Major histocompatibility complex, class II, DQ beta 1 antisense RNA 1 (HLA-DQB1-AS1) conferred the susceptibility to hepatocellular carcinoma. Sustaining cell growth and resisting apoptosis are two hallmarks of hepatocellular carcinoma. The present study explored the role of HLA-DQB1-AS1 in the proliferation and apoptosis of hepatocellular carcinoma cells and investigated its downstream pathway. Colony formation assay was performed to assess cell proliferation. Cell apoptosis was assessed with the TdT-mediated dUTP nick end labeling method. HLA-DQB1-AS1 deficiency exerts antiproliferative and proapoptotic effects on hepatocellular carcinoma cells. Moreover, based on bioinformatic analysis combined with the results of RNA immunoprecipitation assay, HLA-DQB1-AS1 was revealed to bind with zinc finger RANBP2-type containing 2 (ZRANB2) protein. ZRANB2 was upregulated in hepatocellular carcinoma at a clinical and cellular level. HLA-DQB1-AS1 caused no significant effects on ZRANB2 mRNA and protein expression. ZRANB2 knockdown suppressed cell proliferation and enhanced cell apoptosis of hepatocellular carcinoma. Moreover, ZRANB2 overexpression rescued the anticancer effect of silenced HLA-DQB1-AS1 in hepatocellular carcinoma cells. In conclusion, HLA-DQB1-AS1 promotes cell proliferation and inhibits apoptosis in hepatocellular carcinoma by the interaction with ZRANB2 protein.

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Background Despite great advances in the prevention, diagnosis, treatment, and management regarding hepatocellular carcinoma (HCC), the overall prognosis of HCC remains unfavorable. The expression profile, prognostic role, and biological functions of F‐box‐only protein 43 (FBXO43) in HCC remain unclear. Here, we determine the expression profile and prognostic value of FBXO43 in patients with HCC. Materials and Methods A total of 467 HCC patients and their clinicopathological data were collected from the Second Affiliated Hospital of Jiaxing University, the Cancer Genome Atlas (TCGA), and Genotype‐Tissue Expression (GTEx) databases. The expression profile, prognostic value, biological functions, and underlying mechanism of its involvement of FBXO43 were explored based on TCGA, Gene Expression Omnibus (GEO), LinkedOmics, and Cancer Dependency Map (DepMap). The expression of FBXO43 in 93 paired liver tissues was investigated via immunohistochemical staining, tissue microarray analysis, and Western blot. The prognostic value was assessed using survival analysis. Results FBXO43 RNA was upregulated in HCC liver tissues and was associated with an unfavorable prognosis ( p < 0.05). Furthermore, FBXO43 protein was overexpressed in HCC liver tissues compared with that in paired normal liver tissues. Overexpression of FBXO43 protein was significantly associated with advanced TNM stage, large tumor size, lymphatic invasion, distant metastasis, earlier cancer recurrence, and decreased overall survival after radical surgery ( p < 0.05). Cox regression analysis showed that FBXO43 had significant prognostic value in HCC. Importantly, FBXO43 and its co‐expressed genes were mainly involved in cell cycle regulation, DNA replication, metabolic regulation, and so on. FBXO43 knockdown could significantly affect the HCC cell lines growth and proliferation. Conclusions We first revealed that FBXO43 was overexpressed in liver HCC tissues at the RNA and protein levels and served as an independent prognostic factor for HCC patients. Therefore, FBXO43 is worth investigating as a potential HCC treatment target.

Background: Focal nodular hyperplasia (FNH) is a benign liver tumor. The surgical indication of benign liver tumors has expanded due to the minimally invasive surgery (MIS) trend. Whether the tumor located in a specific location (such as under capsule, caudate lobe, left lateral lobe, etc.) or with psychological disorders can be used as an indication for surgery is rarely reported.This study explores the feasibility and safety of laparoscopic liver resection and provides potential surgical indications for FNH. Methods:A retrospective analysis of 29 FNH patients treated surgically at the First Affiliated Hospital of Soochow University from 2013 to 2021, with a median follow-up of 12 months. Data analysis included perioperative indication, mortalities, and prognosis. Results:All patients had surgery for FNH after pathology confirmed the diagnosis. The tumor's mean diameter was 5.5 cm (±1.8 cm). Laparoscopic liver resection was performed on 23 patients. Among them, five patients underwent right posterior lobe resection, and nine received robot-assisted laparoscopic lobectomy. one patient developed subdiaphragmatic fluid and required drainage. The anxiety and depression of all patients have been alleviated compared to the preoperative data(SCL-90).No patients had tumor recurrence or adverse outcomes related to liver resection during the follow-up period. Conclusion:Laparoscopic resection of FNH can be performed with few complications and a short retrieval length using reliable laparoscopic technology and skills. Surgical therapy for FNH is a safe procedure with low morbidity and an excellent prognosis.Resection can be an option for FNH patients with severe psychological problems or specific tumor location.

Background: We performed in vivo and in vitro experiments to observe the expression of long intergenic nonprotein coding RNA 1426 (LINC01426) in pancreatic cancer tissues and cells, investigate the impact of LINC01426 on the proliferation and migration of pancreatic cancer cells, and deduce the underlying molecular mechanism.Methods: LINC01426 expression was measured by fluorescence-based quantitative polymerase chain reaction (PCR) in pancreatic cancer tissues and cell lines. The lentiviral vector was used to create shRNA-NC, shLINC01426#2, pcDNA-NC, and pcDNA-LINC01426 pancreatic cancer cell lines. Cell Counting Kit-8 (CCK-8), clonogenic, and scratch tests were used to measure the effects of LINC01426 knockdown or overexpression on the migration and proliferation of pancreatic cancer cells. The expression levels of genes involved in migration (E-cadherin, N-cadherin, and vimentin) were examined by Western blotting after LINC01426 was either knocked down or overexpressed. The effect of LINC01426 knockdown on the proliferation of pancreatic cancer cells in vivo was verified in nude mice.Results: LINC01426 was highly expressed in pancreatic cancer cells and tissues. Overexpression of LINC01426 might have promoted the proliferation, clonogenicity, and migration of pancreatic cancer cells, while knockdown of LINC01426 decreased these activities. In pancreatic cancer cells, knockdown of LINC01426 dramatically enhanced E-cadherin expression while lowering N-cadherin and vimentin expression, whereas overexpression of LINC01426 had the opposite effect. Knockdown of LINC01426 substantially decreased pancreatic cancer cell proliferation in an in vivo study.Conclusions: Overexpression of LINC01426 was shown to increase the migration and proliferation of pancreatic cancer cells in both in vivo and in vitro experiments. LINC01426 could be a novel predictive biomarker and source of prospective therapeutic targets for patients with pancreatic cancer.