BACKGROUNDHepatocellular carcinoma (HCC) has become a great threat for people’s health. Many long noncoding RNAs are involved in the pathogenesis of HCC. SNHG15, as a tissue specific long noncoding RNAs, has been studied in many human cancers, except HCC.AIMTo explore the regulatory mechanism of SNHG15 in HCC.METHODSIn the present research, 101 HCC patient samples, two HCC cell lines and one normal liver cell line were used. RT-qPCR and Western blot analysis were applied to detect SNHG15, miR-490-3p and histone deacetylase 2 (HDAC2) expression. The regulatory mechanism of SNHG15 was investigated using CCK-8, Transwell and luciferase reporter assays.RESULTSOur research showed that up-regulation of SNHG15 was found in HCC and was related to aggressive behaviors in HCC patients. Moreover, knockdown of SNHG15 restrained HCC cell proliferation, migration and invasion. In addition, SNHG15 served as a molecular sponge for miR-490-3p. Further, miR-490-3p directly targets HDAC2. HDAC2 was involved in HCC progression by interacting with the SNHG15/miR-490-3p axis.CONCLUSIONIn conclusion, long noncoding RNA SNHG15 promotes HCC progression by mediating the miR-490-3p/HDAC2 axis in HCC.

Objective Hepatocellular carcinoma (HCC) is one of the most common causes of cancer-related deaths worldwide. This study investigated the relationship between cyclin-dependent kinase inhibitor (CDKN)3 and prognosis and pathological characteristics in HCC patients to determine whether it could be used as a prognostic factor and/or therapeutic target for HCC drug development. Methods We previously showed that CDKN3 is deregulated in HCC tumor samples. Here, bioinformatics analysis was used to assess the relationship between CDKN3 gene expression and the characteristics of HCC patients from Gene Expression Omnibus and The Cancer Genome Atlas databases. Additionally, CDKN3 expression was silenced by small interfering RNA to determine its effect on HCC cell proliferation and on HCC cell sensitivity to adriamycin chemotherapy. Results Bioinformatics analysis showed a negative correlation between CDKN3 expression and both disease-free survival and overall survival. CDKN3 silencing did not significantly suppress the proliferation of HCC cells, but did decrease their sensitivity to adriamycin. Conclusions CDKN3 may have a dual role during the development of HCC, and could be used as an independent prognostic factor and therapeutic target for HCC treatment.

Liver fibrosis is a critical pathological process in the early stage of many liver diseases, including hepatic cirrhosis and liver cancer. However, the molecular mechanism is not fully revealed. In this study, we investigated the role of F‐box protein 31 (FBXO31) in liver fibrosis. We found FBXO31 upregulated in carbon tetrachloride (CCl4) induced liver fibrosis and in activated hepatic stellate cells, induced by transforming growth factor‐β (TGF‐β). The enforced expression of FBXO31 caused enhanced proliferation and increased expression of α‐smooth muscle actin (α‐SMA) and Col‐1 in HSC‐T6 cells. Conversely, suppression of FBXO31 resulted in inhibition of proliferation and decreased accumulation of α‐SMA and Col‐1 in HSC‐T6 cells. In addition, upregulation of FBXO31 in HSC‐T6 cells decreased accumulation of Smad7, the negative regulator of the TGF‐β/smad signaling pathway, and suppression of the FBXO31 increased accumulation of Smad7. Immunofluorescence staining showed FBXO31 colocalized with Smad7 in HSC‐T6 cells and in liver tissues of BALB/c mice treated with CCl4. Immunoprecipitation demonstrated FBXO31 interacted with Smad7. Moreover, FBXO31 enhanced ubiquitination of Smad7. In conclusion, FBXO31 modulates activation of HSCs and liver fibrogenesis by promoting ubiquitination of Smad7.

Introduction: Pheochromocytoma (PCC) is a rare tumor which derives from adrenal medulla, when maximum diameter of pheochromocytoma is greater than 10CM, it is divided into Giant pheochromocytoma(GPCC), which is extremely rare and usually asymptomatic.Clinically, a huge and asymptomatic adrenal pheochromocytoma was usually misdiagnosed as other types of tumors, which result in notable increase of complication rates and death rates.Case presentation:In this case report, we described a clinically asymptomatic GPCC patient. Diagnosis:According to computed tomography (CT) scan, nuclear magnetic resonance(MR) scan, the patient is initially diagnosed as liposarcoma.After laparotomy, biochemical detection of catecholamine (CA) intermediate metabolites methoxyepinephrine (MN) and methoxy norepinephrine (NMN) and the pathological examination , diagnosis of GPCC was obtained. Intervention：The laparotomy was suspended and a diagnosis of pheochromocytoma was confirmed, because of unstable blood pressure and hypertension during separating and moving the mass during surgery. After consultation of multi-disciplinary team, adequate preoperative preparation was conducted according to the procedure of PCC surgical preparation. By the end of the regular phenoxybenzamine and intravenous fluids treatment for three weeks, the blood pressure of the patient was kept at an acceptable average. Therefore, the patient underwent the operationagain for radical resection. Outcome: After the operation, CA was basically normal in rechecking process, and the tumor was successfully removed. Pathological diagnosis of the mass after operation: Immunohistochemical resulted conformed to (epigastrium) pheochromocytoma. Immunohistochemistry: CgA(+), Inhibin-α(-), ki-67(<1%+), Syn(+). Pheochromocytoma had the definite pathological diagnosis. Conclusion: GPCC has the high diagnostic identification difficulty, it should be combined with imaging examination and biochemical measurement to identify. Before operation, the detailed imageological examination provides important reference for excision and surgical planning. Individualized and multi-disciplinary cooperation of management strategy in perioperative period should be recommended. Patients should conduct long-term follow-up.