lncRNAs and discuss their potential use as both prognostic biomarkers and targets for the development of future therapies.
MeSH term(s)	Animals ; Humans ; Neoplasms/blood supply ; Neoplasms/genetics ; Neoplasms/pathology ; Neoplasms/therapy ; Neovascularization, Pathologic/pathology ; RNA, Long Noncoding/genetics
Chemical Substances	RNA, Long Noncoding
Language	English
Publishing date	2022-01-15
Publishing country	Switzerland
Document type	Journal Article ; Research Support, Non-U.S. Gov't ; Review
ZDB-ID	2527218-4
ISSN	2073-4425 ; 2073-4425
ISSN (online)	2073-4425
ISSN	2073-4425
DOI	10.3390/genes13010152
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Article: LncRNAs and the Angiogenic Switch in Cancer: Clinical Significance and Therapeutic Opportunities

Mabeta, Peace / Hull, Rodney / Dlamini, Zodwa

Genes. 2022 Jan. 15, v. 13, no. 1

2022

Abstract: Angiogenesis is one of the hallmarks of cancer, and the establishment of new blood vessels is vital to allow for a tumour to grow beyond 1–2 mm in size. The angiogenic switch is the term given to the point where the number or activity of the pro- ... ...

Abstract	Angiogenesis is one of the hallmarks of cancer, and the establishment of new blood vessels is vital to allow for a tumour to grow beyond 1–2 mm in size. The angiogenic switch is the term given to the point where the number or activity of the pro-angiogenic factors exceeds that of the anti-angiogenic factors, resulting in the angiogenic process proceeding, giving rise to new blood vessels accompanied by increased tumour growth, metastasis, and potential drug resistance. Long noncoding ribonucleic acids (lncRNAs) have been found to play a role in the angiogenic switch by regulating gene expression, transcription, translation, and post translation modification. In this regard they play both anti-angiogenic and pro-angiogenic roles. The expression levels of the pro-angiogenic lncRNAs have been found to correlate with patient survival. These lncRNAs are also potential drug targets for the development of therapies that will inhibit or modify tumour angiogenesis. Here we review the roles of lncRNAs in regulating the angiogenic switch. We cover specific examples of both pro and anti-angiogenic lncRNAs and discuss their potential use as both prognostic biomarkers and targets for the development of future therapies.
Keywords	angiogenesis ; biomarkers ; blood ; drug resistance ; drugs ; gene expression ; metastasis ; neoplasms ; patients ; therapeutics
Language	English
Dates of publication	2022-0115
Publishing place	Multidisciplinary Digital Publishing Institute
Document type	Article
ZDB-ID	2527218-4
ISSN	2073-4425
ISSN	2073-4425
DOI	10.3390/genes13010152
Database	NAL-Catalogue (AGRICOLA)

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Article ; Online: Sunitinib malate inhibits hemangioma cell growth and migration by suppressing focal adhesion kinase signaling.

Scholtz, Wihan / Mabeta, Peace

Journal of applied biomedicine

2020 Volume 18, Issue 4, Page(s) 143–151

Abstract: Sunitinib malate is a small molecule that targets multiple receptor tyrosine kinases and blocks their activity. Receptors targeted by sunitinib are implicated in tumor vascularization and are overexpressed by vascular tumors encountered in infants, ... ...

Abstract	Sunitinib malate is a small molecule that targets multiple receptor tyrosine kinases and blocks their activity. Receptors targeted by sunitinib are implicated in tumor vascularization and are overexpressed by vascular tumors encountered in infants, namely, hemangiomas. Of note is that there is still no definitive treatment for these commonly occurring tumors of infancy. The purpose of this study was to investigate the effects of sunitinib malate on hemangioma using endothelial cells isolated from a murine model of the neoplasm (sEnd.2). The effects of the drug on cell growth were evaluated using the crystal violet assay and flow cytometry, while the scratch assay was employed to measure cell migration. Proteins associated with cell migration and angiogenesis were detected using western blotting. Sunitinib was investigated further to determine its effects on the production of reactive oxygen species, a parameter associated with the promotion of neovascularization in tumors. The results showed that sunitinib significantly reduced the growth of sEnd.2 cells by causing the cells to accumulate in the sub-G1 phase of the cell cycle, and also induced a significant decrease in the migration of these hemangioma cells (P < 0.05). The western blot assay showed a decrease in the expression of adhesion proteins, focal adhesion kinase and paxillin at IC50 doses, although the expression of cadherin did not change significantly (P < 0.05). In addition, transforming growth factor-β1 (TGF-β1) expression was decreased in sunitinib-treated cells at the same dose. The adhesion proteins as well as TGF-β1 regulate cell movement and have been implicated in tumor progression. Thus, sunitinib malate may have potential in the treatment of hemangiomas.
MeSH term(s)	Animals ; Cell Cycle ; Endothelial Cells ; Focal Adhesion Protein-Tyrosine Kinases/antagonists & inhibitors ; Focal Adhesion Protein-Tyrosine Kinases/metabolism ; Hemangioma/drug therapy ; Mice ; Neovascularization, Pathologic/drug therapy ; Sunitinib/pharmacology ; Transforming Growth Factor beta1/pharmacology
Chemical Substances	Transforming Growth Factor beta1 ; Focal Adhesion Protein-Tyrosine Kinases (EC 2.7.10.2) ; Sunitinib (V99T50803M)
Language	English
Publishing date	2020-12-07
Publishing country	Poland
Document type	Journal Article ; Research Support, Non-U.S. Gov't
ZDB-ID	2171142-2
ISSN	1214-0287 ; 1214-0287
ISSN (online)	1214-0287
ISSN	1214-0287
DOI	10.32725/jab.2020.019
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Article ; Online: Insights into the mechanism of antiproliferative effects of primaquine-cinnamic acid conjugates on MCF-7 cells.

Mabeta, Peace / Pavić, Kristina / Zorc, Branka

Acta pharmaceutica (Zagreb, Croatia)

2019 Volume 68, Issue 3, Page(s) 337–348

Abstract: In our previous paper, we showed that three primaquine-cinnamic acid conjugates composed of primaquine (PQ) residue and cinnamic acid derivatives (CADs) bound directly by an amide linkage (1) or through an acylsemicarbazide spacer (2 and 3) had ... ...

Abstract	In our previous paper, we showed that three primaquine-cinnamic acid conjugates composed of primaquine (PQ) residue and cinnamic acid derivatives (CADs) bound directly by an amide linkage (1) or through an acylsemicarbazide spacer (2 and 3) had significant growth inhibitory effects on some cancer cell lines. Compound 1 induced significant growth inhibition in the colorectal adenocarcinoma (SW620), human breast adenocarcinoma (MCF-7) and cervical carcinoma (HeLa) cell lines, while compounds 2 and 3 selectively inhibited the growth of MCF-7 cells. To better understand the underlying mechanisms of action of these PQ-CADs, morphological studies of the effects of test compounds on MCF-7 cells were undertaken using haematoxylin and eosin stain. Further analysis to determine the effects of test compounds on caspase activity and on the levels of apoptosis proteins were undertaken using the enzyme-linked immunosorbent assay (ELISA). Haematoxylin and eosin staining revealed that compounds 1 and 3 induced morphological changes in MCF-7 cells characteristic of apoptosis, while 2-treated cells were in interphase. Cell cycle analysis showed that cells treated with 1 and 3 were in sub-G1, while cells treated with 2 were mainly in interphase (G1 phase). Further, the study showed that the treatment of MCF-7 cells with 1 and 3 resulted in poly ADP ribose polymerase (PARP) cleavage as well as caspase-9 activation, indicating that they induced apoptotic cell death. We further investigated their effects on two important processes during metastasis, namely, migration and invasion. Compounds 1 and 3 inhibited the migration and invasion of MCF-7 cells, while compound 2 had a marginal effect.
MeSH term(s)	Adenocarcinoma/drug therapy ; Antineoplastic Agents/chemistry ; Antineoplastic Agents/pharmacology ; Apoptosis/drug effects ; Breast Neoplasms/drug therapy ; Cell Line, Tumor ; Cell Movement/drug effects ; Cell Proliferation/drug effects ; Cinnamates/chemistry ; Cinnamates/pharmacology ; Colorectal Neoplasms/drug therapy ; Enzyme-Linked Immunosorbent Assay ; Female ; HeLa Cells ; Humans ; MCF-7 Cells ; Neoplasm Invasiveness/prevention & control ; Primaquine/chemistry ; Primaquine/pharmacology ; Uterine Cervical Neoplasms/drug therapy
Chemical Substances	Antineoplastic Agents ; Cinnamates ; cinnamic acid (140-10-3) ; Primaquine (MVR3634GX1)
Language	English
Publishing date	2019-06-28
Publishing country	Croatia
Document type	Comparative Study ; Journal Article
ZDB-ID	1111806-4
ISSN	1846-9558 ; 1330-0075
ISSN (online)	1846-9558
ISSN	1330-0075
DOI	10.2478/acph-2018-0021
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