Background: Pituitary adenoma (PA) is a kind of common primary brain tumor with invasive properties. Although the fact that long noncoding RNA (lncRNA) small nucleolar RNA host gene 6 (SNHG6) exerts oncogenic function in cancer cells and that miR-944 inhibits epithelial-mesenchymal transition (EMT) of cancer cells are well documented, few studies explore the function and mechanism of SNHG6 and miR-944 in invasive pituitary adenoma (IPA). Materials and Methods: Quantitative real-time polymerase chain reaction (qRT-PCR) was used to detect the expressions of SNHG6 and miR-944 in PA samples. Human PA cell line HP75 was used as a cell model. The biological effects of SNHG6 and miR-944 on HP75 cells were investigated with cell counting kit-8 (CCK-8) assay, Transwell assay, and scratch healing assay in vitro, respectively. Markers of EMT, including E-cadherin and vimentin, were detected by western blot. Interactions between SNHG6 and miR-944, miR-944 and RAB11A were determined by bioinformatics analysis, qRT-PCR, and dual luciferase reporter assay. Results: SNHG6 was significantly upregulated in IPA samples, whereas miR-944 was downregulated. SNHG6 markedly promoted viability, migration, invasion, and EMT of PA cells, whereas miR-944 transfection had the opposite effects. SNHG6 could downregulate miR-944, and there was a negative correlation between SNHG6 expression and miR-944 expression in IPA samples. Besides, it was confirmed that miR-944 could pair with the 3¢-untranslated region of RAB11A and repress its expression. Conclusions: This study authenticates that the SNHG6/miR-994/RAB11A axis plays a crucial role in regulating proliferation, migration, invasion, and EMT of IPA cells. SNHG6 and miR-994 can serve as novel valuable therapeutic targets for IPA.
Abstract. The aquaporin (AQP) family, which includes 13 members identified in mammalian cells, is involved in cancer development and progression. AQP9 expression is upregulated in several tumor tissue types. However, the functions of AQP9 in astrocytoma remain elusive. The present study identified that AQP9 was expressed in astrocytoma cells. AQP9 expression was silenced by transfection with small interfering RNAs and increased by transfection with a plasmid containing the AQP9 gene. Using invasion and wound-healing assays, it was revealed that the knockdown of AQP9 suppressed astrocytoma cell invasion and motility, whereas overexpression of AQP9 promoted the invasion and motility of astrocytoma cells. It was further revealed that AQP9 could induce RAC serine/threonine-protein kinase (AKT) activation and decrease E-cadherin expression in astrocytoma cells. Inhibition of the AKT pathway attenuated AQP9-mediated invasion, motility and E-cadherin expression. Taken together, the results of the present study indicated that AQP9 promoted the invasion and motility of cells via the AKT pathway. Therefore, AQP9 may represent a potential target for therapeutic use of astrocytoma.
BackgroundTranssphenoidal surgery (TSS) is first-line treatment for giant pituitary adenomas (PAs). Although PA is a benign neuroendocrine tumor that originates from adenohypophysial cells, the surgical outcomes and prognosis of giant PAs differ significantly due to multiple factors such as tumor morphology, invasion site, pathological characteristics and so on. The aim of this study was to evaluate surgical outcomes of giant PAs in a single-center cohort.MethodsThe clinical features and outcomes of 239 patients with giant PA who underwent sphenoidal surgery at the Second Affiliated Hospital of Zhejiang University School of Medicine from January 2015 to October 2021 were collected from medical records. The basic clinical information (age, gender, function etc.), surgical procedure, imaging features (maximum diameter, invasion characteristics, tumor shape etc.) and histopathological characteristics (pathological results, Ki-67, P53 etc.) were retrospectively reviewed. SPSS 25.0 and Stata 12.0 software were used for statistical analysis.ResultsA total of 239 patients with giant PAs underwent TSS, of which 168 surgeries (70.29%) were endoscopic endonasal transsphenoidal (EETS) and 71 (29.71%) were microscopic transsphenoidal (MTS). The mean preoperative maximum diameter in the cohort was 45.64 mm. Gross-total resection was achieved in 46 patients (19.25%), near-total in 56 (23.43%), subtotal in 68 (28.45%), and partial in 69 (28.87%) patients. The maximum tumor diameter and Knosp grade were the significant factors that limited the extent of the resection of giant PAs. A total of 193 patients (80.75%) experienced surgical complications, and the most common complications were postoperative diabetes insipidus (DI) (91, 38.08%), intracranial infection (36, 15.06%) and cerebrospinal fluid (CSF) leaks (37, 15.48%). In addition, there was a significant difference in the incidence of CSF leaks between the neuroendoscopy group and the microscopic group (P < 0.05).ConclusionThe management of giant PAs remains a therapeutic challenge due to their large size and postoperative complications. The maximum diameter and Knosp grade of giant PAs significantly limited the extent of resection, which warrants a reasonable surgical plan.
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