Primary small intestinal extranodal NK/T cell lymphoma, nasal type with kidney involvement: a rare case report and literature review.

BACKGROUND: Extranodal NK/T cell lymphoma, nasal type (EN-NK/T-NT) is a rare and aggressive type of non-Hodgkin's lymphoma. EN-NK/T-NT seldom occurs in the gastrointestinal tract, and renal involvement is relatively rare. CASE PRESENTATION: Here we report a case of primary small intestinal EN-NK/T-NT with kidney involvement. We present the case of a 71-year-old female who was admitted to our hospital for coronary heart disease with a fever of unknown origin. Laboratory examination showed renal impairment and PET/CT showed a locally thickened wall of the small intestine, abnormally increased FDG metabolism in the right lower abdomen, and multiple slightly high-density masses with abnormal increased FDG metabolism in the right kidney. The gross specimen showed a grayish-white lump located in the ileum approximately 15 cm away from the ileocecum, and two grayish-white lumps located in the upper and lower poles of the right kidney, respectively. The pathological diagnosis was EN-NK/T-NT. The patient died approximately 10 months after the operation. CONCLUSION: EN-NK/T-NT is a rare type of non-Hodgkin's lymphoma and may develop insidiously, with fever as the only clinical manifestation. The disease was found to be difficult to diagnose in the early stage, resulting in a highly aggressive clinical course and short survival time.

Blocking OLFM4/HIF-1α axis alleviates hypoxia-induced invasion, epithelial-mesenchymal transition, and chemotherapy resistance in non-small-cell lung cancer.

Hypoxia is a common biological hallmark of solid cancers, which has been proposed to be associated with oncogenesis and chemotherapy resistance. The purpose of the present study was to investigate the role and underlying mechanisms of olfactomedin 4 (OLFM4) in the hypoxia-induced invasion, epithelial-mesenchymal transition (EMT), and chemotherapy resistance of non-small-cell lung cancer (NSCLC). We observed dramatically upregulated expression of OLFM4 in several NSCLC cell lines, and this effect was more pronounced in A549 and H1299 cells. In addition, our data revealed that OLFM4 expression was remarkably increased in both A549 and H1299 cells under hypoxic microenvironment, accompanied by enhanced levels of hypoxia-inducible factor (HIF)-1α protein. The HIF-1α level was elevated in response to hypoxia, resulting in the regulation of OLFM4. Interestingly, OLFM4 was a positive regulator of hypoxia-driven HIF-1α production. Moreover, depletion of OLFM4 modulated multiple EMT-associated proteins, as evidenced by the enhanced E-cadherin levels along with the diminished expression of N-cadherin and vimentin in response to hypoxia, and thus blocked invasion ability of A549 and H1299 cells following exposure to hypoxia. Furthermore, ablation of OLFM4 accelerated the sensitivity of A549 cells to cisplatin under hypoxic conditions, implying that OLFM4 serves as a key regulator in chemotherapeutic resistance under hypoxia. In conclusion, OLFM4/HIF-1α axis might be a potential therapeutic strategy for NSCLC.

MiR-543 Promotes Migration, Invasion and Epithelial-Mesenchymal Transition of Esophageal Cancer Cells by Targeting Phospholipase A2 Group IVA.

BACKGROUND/AIMS: The aim of this study was to investigate the roles of miR-543 and phospholipase A2 group IVA (PLA2G4A) in cell mobility and the invasiveness cascade in esophageal squamous cell carcinoma (ESCC) and to validate the interactive relationship between miR-543 and PLA2G4A. METHODS: Microarray analysis showed the different expression levels of PLA2G4A in two ESCC cell lines (KYSE30 and KYSE180). The expression levels of miR-543 and PLA2G4A in ESCC tissues were confirmed by qRT-PCR and Western blotting. The targeted relationship between miR-543 and PLA2G4A was studied and verified by a luciferase activity assay. Then, the invasion and metastasis ability of ESCC cell lines transfected with miR-543 mimics, miR-543 inhibitor, or PLA2G4A and miR-543 mimics were analyzed separately by Transwell migration and invasion assays. In addition, the roles of miR-543 and PLA2G4A in the expression of E-cadherin and vimentin were also investigated. RESULTS: PLA2G4A up-regulated the level of E-cadherin and down-regulated the level of vimentin, which curbed ESCC cell mobility and invasion. In ESCC cells, the expression of miR-543 was significantly higher, whereas the expression of PLA2G4A was markedly lower. MiR-543 facilitated ESCC cell mobility and invasion by repressing PLA2G4A. CONCLUSIONS: MiR-543 enhanced the cell mobility and the invasiveness cascade in ESCC cells via the down-regulation of PLA2G4A expression.

LncRNA BDNF-AS inhibits proliferation, migration, invasion and EMT in oesophageal cancer cells by targeting miR-214.

This study was aimed at exploring the effect of lncRNA BDNF-AS on cell proliferation, migration, invasion and epithelial-to-mesenchymal transition (EMT) of oesophageal cancer (EC) cells. The expression of BDNF-AS and miR-214 in tissue samples and cells was measured by qRT-PCR. The targeted relationship between BDNF-AS and miR-214 was analysed by dual-luciferase reporter assay. After cell transfection, the cell proliferation activity was assessed by MTS method, while the migrating and invading abilities were evaluated by transwell assay. LncRNA BDNF-AS was remarkably down-regulated, while miR-214 was up-regulated in EC tissues and cells in comparison with normal tissues and cells. Overexpression of BDNF-AS significantly inhibited the abilities of cell proliferation, migration and invasion as well as the EMT processes of EC cells. The bioinformatics analysis and luciferase assay indicated that BDNF-AS could be directly bound by miR-214. Furthermore, overexpression of miR-214 and BDNF-AS exerted suppressive influence on EC cell multiplication, migration, invasion and EMT processes. LncRNA BDNF-AS restrained cell proliferation, migration, invasion and EMT processes in EC cells by targeting miR-214.

miR-455-3p serves as prognostic factor and regulates the proliferation and migration of non-small cell lung cancer through targeting HOXB5.

MicroRNAs (miRs) have been reported to play significantly roles in the initiation and progression of human cancers. miR-455-3p has been recently found could function as tumor suppressor in various human cancers. However, its expression and biological role in non-small cell lung cancer (NSCLC) remains elusive. In this study, we found miR-455-3p was markedly downregulated in NSCLC tissues and cell lines. Chi-square test to analyze the correlations between miR-455-3p expression and clinicopathological features revealed that miR-455-3p expression was correlated with poorly differentiated cancer and advanced tumor stage (P < 0.05). Kaplan-Meier curve revealed that low expression of miR-455-3p was correlated with shorter 5-year survival time (P = 0.029). Univariate and multivariate analyses identified low miR-455-3p expression was an unfavorable prognostic factor for overall survival. Gain-of-function and loss-of-function studies revealed that miR-455-3p inhibits cell proliferation and migration in vitro. Computer algorithm and dual-luciferase reporter assay revealed that miR-455-3p directly targets and suppresses HOXB5 in NSCLC. Further studies demonstrated that knockdown of HOXB5 attenuated the effect of miR-455-3p downregulation on cell proliferation and migration. Taken together, our results for the first time suggested that miR-455-3p was downregulated in NSCLC and was correlated with the poor prognosis of NSCLC patients. Also, miR-455-3p functions as tumor suppressor by directly targeting HOXB5 in NSCLC progression and may be used as a potential target for NSCLC treatment.

Prognosis of surgery combined with different adjuvant therapies in esophageal cancer treatment: a network meta-analysis.

This network meta-analysis was conducted to assess whether the efficacy of surgery with adjuvant therapies, including radiotherapy (RT+S), chemotherapy (CT+S), and chemoradiotherapy (CRT+S) have better performance in esophageal cancer treatment and management. PubMed and EMBASE were used to search for relevant trials. Both conventional pair-wise and network meta-analyses were carried out. The surface under the cumulative ranking curve (SUCRA) was used to rank interventions based on the efficacy of the treatment method. As for 3-year overall survival (OS), CRT+S showed the highest efficacy (CRT+S vs. SURGERY: HR=0.81, 95% CrI =0.73-0.90; CRT+S vs. CT+S: HR=0.82, 95% CrI =0.70-0.95; CRT+S vs. RT+S: HR=0.77, 95% CrI =0.62-0.95). For disease-free survival, CRT+S showed efficacy over CT+S ((HR =0.70, 95% CrI =0. 59-0.83). In conclusion, CRT+S showed a better performance for survival outcomes and ranks best among all therapies. The results of our study can provide guidance for medical decisions and treatment options that may help clinical practitioners improve the efficacy of EC treatment.