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In China, Budd-Chiari syndrome has been transliterated into six names according to the pronunciation of the letters. To standardize and unify the Chinese names of the disease, multi-disciplinary experts suggest translating Budd-Chiari syndrome into hepatic vein inferior venal cava obstruction syndrome as its Chinese name after reaching a consensus through discussion.

Dan Cui, Caifang Ni Department of Interventional Radiology, The First Affiliated Hospital of Soochow University, Suzhou City, Jiangsu Province 215006, People’s Republic of ChinaCorrespondence: Caifang NiDepartment of Interventional Radiology, The First Affiliated Hospital of Soochow University, No.188 Shizi Street, Suzhou City, Jiangsu Province 215006, People’s Republic of ChinaTel +86-512-65223637Email np0973@163.comBackground: It is known that Lnc712 plays an important role in the pathogenesis of breast cancer. However, whether it is involved in hepatocellular carcinoma (HCC) remains unknown. In this study, we aimed to investigate the role and underlying mechanism of Lnc712 in HCC.Methods: Sixty-four HCC patients were enrolled and followed up for 5 years to analyze the prognostic value of Lnc712 for HCC. HCC cells were transfected with Lnc712 expression vector, Bach-1 expression vector (or siRNA) and miR-142-3p mimic (or inhibitor) to explore the interactions among Lnc712, miR-142-3p and Bach-1. Cell proliferation, migration, invasion and cell cycle were analyzed by CCK-8 assay, transwell assay, wound healing assay and flow cytometry assay, respectively.Results: The expression of Lnc712 was upregulated in HCC, and the upregulated Lnc712 expression was significantly related to poor overall survival in HCC patients. In HCC cells, Lnc712 interacted with miR-142-3p and upregulated Bach-1, a target of miR-142-3p. In addition, Lnc712 promoted HCC cell proliferation, migration, invasion and cell cycle, while its effects were abolished by miR-142-3p mimic. Moreover, miR-142-3p mimic enhanced HCC cell proliferation, migration, invasion and cell cycle, while its effects were abolished by Bach-1 overexpression. miR-142-3p inhibitor repressed cell proliferation, migration, invasion and cell cycle in HCC cells, while its effects were abolished by Bach-1 knockdown. Furthermore, Lnc712 knockdown remarkably inhibited HCC tumor growth in nude mice.Conclusion: Lnc712 may promote the development of HCC by targeting the miR-142-3p/Bach-1 axis.Keywords: hepatocellular carcinoma, Lnc712, Bach-1, miR-142-3p

Yuxia Duan,1,2 Mengjing Zhao,2 Mengmeng Jiang,2 Zhi Li,1 Caifang Ni1 1Department of Interventional Radiology, The First Affiliated Hospital of Soochow University, Suzhou 215006, People’s Republic of China; 2Department of Radiology, The First Affiliated Hospital of Wenzhou Medical University, Wenzhou 325000, People’s Republic of ChinaCorrespondence: Caifang Ni Email caifangni@yeah.netBackground: Long noncoding RNAs (lncRNAs) can promote hepatocellular carcinoma (HCC) initiation and progression. In this report, we examined the role of lncRNA LINC02476 in HCC.Methods: The expression levels of different lncRNAs in HCC were explored using the TCGA database and lncRNA LINC02476 was selected for further study. The expression of LINC02476 in HCC tissues was determined by real-time PCR. The clinicopathological characteristics of HCC patients were analyzed relative to the expression of LINC02476.The expression of LINC02476 was downregulated in HCC cells using a lentiviral vector and different assays were performed to study cell growth, proliferation, invasion, apoptosis and the cell cycle. MiR-497 was selected as a miRNA that could interact with LINC02476 which was further tested by RNA immunoprecipitation. HMGA2 was selected as a possible target of miR-497, and their interaction was examined by a luciferase reporter assay.Results: LINC02476 expression was elevated in HCC cell lines and HCC tissues. When LINC02476 was downregulated, the growth and the invasion of HCC cells decreased in vitro and in vivo. LINC02476 negatively regulated the expression of miR-497 by acting as a ceRNA. HMGA2 was directly targeted and inhibited by miR-497.Conclusion: The results indicate that LINC02476 functions through the miR-497/HMGA2 axis and that it has a role in the growth and metastasis of HCC cells. Therefore,LINC02476 could be an interesting new molecular target in HCC therapies.Keywords: LINC02476, miR-497, HMGA2, hepatocellular carcinoma

Qingyun Zhu,1,2 Yuehui Guo,2 Shiwei Chen,2 Daiquan Fu,2 Yanxiang Li,2 Zhi Li,1 Caifang Ni1 1Department of Interventional Radiology, The First Affiliated Hospital of Soochow University, Suzhou 215006, People’s Republic of China; 2Department of Intervention, Gongli Hospital of Shanghai Pudong New Area, Shanghai 200135, People’s Republic of ChinaCorrespondence: Caifang Ni; Zhi Li Email nicaifangsz@163.com; zhilisoochow1983@163.comBackground: Irinotecan (IRI) is considered an option for second-line treatment of advanced gastric cancer; however, acquired drug resistance currently limits its clinical application. Recently, many researchers have shown that autophagy plays a crucial role in the resistance of tumor cells to chemotherapy and radiotherapy. In this study, we investigated the relationship between autophagy and antitumor activity of IRI in gastric cancer cells.Methods: We used MTT assay, flow cytometry and immunofluorescence staining to detect viability, apoptosis and autophagy in gastric cancer. Western blotting assay was used to determine the expression of LC3, Beclin-1, P62, cleaved PARP and Caspase 3. In vivo animal study was performed finally.Results: We found that IRI treatment dose- and time-dependently inhibited growth and induced apoptosis in gastric cancer cells. Moreover, IRI treatment caused autophagy in these cells, whereas autophagy inhibitors— 3-methyladenine (3-MA), chloroquine (CQ), and Beclin-1 small interfering RNA (siRNA)—suppressed cytotoxicity of IRI. A mechanistic analysis showed that IRI-induced autophagy and apoptosis were related to increased reactive oxygen species (ROS) accumulation and activation of the JNK- and p38-MAPK pathways. Further in vivo experiments revealed that IRI suppressed tumor growth, induced autophagy, and stimulated the JNK- and p38-MAPK pathways, whereas 3-MA attenuated these effects.Conclusion: Taken together, these results indicate that IRI stimulates the ROS-related JNK- and p38-MAPK pathways to promote autophagy-dependent apoptosis. Thus, a combination of IRI with a pharmacological autophagy enhancer may be a promising therapeutic strategy against gastric cancer.Keywords: gastric cancer, irinotecan, autophagy, ROS, JNK, p38