Xia Zhang

Ovarian teratoma-associated anti- Anti-N-methyl-D-aspartate receptor encephalitis: a clinical analysis of 5 cases

To analyse the clinical features, diagnosis, treatment, and prognosis of anti-N-methyl-D-aspartic acid receptor (NMDAR) encephalitis associated with ovarian mature teratomas. Retrospectively analysed the clinical-laboratory data of five patients with anti-NMDAR encephalitis combined with ovarian teratoma at a single centre between March 2016 and June 2019. The mean age of the patients was 22.40 ± 2.89 years (range, 19-26 years). Five patients had premonitory fever symptoms, clinical manifestations of mental disorder or convulsions for starting, with varying degrees of involuntary movement. Brain MRI and electroencephalography lacked specificity, and cerebrospinal fluid resistance NMDAR antibody detection was the key to diagnosis. All patients experienced good outcomes in response to immunotherapy combined with ovarian tumour resection, with a median follow-up time of 36 months (range, 16-55 months). The MRS value of five patients decreased significantly half a year after surgery, and no encephalitis or ovarian tumour relapses were reported. Anti-NMDA encephalitis caused by ovarian teratoma is mostly a non-specific clinical manifestation of neurological and mental abnormalities, which can be easily misdiagnosed and delayed, and doctors should fully recognise the disease, early diagnosis, and timely surgical intervention to improve the prognosis of patients.

CircFAT1 facilitates cervical cancer malignant progression by regulating ERK1/2 and p38 MAPK pathway through miR‐409‐3p/CDK8 axis

AbstractCircular RNA FAT atypical cadherin 1 (circFAT1) has been reported to play vital roles in the progression of some cancers. However, the regulatory role and underlying mechanisms of circFAT1 in cervical cancer (CC) remain largely unknown. The expression of circFAT1, microRNA (miR)‐409‐3p and cyclin‐dependent kinase 8 (CDK8) was detected using qRT‐PCR and Western blot assays. Cell proliferation, apoptosis, migration and invasion in vitro were investigated using cell counting kit‐8, colony formation, flow cytometry, and transwell assays, respectively. Western blot assay was used to determine the activation of ERK1/2 and p38 MAPK pathway. The interaction miR‐409‐3p and circFAT1 or CDK8 was confirmed by dual‐luciferase reporter, pull‐down or RIP assays. The effects of circFAT1 in vivo were determined using xenograft models. CircFAT1 was highly expressed in CC, and closely associated with poor prognosis. CircFAT1 knockdown resulted in the suppression of proliferation, migration and invasion, and promotion of apoptosis in CC cells via the inactivation of ERK1/2 and p38 MAPK pathway; also, circFAT1 silencing could inactivate this pathway and repressed CC tumor growth in vivo. Mechanistic analysis showed that circFAT1 directly sponged miR‐409‐3p and then relieved the repressive effect of miR‐409‐3p on its target CDK8. Furthermore, miR‐409‐3p inhibition reversed the effects of circFAT1 silencing on CC cells. Whereas, miR‐409‐3p overexpression impeded CC cell growth and motility, which was attenuated by CDK8. CircFAT1 promoted CC progression via activating ERK1/2 and p38 MAPK pathway through the miR‐409‐3p/CDK8 axis, suggesting a promising prognostic biomarker and therapeutic target for CC.