Solitary Fibrous Tumors of the Chest: An Analysis of Fifty Patients.

BACKGROUND: A solitary fibrous tumor of the chest (SFTC) is a subtype of solitary fibrous tumor (SFT) with a low incidence rate. The purpose of this study is to analyze the diagnosis and treatment of SFTC and the difference between benign and malignant solitary fibrous tumor of the pleura (SFTP) to improve the understanding of this rare disease. METHODS: A retrospective analysis of fifty patients with SFTC (33 cases in the pleura and 17 in the lung) was performed. Clinical and imaging characteristics, pathological features, and treatment follow-up outcomes were analyzed. RESULTS: The common symptoms of the 50 patients included a cough, expectoration, chest tightness, fever, and chest pain. Space occupying lesions were found via plain computed tomography (CT) and enhanced CT was used for enhancement of the tumors. It was also found that 18 cases had necrosis, and 5 cases had calcification. The histopathology results showed that frequent nuclear division, obvious morphological variation, necrosis, and the high expression of Ki-67 cells are markers of malignant SFTC. There were significant differences in age, chest tightness, necrotic foci in CT, and expression of Ki-67 between the benign and malignant SFTP cases. All the patients who received treatment were given an excellent prognosis. CONCLUSION: A combination of enhanced CT, histopathology, and immunohistochemistry can be used for the accurate diagnosis of SFTC. Advanced age, chest tightness, necrotic foci in CT, and a high Ki-67 index were more likely to be malignant SFTP. Operation and radiofrequency ablation can provide favorable outcomes for both benign and malignant SFTC.

KLF5-induced BBOX1-AS1 contributes to cell malignant phenotypes in non-small cell lung cancer via sponging miR-27a-5p to up-regulate MELK and activate FAK signaling pathway.

BACKGROUND: Non-small cell lung cancer (NSCLC) is a major histological subtype of lung cancer with high mortality and morbidity. A substantial amount of evidence demonstrates long non-coding RNAs (lncRNA) as critical regulators in tumorigeneis and malignant progression of human cancers. The oncogenic role of BBOX1 anti-sense RNA 1 (BBOX1-AS1) has been reported in several tumors. As yet, the potential functions and mechanisms of BBOX1-AS1 in NSCLC are obscure. METHODS: The gene and protein expression was detected by qRT-PCR and western blot. Cell function was determined by CCK-8, colony forming, would healing and transwell assays. Bioinformatics tools, ChIP assays, dual luciferase reporters system and RNA pull-down experiments were used to examine the interaction between molecules. Subcutaneous tumor models in nude mice were established to investigate in vivo NSCLC cell behavior. RESULTS: BBOX1-AS1 was highly expressed in NSCLC tissues and cells. High BBOX1-AS1 expression was associated with worse clinical parameters and poor prognosis. BBOX1-AS1 up-regulation was induced by transcription factor KLF5. BBOX1-AS1 deficiency resulted in an inhibition of cell proliferation, migration, invasion and EMT in vitro. Also, knockdown of BBOX1-AS1 suppressed NSCLC xenograft tumor growth in mice in vivo. Mechanistically, BBOX1-AS1 acted act as a competetive "sponge" of miR-27a-5p to promote maternal embryonic leucine zipper kinase (MELK) expression and activate FAK signaling. miR-27a-5p was confirmed as a tumor suppressor in NSCLC. Moreover, BBOX1-AS1-induced increase of cell proliferation, migration, invasion and EMT was greatly reversed due to the overexpression of miR-27a-5p. In addition, the suppressive effect of NSCLC progression owing to BBOX1-AS1 depletion was abated by the up-regulation of MELK. Consistently, BBOX1-AS1-mediated carcinogenicity was attenuated in NSCLC after treatment with a specific MELK inhibitor OTSSP167. CONCLUSIONS: KLF5-induced BBOX1-AS1 exerts tumor-promotive roles in NSCLC via sponging miR-27a-5p to activate MELK/FAK signaling, providing the possibility of employing BBOX1-AS1 as a therapeutic target for NSCLC patients.

Ganoderic acid B attenuates LPS-induced lung injury.

Acute lung injury (ALI)/acute respiratory distress syndrome (ARDS) is a serious respiratory disease, the mechanism is unclear. This paper revealed the mechanism of ganoderic acid B (BB) on lipopolysaccharide-induced pneumonia in mice. Pneumonia model was induced by LPS in mice and A549 cells. Lung dry/wet weight (W/D) and myeloperoxidase (MPO) activity in lung were examined. Lung histopathological changes was observed by HE staining. Superoxide dismutase (SOD), malondialdehyde (MDA) and proinflammatory cytokines, including tumor necrosis factor-α (TNF-α), interleukin-1ß (IL-1ß) and interleukin-6 (IL-6) in mice and A549 cells were detected. Rho/NF-κB pathway in mice and A549 cells were examined by Western Blot. BB significantly reduced W/D and MPO activity, restored lung histopathological changes. BB also increased SOD, decreased MDA, TNF-α, IL-1ß and IL-6 in mice and A549 cells. In addition, BB inhibited Rho/NF-κB pathway in mice and A549 cells. BB has protective effect on LPS-induced pneumonia in mice, and its mechanism is related to the regulation of Rho/NF-κB signaling pathway.

EPHA5 mutation impairs natural killer cell-mediated cytotoxicity against non-small lung cancer cells and promotes cancer cell migration and invasion.

AIM: This study aims to evaluate the role of the EPHA5 mutation in the migration and invasion of non-small cell lung cancer (NSCLC) cells and in modulating the killing effect of natural killer (NK) cells to NSCLC cells. METHODS: EPHA5-wt (wild type) and EPHA5-mut (mutation) plasmids were constructed. EPHA5 was silenced using si-EPHA5. NSCLC cell migration and invasion were determined using Transwell assays. NK cell proliferation and apoptosis were determined using CCK-8 assay and flow cytometry, respectively. The killing effect of NK cells to NSCLC cells was also examined. RESULTS: EPHA5 mutation significantly promoted migration and invasion in NSCLC cells. Furthermore, EPHA5 mutation notably impaired the cytotoxicity of NK cells against NSCLC cells. In contrast, EPHA5-wt overexpression and EPHA5 silencing exerted the opposite effect. CONCLUSION: EPHA5 mutation impairs the NK cell-mediated cytotoxicity against NSCLC cells and promotes migration and invasion in NSCLC cells.