Raquel Sitcheran

About

Dr. Raquel Sitcheran received her Bachelor of Arts in biology from Columbia University in 1992 and her PhD in physiology and genetics from the University of California, San Francisco in 2000, working with Dr. Keith Yamamoto. Her postdoctoral work was conducted with Dr. Albert Baldwin at the University of North Carolina, Chapel Hill. She served as a research associate at the Lineberger Comprehensive Cancer Center at UNC Chapel Hill from 2006 to 2009 before joining the faculty at the Texas A&M University Naresh K. Vashisht College of Medicine in September 2009. Her research focuses on the role of NF-κB regulatory proteins in regulating cancer cell behavior, particularly their motility and invasive potential. She studies how signals regulate NF-κB and how deregulation of this pathway impacts cancer cell growth, self-renewal, and survival. Her laboratory has established a critical role for NIK and noncanonical NF-κB signaling in promoting the migratory and invasive potential of glioma cells. Current efforts include elucidating mediators of NIK signaling in mitochondria within cancer and normal cells to understand how mitochondrial dysfunction contributes to disease and cancer progression.

Research topics

• Biology
• Genetics
• Cancer research
• Cell biology
• Immunology
• Neuroscience
• Chemistry
• Biochemistry

Selected publications

• Targeting NF-κB-Inducing Kinase (NIK) in Immunity, Inflammation, and Cancer

  International Journal of Molecular Sciences · 2020 · 154 citations

  Senior authorCorresponding

  NF-κB-inducing kinase (NIK), the essential upstream kinase, which regulates activation of the noncanonical NF-κB pathway, has important roles in regulating immunity and inflammation. In addition, NIK is vital for maintaining cellular health through its control of fundamental cellular processes, including differentiation, growth, and cell survival. As such aberrant expression or regulation of NIK is associated with several disease states. For example, loss of NIK leads to severe immune defects, w…

  PublisherOA PDFDOI

• NIK promotes metabolic adaptation of glioblastoma cells to bioenergetic stress

  Cell Death and Disease · 2021 · 34 citations

  Senior authorCorresponding

  cells without inducing IKK. Thus, we establish that NIK is critical for bioenergetic stress responses to promote GBM cell pathogenesis independently of IKK. Our data suggest that targeting NIK may be used to exploit metabolic vulnerabilities and improve therapeutic strategies for GBM.

  PublisherOA PDFDOI

• Atomic vacancies of molybdenum disulfide nanoparticles stimulate mitochondrial biogenesis

  Nature Communications · 2024-09-17 · 19 citations

  articleOpen access

  Diminished mitochondrial function underlies many rare inborn errors of energy metabolism and contributes to more common age-associated metabolic and neurodegenerative disorders. Thus, boosting mitochondrial biogenesis has been proposed as a potential therapeutic approach for these diseases; however, currently we have a limited arsenal of compounds that can stimulate mitochondrial function. In this study, we designed molybdenum disulfide (MoS2) nanoflowers with predefined atomic vacancies that ar…

  PublisherOA PDFDOI

• NF-κB–Inducing Kinase Governs the Mitochondrial Respiratory Capacity, Differentiation, and Inflammatory Status of Innate Immune Cells

  The Journal of Immunology · 2023-03-06 · 10 citations

  articleOpen access

  NF-κB-inducing kinase (NIK), which is essential for the activation of the noncanonical NF-κB pathway, regulates diverse processes in immunity, development, and disease. Although recent studies have elucidated important functions of NIK in adaptive immune cells and cancer cell metabolism, the role of NIK in metabolic-driven inflammatory responses in innate immune cells remains unclear. In this study, we demonstrate that murine NIK-deficient bone marrow-derived macrophages exhibit defects in mitoc…

  PublisherOA PDFDOI

• Transcriptional induction of NF-κB-inducing kinase by E2F4/5 facilitates collective invasion of GBM cells

  Scientific Reports · 2023 · 8 citations

  Senior authorCorresponding

  The prognosis of high-grade gliomas, such as glioblastoma multiforme (GBM), is extremely poor due to the highly invasive nature of these aggressive cancers. Previous work has demonstrated that TNF-weak like factor (TWEAK) induction of the noncanonical NF-κB pathway promotes the invasiveness of GBM cells in an NF-κB-inducing kinase (NIK)-dependent manner. While NIK activity is predominantly regulated at the posttranslational level, we show here that NIK (MAP3K14) is upregulated at the transcripti…

  PublisherOA PDFDOI

Recent grants

• Investigating Novel Functions for NIK/MAP3K14 in High-Grade Glioma

  NIH · $2.5M · 2014–2024

• NF-kappaB N-myc in Oncogenic Pathways of the CNS

  NIH · $780k · 2006–2012

Frequent coauthors

• Kathryn M. Pflug

  Bryan College

  35 shared

• Dong W. Lee

  Texas A&M Health Science Center

  27 shared

• Albert S. Baldwin

  26 shared

• Justin Keeney

  Texas A&M University

  18 shared

• Jonathan S. Serody

  15 shared

• Matthew J. O’Shaughnessy

  Memorial Sloan Kettering Cancer Center

  15 shared

• Bruce R. Blazar

  University of Minnesota

  15 shared

• Patricia C. Cogswell

  Chordoma Foundation

  10 shared

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