Tumor angiogenesis and anti‑angiogenic gene therapy for cancer (Review)

Abstract

When Folkman first suggested a theory about the association between angiogenesis and tumor growth in 1971, the hypothesis of targeting angiogenesis to treat cancer was formed. Since then, various studies conducted across the world have additionally confirmed the theory of Folkman, and numerous efforts have been made to explore the possibilities of curing cancer by targeting angiogenesis. Among them, anti-angiogenic gene therapy has received attention due to its apparent advantages. Although specific problems remain prior to cancer being fully curable using anti-angiogenic gene therapy, several methods have been explored, and progress has been made in pre-clinical and clinical settings over previous decades. The present review aimed to provide up-to-date information concerning tumor angiogenesis and gene delivery systems in anti-angiogenic gene therapy, with a focus on recent developments in the study and application of the most commonly studied and newly identified anti-angiogenic candidates for anti-angiogenesis gene therapy, including interleukin-12, angiostatin, endostatin, tumstatin, anti-angiogenic metargidin peptide and endoglin silencing.

Tumor Angiogenesis and Anti-Angiogenic Strategies for Cancer Treatment

“…Similarly, there is also a set of chemical signals that inhibit angiogenesis by disrupting blood vessel formation or supporting the removal of existing vessels, i.e., at the end of an inflammatory response [25]. Examples of such molecules that facilitate the termination of neovascularization through anti-apoptosis gene suppression are angiostatin, endostatin, platelet factor 4 (PF4), thrombospondin-1 and 2, interleukin-12, tumstatin, osteopontin, anti-angiogenic metargidin peptide, and endoglin silencing [22,25,61].…”

Endoglin (CD105) expression in neurofibromatosis type 2 vestibular schwannoma

“…If these preliminary evidences were confirmed by further investigations, predicting tumor growth might have a role in treatment planning and the choice between observation and early surgery. 9 In the field of gene therapies, silencing endoglin by interfering with its RNA is seen as a potential alternative approach to endoglin targeting. Abstaining from therapy might be a valid conservative option if tumor growth can be predicted (not just monitored), bearing in mind that both surgery and the persistent presence of the tumor pose a risk to hearing function.…”

“…Several studies using different anti-endoglin antibodies (including monoclonal, immunotoxinconjugated, or radiolabeled antibodies) have demonstrated good anti-angiogenic and antitumor responses. 9 In the field of gene therapies, silencing endoglin by interfering with its RNA is seen as a potential alternative approach to endoglin targeting. The chimeric IgG1 anti-CD105 monoclonal antibody (TRC105) binds human endoglin with a high avidity.…”

“…9 The angiogenic process includes cell migration, proliferation, microvessel differentiation and anastomosis, extracellular matrix degradation, and structural reorganization. 9 The angiogenic process includes cell migration, proliferation, microvessel differentiation and anastomosis, extracellular matrix degradation, and structural reorganization.…”

“…Angiogenesis is a biological process in which novel capillary blood vessels grow from preexisting vasculature, providing tissues with oxygen and nutrients. 9 The angiogenic process includes cell migration, proliferation, microvessel differentiation and anastomosis, extracellular matrix degradation, and structural reorganization. 10 Neovascularization is fundamental to tumor survival and growth.…”