APLN/APLNR Signaling Controls Key Pathological Parameters of Glioblastoma
Glioblastoma (GBM) is the most common and aggressive primary brain tumor in adults. GBM-expansion depends on a dense vascular network and, coherently, GBMs are highly angiogenic. However, new intratumoral blood vessels are often aberrant with consequences for blood-flow and vascular barrier function...
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| Format: | Article |
| Language: | English |
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MDPI AG
2021-08-01
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| Series: | Cancers |
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| Online Access: | https://www.mdpi.com/2072-6694/13/15/3899 |
| _version_ | 1797525709822885888 |
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| author | Roland E. Kälin Rainer Glass |
| author_facet | Roland E. Kälin Rainer Glass |
| author_sort | Roland E. Kälin |
| collection | DOAJ |
| description | Glioblastoma (GBM) is the most common and aggressive primary brain tumor in adults. GBM-expansion depends on a dense vascular network and, coherently, GBMs are highly angiogenic. However, new intratumoral blood vessels are often aberrant with consequences for blood-flow and vascular barrier function. Hence, the delivery of chemotherapeutics into GBM can be compromised. Furthermore, leaky vessels support edema-formation, which can result in severe neurological deficits. The secreted signaling peptide Apelin (APLN) plays an important role in the formation of GBM blood vessels. Both APLN and the Apelin receptor (APLNR) are upregulated in GBM cells and control tumor cell invasiveness. Here we summarize the current evidence on the role of APLN/APLNR signaling during brain tumor pathology. We show that targeting APLN/APLNR can induce anti-angiogenic effects in GBM and simultaneously blunt GBM cell infiltration. In addition, we discuss how manipulation of APLN/APLNR signaling in GBM leads to the normalization of tumor vessels and thereby supports chemotherapy, reduces edema, and improves anti-tumorigenic immune reactions. Hence, therapeutic targeting of APLN/APLNR signaling offers an interesting option to address different pathological hallmarks of GBM. |
| first_indexed | 2024-03-10T09:16:54Z |
| format | Article |
| id | doaj.art-43f4cd42eeb44cb3bbc19c827dbc7a68 |
| institution | Directory Open Access Journal |
| issn | 2072-6694 |
| language | English |
| last_indexed | 2024-03-10T09:16:54Z |
| publishDate | 2021-08-01 |
| publisher | MDPI AG |
| record_format | Article |
| series | Cancers |
| spelling | doaj.art-43f4cd42eeb44cb3bbc19c827dbc7a682023-11-22T05:29:43ZengMDPI AGCancers2072-66942021-08-011315389910.3390/cancers13153899APLN/APLNR Signaling Controls Key Pathological Parameters of GlioblastomaRoland E. Kälin0Rainer Glass1Neurovascular Research, Department of Neurosurgery, University Hospital, LMU Munich, 81377 Munich, GermanyWalter Brendel Center of Experimental Medicine, Faculty of Medicine, LMU Munich, 81377 Munich, GermanyGlioblastoma (GBM) is the most common and aggressive primary brain tumor in adults. GBM-expansion depends on a dense vascular network and, coherently, GBMs are highly angiogenic. However, new intratumoral blood vessels are often aberrant with consequences for blood-flow and vascular barrier function. Hence, the delivery of chemotherapeutics into GBM can be compromised. Furthermore, leaky vessels support edema-formation, which can result in severe neurological deficits. The secreted signaling peptide Apelin (APLN) plays an important role in the formation of GBM blood vessels. Both APLN and the Apelin receptor (APLNR) are upregulated in GBM cells and control tumor cell invasiveness. Here we summarize the current evidence on the role of APLN/APLNR signaling during brain tumor pathology. We show that targeting APLN/APLNR can induce anti-angiogenic effects in GBM and simultaneously blunt GBM cell infiltration. In addition, we discuss how manipulation of APLN/APLNR signaling in GBM leads to the normalization of tumor vessels and thereby supports chemotherapy, reduces edema, and improves anti-tumorigenic immune reactions. Hence, therapeutic targeting of APLN/APLNR signaling offers an interesting option to address different pathological hallmarks of GBM.https://www.mdpi.com/2072-6694/13/15/3899Apelin (APLN)APLNRGlioblastoma (GBM)tumor microenvironment (TME)tumor associated myeloid cells (TAM)pericytes |
| spellingShingle | Roland E. Kälin Rainer Glass APLN/APLNR Signaling Controls Key Pathological Parameters of Glioblastoma Cancers Apelin (APLN) APLNR Glioblastoma (GBM) tumor microenvironment (TME) tumor associated myeloid cells (TAM) pericytes |
| title | APLN/APLNR Signaling Controls Key Pathological Parameters of Glioblastoma |
| title_full | APLN/APLNR Signaling Controls Key Pathological Parameters of Glioblastoma |
| title_fullStr | APLN/APLNR Signaling Controls Key Pathological Parameters of Glioblastoma |
| title_full_unstemmed | APLN/APLNR Signaling Controls Key Pathological Parameters of Glioblastoma |
| title_short | APLN/APLNR Signaling Controls Key Pathological Parameters of Glioblastoma |
| title_sort | apln aplnr signaling controls key pathological parameters of glioblastoma |
| topic | Apelin (APLN) APLNR Glioblastoma (GBM) tumor microenvironment (TME) tumor associated myeloid cells (TAM) pericytes |
| url | https://www.mdpi.com/2072-6694/13/15/3899 |
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