Kurtis Willingham

Tulane University

Author Statistics

Papers

Citation

H-Index

i-10 index

Research Trends

Author Order

Document Type

Co-Authors

Bysani Chandrasekar

Harry S. Truman Memorial Veterans' Hospital

Reza Izadpanah

Tulane University

Amin Izadpanah

Tulane University

Eckhard Alt

Tulane University

Ricardo Mostany

Tulane University

Aaron S. Dumont

Tulane University

Zahra Barabadi

Hamedan University of Medical Sciences

Fatemeh Daneshimehr

Tehran University of Medical Sciences

Stephen E. Braun

Tulane University

Cooperative Institutions

Tulane University

Tehran University of Medical Sciences

University of California, Los Angeles

Universidad de Cantabria

Instituto de Biomedicina y Biotecnología de Cantabria

Unidades Centrales Científico-Técnicas

Consejo Superior de Investigaciones Científicas

Universidad de León

Neurological Surgery

Ochsner Health System

Author Statistics

Papers

Citation

H-Index

i-10 index

Research Field

Targeting TRAF3IP2 inhibits angiogenesis in glioblastoma

Frontiers in Oncology (2022)

Amin Izadpanah Fatemeh Daneshimehr Kurtis Willingham Zahra Barabadi Stephen E. Braun

Increased vascularization, also known as neoangiogenesis, plays a major role in many cancers, including glioblastoma multiforme (GBM), by contributing to their aggressive growth and metastasis. Although anti-angiogenic therapies provide some clinical improvement, they fail to significantly improve the overall survival of GBM patients. Since various pro-angiogenic mediators drive GBM, we hypothesized that identifying targetable genes that broadly inhibit multiple pro-angiogenic mediators will significantly promote favorable outcomes. Here, we identified TRAF3IP2 (TRAF3-interacting protein 2) as a critical regulator of angiogenesis in GBM. We demonstrated that knockdown of TRAF3IP2 in an intracranial model of GBM significantly reduces vascularization. Targeting TRAF3IP2 significantly downregulated VEGF, IL6, ANGPT2, IL8, FZGF2, PGF, IL1β, EGF, PDGFRB, and VEGFR2 expression in residual tumors. Our data also indicate that exogenous addition of VEGF partially restores angiogenesis by TRAF3IP2-silenced cells, suggesting that TRAF3IP2 promotes angiogenesis through VEGF- and non-VEGF-dependent mechanisms. These results indicate the anti-angiogenic and anti-tumorigenic potential of targeting TRAF3IP2 in GBM, a deadly cancer with limited treatment options.

10.3389/fonc.2022.893820

Cite

Citations (4)

Unfolded protein response and angiogenesis in malignancies

Biochimica et Biophysica Acta (BBA) - Reviews on Cancer (2022)

Amin Izadpanah Kurtis Willingham Bysani Chandrasekar Eckhard Alt Reza Izadpanah

Crosstalk

10.1016/j.bbcan.2022.188839

Cite

Citations (4)