Multi-omics pan-cancer study of SPTBN2 and its value as a potential therapeutic target in pancreatic cancer.

SPTBN2 is a protein-coding gene that is closely related to the development of malignant tumors. However, its prognostic value and biological function in pan-cancer, especially pancreatic cancer (PAAD), have not been reported. In the present study, a novel exploration of the value and potential mechanism of SPTBN2 in PAAD was conducted using multi-omics in the background of pan-cancer. Via various database analysis, up-regulated expression of SPTBN2 was detected in most of the tumor tissues examined. Overexpression of SPTBN2 in PAAD and kidney renal clear cell cancer patients potentially affected overall survival, disease-specific survival, and progression-free interval. In PAAD, SPTBN2 can be used as an independent factor affecting prognosis. Mutations and amplification of SPTBN2 were detected, with abnormal methylation of SPTBN2 affecting its expression and the survival outcome of PAAD patients. Immunoassay results demonstrate that SPTBN2 was a potential biomarker for predicting therapeutic response in PAAD, and may influence the immunotherapy efficacy of PAAD by regulating levels of CD8 + T cells and neutrophil infiltration. Results from an enrichment analysis indicated that SPTBN2 may regulate the development of PAAD via immune pathways. Thus, SPTBN2 is a potential prognostic biomarker and immunotherapy target based on its crucial role in the development of PAAD.

Potential prognostic biomarkers of hepatocellular carcinoma based on 4D label-free quantitative proteomics analysis pilot investigation.

BACKGROUND: Hepatocellular carcinoma carries a poor prognosis and poses a serious threat to global health. Currently, there are few potential prognostic biomarkers available for the prognosis of hepatocellular carcinoma. METHODS: This pilot study used 4D label-free quantitative proteomics to compare the proteomes of hepatocellular carcinoma and adjacent non-tumor tissue. A total of 66,075 peptides, 6363 identified proteins, and 772 differentially expressed proteins were identified in specimens from three hepatocellular carcinoma patients. Through functional enrichment analysis of differentially expressed proteins by Gene Ontology, KEGG pathway, and protein domain, we identified proteins with similar functions. RESULTS: Twelve differentially expressed proteins (RPL17, RPL27, RPL27A, RPS5, RPS16, RSL1D1, DDX18, RRP12, TARS2, YARS2, MARS2, and NARS1) were selected for identification and validation by parallel reaction monitoring. Subsequent Western blotting confirmed overexpression of RPL27, RPS16, and TARS2 in hepatocellular carcinoma compared to non-tumor tissue in 16 pairs of clinical samples. Analysis of The Cancer Genome Atlas datasets associated the increased expression of these proteins with poor prognosis. Tissue microarray revealed a negative association between high expression of RPL27 and TARS2 and the prognosis of hepatocellular carcinoma patients, although RPS16 was not significant. CONCLUSIONS: These data suggest that RPL27 and TARS2 play an important role in hepatocellular carcinoma progression and may be potential prognostic biomarkers of overall survival in hepatocellular carcinoma patients.

Effect of RPL27 knockdown on the proliferation and apoptosis of human liver cancer cells.

RPL27 is linked to the development of various diseases including malignant tumors. RPL27 may play an oncogenic function in hepatocellular carcinoma (HCC), but this is unknown. So, the aim of this study was to investigate how the human liver cancer cell lines SNU449 and HepG2 responded to RPL27 knockdown in terms of proliferation and apoptosis. SNU449 and HepG2 were cultured and infected with shCon and shRPL27 lentiviral particles to induce RPL27 knockdown, and then RPL27 expression was detected using qPCR and Western blot. Cell proliferation was measured using CCK8, cell cloning, cell scraping, and transwell migration and invasion, while apoptosis was measured using flow cytometry (FCM). The qPCR revealed that mRNA expression of RPL27 decreased after knocking down RPL27 in cells. The CCK8 and cell cloning assay confirmed that knocking down RPL27 significantly reduced cell viability. The cell scratch assay and transwell assays showed that the proliferation rate decreased after knocking down RPL27. A substantial increase in apoptotic cells was discovered by FCM. According to WB, RPL27 knockdown increased the expression of Bax and Caspase-3 while decreasing the expression of bcl-2. The findings showed that RPL27 knockdown inhibited cell proliferation in SNU449 and HepG2 via inducing apoptosis, proving that RPL27 is a novel gene linked with HCC and is crucial for both proliferation and apoptosis. These outcomes imply that RPL27 may be a potential target for liver cancer diagnosis and therapy.

Risk Factors Related to Early Biliary Complications After Liver Transplantation: a Single-Center Analysis.

BACKGROUND: The aim of this study was to evaluate the risk factors of early biliary complications (EBC) after liver transplantation (LT) and seek effective treatments based on our single-center experience. METHODS: A total of 124 adult patients were divided into a non-EBC group and EBC group. EBC usually accounts for biliary leakage, biliary stricture, biliary stones, sphincter of Oddi dysfunction, and transient jaundice within 3 months after LT. Statistical analysis including logistic regression was performed to determine EBC risk factors. All procedures complied with the Helsinki Congress and the Declaration of Istanbul. RESULTS: Non-EBC (n = 95) and EBC (n = 29) were finally compared, which had no difference in their general characteristics. EBC occurred in 29 patients (26.92%): 1 biliary hemorrhage (3.45%), 7 biliary leakage (24.13%), and 16 biliary stricture (55.18%), and 5 others (17.24%). Of all EBC patients, endoscopic retrograde cholangiopancreatography (68.96%) was higher used to deal with complications than conservative treatment (10.35%), percutaneous transhepatic cholangial drainage (17.24%), and surgical treatment (3.45%). On univariate analyses, risk factors for EBC were bilirubin (P = .014), warm ischemia time (WIT) (P = .020), second WIT (P = .042), and operative time (OT) (P = .033). On multivariate analysis, independent risk factors for BC were WIT (P = .011) and OT (P = .049). CONCLUSIONS: The presence of WIT and OT were the independent risk factors for the development of EBC. In addition, we also confirmed that endoscopic retrograde cholangiopancreatography was beneficial and safe in the management of EBC after LT.