Abstract
PurposeRecent studies have suggested that molecular targets for the anti-angiogenic therapy might constitute a basis for additional therapy in gastric cancer treatment. A vast number of molecules, receptors, pathways, specific interactions, and thus strategies that target gastric cancer angiogenesis specifically have been reported in numerous research articles and clinical trials.MethodsWe conducted a systematic literature review of molecularly targeted treatment strategies in gastric cancer on the following databases—PubMed, Google Scholar, and Scopus—on September 20, 2020. Multiple articles and evaluations were searched for studies reporting newly found and promising molecular anti-angiogenic therapy pathways. Eventually, 39 articles regarding the anti-angiogenic therapy in gastric cancer were included in the final analysis.ResultsAs a consequence of the release of the pro-angiogenic molecules from the tumour cells, gastric cancer presents high angiogenic capability. Therefore, potential schemes for future treatment strategies include the decrease of the process ligands as well as the expression of their receptors. Moreover, the increase in the angiogenic inhibitor levels and direct aim for the inner walls of the endothelial cells appear as a promising therapeutic strategy. Beyond that, angiogenesis process inhibition seems to indirectly exaggerate the effects of chemotherapy in the considered patients.ConclusionsThe anti-angiogenic treatment in gastric cancer patients evaluates its significance especially in the early stages of the malignancy. The studies conducted so far show that most of the meaningful angiogenic factors and receptors with the potential molecular pathways should be further evaluated since they could potentially play a substantial role in future therapies.
Highlights
With more than 990,000 new diagnoses and over 738,000 death cases reported every year, gastric cancer (GC) is estimated to be the fourth most prevalent cancer and currently, it is in the second position in terms of cancer-related deaths [1–3]
Several studies showed that miRNAs can regulate tumour angiogenesis through targeting both the pro- and antiangiogenic factors, such as RTK signalling protein, HIF, vascular endothelial growth factor (VEGF), and epidermal growth factor (EGF) [71]. miRNA-126 has an essential role in regulating the angiogenesis processes; elevated expression of miRNA-126 is associated with the increased VEGF-A signalling in endothelial cells (EC)
Circulating tumour cells (CTCs) and free nucleic acid (CTNA) are metastatic cells that are released into the bloodstream by the primary tumour cells; they are involved in the recognition of the hematogenous metastasis [74]
Summary
With more than 990,000 new diagnoses and over 738,000 death cases reported every year, gastric cancer (GC) is estimated to be the fourth most prevalent cancer and currently, it is in the second position in terms of cancer-related deaths [1–3]. Over the last few decades, it was observed that GC incidence rates decreased in most parts of the world This data, concerns only the sporadic intestinal type of GC, whereas the prevalence of the diffuse type of GC has increased [8, 9]. Tumour cells release a significant number of molecules that induce the growth of new vasculature, promoting angiogenesis. Studies have shown that GC cells present a high angiogenic potential; the major pro-angiogenic factors include the vascular endothelial growth factor (VEGF) family with placental growth factor (PIGF) [26, 27], Fig. 1 Regulation of angiogenesis and vascular homeostasis through the angiogenic activators and inhibitors. The potential strategies of GC treatment include the decrease of the proangiogenic ligands and the expression of their receptors and the increase of the angiogenic inhibitor levels, as well as targeting the inner walls of the endothelial cells (EC) directly [34]. We summarized the most significant angiogenetic factors and receptors together with potential molecular pathways, their effects, and possible involvement in the anti-angiogenic therapy of GC
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