NIK/MAP3K14 Regulates Mitochondrial Dynamics and Trafficking to Promote Cell Invasion.

Although the role of NF-κB-inducing kinase (NIK) in immunity is well established, its relevance in cancer is just emerging. Here we describe novel functions for NIK in regulating mitochondrial dynamics and motility to promote cell invasion. We show that NIK is localized to mitochondria in cancer cell lines, ex vivo tumor tissue, and mouse embryonic fibroblasts (MEFs).

Asphyxia due to laryngeal spasm as a severe complication of awake deep brain stimulation for Parkinson's disease: a case report.

Background: In accordance with German neurosurgical and neurological consensus recommendations, lead placements for deep brain stimulation (DBS) in patients with Parkinson's disease (PD) are usually performed with the patient awake and in "medication off" state. This allows for optimal lead position adjustment according to the clinical response to intraoperative test stimulation. However, exacerbation of Parkinsonian symptoms after withdrawal of dopaminergic medication may endanger the patient by inducing severe "off" state motor phenomena.

NIK regulates MT1-MMP activity and promotes glioma cell invasion independently of the canonical NF-κB pathway.

A growing body of evidence implicates the noncanonical NF-κB pathway as a key driver of glioma invasiveness and a major factor underlying poor patient prognoses. Here, we show that NF-κB-inducing kinase (NIK/MAP3K14), a critical upstream regulator of the noncanonical NF-κB pathway, is both necessary and sufficient for cell-intrinsic invasion, as well as invasion induced by the cytokine TWEAK, which is strongly associated with tumor pathogenicity. NIK promotes dramatic alterations in glioma cell morphology that are characterized by extensive membrane branching and elongated pseudopodial protrusions.

MicroRNA-145 Promotes the Phenotype of Human Glioblastoma Cells Selected for Invasion.

Background/aim: Novel treatment strategies aiming to eliminate or attenuate the invasive phenotype of glioblastoma multiforme (GBM), the most common and aggressive primary brain tumor, could offer a profound therapeutic benefit to patients. We previously demonstrated one method to create invasive sub-populations of GBM cells (IM3 cells) and a positive regulatory role for the miR-143/-145 locus in enhancing the invasion of GBM cells. Herein, we investigated the correlation between miR-145 and srGAP1 (SLIT-ROBO Rho GTPase-activating protein1) that is purported to be a target of miR-145 and involved in migration and invasion.

Tumor necrosis factor-like weak inducer of apoptosis (TWEAK) promotes glioma cell invasion through induction of NF-κB-inducing kinase (NIK) and noncanonical NF-κB signaling.

Background: High-grade gliomas are one of the most invasive and therapy-resistant cancers. We have recently shown that noncanonical NF-κB/RelB signaling is a potent driver of tumorigenesis and invasion in the aggressive, mesenchymal subtype of glioma. However, the relevant signals that induce activation of noncanonical NF-κB signaling in glioma and its function relative to the canonical NF-κB pathway remain elusive.

Synovial cyst mimicking an intraspinal sacral mass.

A 68-year-old female had a three-week history of severe low back pain radiating down the posterior left buttocks and left leg exacerbated by standing and walking. Lumbar spine MRI revealed cystic mass with similar intensity to cerebrospinal fluid located on dorsolateral left side of the sacral spinal canal inferior to the S1 pedicle. There was compression of left exiting S1 and traversing S2 nerve roots.

Galectin-1, a gene preferentially expressed at the tumor margin, promotes glioblastoma cell invasion.

Background: High-grade gliomas, including glioblastomas (GBMs), are recalcitrant to local therapy in part because of their ability to invade the normal brain parenchyma surrounding these tumors. Animal models capable of recapitulating glioblastoma invasion may help identify mediators of this aggressive phenotype.

Methods: Patient-derived glioblastoma lines have been propagated in our laboratories and orthotopically xenografted into the brains of immunocompromized mice.