Hemifacial spasms triggered by compression of tortuous anterior inferior cerebellar artery loop on the facial nerve in the internal auditory canal: A case report.

RATIONALE: Hemifacial spasm (HFS) is triggered by neurovascular compression mostly at the root entry/exit zone of the facial nerve. HFS with the responsible blood vessel located in the internal auditory canal (IAC) is a very rare occurrence. In our case, the HFS was triggered by compression of the anterior inferior cerebellar artery (AICA) loop on the facial nerve in the IAC. PATIENT CONCERNS: A 27-year-old female presented with a 5-year history of right-sided facial twitching with no obvious course. The frequency and severity of the attacks increases when the patient was anxious or agitated which severely affected her quality of life. DIAGNOSIS: Preoperative 3D-TOF magnetic resonance imaging (MRI) evaluation of cranial nerves showed that the right AICA loop had a tortuous course within the IAC and compressed the facial nerve. INTERVENTION: Microvascular decompression (MVD) surgery was carried out to separate the tortuous AICA loop and facial nerve in the IAC using a Teflon pad. OUTCOMES: The abnormal muscle response disappeared intraoperatively and 2-years follow-up revealed no recurrence of her symptomatology. She is current well and go about her daily activities with no neurological deficits. LESSON: The attachment of the facial nerve to the tortuous AICA loop coupled with the pulsatile impulse of tortuous AICA loop may have resulted in the entrapment and compression of the CN VII in the IAC.

Suppression of PTTG1 inhibits cell angiogenesis, migration and invasion in glioma cells.

Pituitary tumor-transforming gene 1 (PTTG1) has been identified as an oncogene and is overexpressed in many tumor types. However, the role of PTTG1 in glioblastoma (GBM) has not been well characterized, especially in relation to angiogenesis, migration, and invasion. In the present study, our results showed that the expression of PTTG1 was significantly higher in patients with GBM. Bioinformatic analysis showed that angiogenesis and the cell migration-related process were increased in patients with high PTTG1 expression levels; meanwhile, PTTG1 was positively correlated with marker genes of angiogenesis, migration and the evasion of apoptosis. In vitro assays showed that PTTG1 knockdown dramatically suppressed angiogenesis, migration and invasion, and increased the apoptosis of GBM cells. Moreover, our results also showed that silencing PTTG1 suppressed the activity of the TGF-ß/PI3K-AKT-mTOR pathway, which induced tumor deterioration in multiple organs. Overall, our findings indicate that PTTG1 is a glioma malignant factor that promotes angiogenesis, migration, invasion, and the evasion of apoptosis, and these roles may be related to the TGF-ß/PI3K-AKT-mTOR pathway. Thus, the targeted inhibition of PTTG1 might be a novel therapeutic strategy and a potential diagnostic biomarker for GBM-targeted therapies.

STAT3-PTTG11 abrogation inhibits proliferation and induces apoptosis in malignant glioma cells.

Pituitary tumor transforming gene 1 (PTTG11) is abundantly expressed in glioma. Our previous study demonstrated that the downregulation of PTTG11 gene expression significantly inhibited the proliferation, migration and invasion ability, and increased the apoptosis of SHG44 glioma cells. However, the molecular mechanisms that regulate PTTG11 and its actions remain elusive. In the present study, CCK-8 and flow cytometry assays were used to assess the proliferation/viability and apoptosis, respectively, of the human glioma U251 cell line. STAT3-PTTG1 signals were further evaluated by western blotting. The findings of the present study revealed that STAT3 induced PTTG11 expression, which subsequently induced downstream c-Myc and Bcl-2 expression while inhibiting Bax expression, thereby promoting cell viability and inhibiting apoptosis. PTTG11 suppression via siRNA inhibited the viability and increased the apoptosis of glioma cells induced by the STAT3 activator S3I-201. c-Myc and Bcl-2 expression was suppressed by PTTG11 inhibition. The findings of the present study suggest that the STAT3-PTTG11 signaling pathway may play an important role in glioma progression by regulating cell proliferation and apoptosis.