Plastin-3 is a diagnostic and prognostic marker for pancreatic adenocarcinoma and distinguishes from diffuse large B-cell lymphoma

Abstract

Background Altered Plastin-3 (PLS3; an actin-binding protein) expression was associated with human carcinogenesis, including pancreatic ductal adenocarcinoma (PDA). This study first assessed differentially expressed genes (DEGs) and then bioinformatically and experimentally confirmed PLS3 to be able to predict PDA prognosis and distinguish PDA from diffuse large B-cell lymphoma. Methods This study screened multiple online databases and revealed DEGs among PDA, normal pancreas, diffuse large B-cell lymphoma (DLBCL), and normal lymph node tissues and then focused on PLS3. These DEGs were analyzed for Gene Ontology (GO) terms, Kaplan–Meier curves, and the log-rank test to characterize their association with PDA prognosis. The receiver operating characteristic curve (ROC) was plotted, and Spearman’s tests were performed. Differential PLS3 expression in different tissue specimens (n = 30) was evaluated by reverse transcription quantitative polymerase chain reaction (RT-qPCR). Results There were a great number of DEGs between PDA and lymph node, between PDA and DLBCL, and between PDA and normal pancreatic tissues. Five DEGs (NET1, KCNK1, MAL2, PLS1, and PLS3) were associated with poor overall survival of PDA patients, but only PLS3 was further verified by the R2 and ICGC datasets. The ROC analysis showed a high PLS3 AUC (area under the curve) value for PDA diagnosis, while PLS3 was able to distinguish PDA from DLBCL. The results of Spearman's analysis showed that PLS3 expression was associated with levels of KRT7, SPP1, and SPARC. Differential PLS3 expression in different tissue specimens was further validated by RT-qPCR. Conclusions Altered PLS3 expression was useful in diagnosis and prognosis of PDA as well as to distinguish PDA from DLBCL.

Detection of Marker Associated with CTC in Colorectal Cancer in Mononuclear Cells of Patients with Benign Inflammatory Intestinal Diseases

“…PLS3 has been identified as a suitable and prognostic marker for CTC detection in metastatic CRC, being also expressed in CTC which have undergone EMT [ 25 , 26 ]. Besides, PLS3 has been proven to be a prognostic and/or diagnostic tumor marker also in other tumor entities, e.g., non-small-cell lung cancer (NSCLC) or pancreatic ductal adenocarcinoma (PDAC) [ 27 , 28 ].…”

The H2A.Z-KDM1A complex promotes tumorigenesis by localizing in the nucleus to promote SFRP1 promoter methylation in cholangiocarcinoma cells

“…Two microarrays containing the mRNA sequencing data of cholangiocarcinoma tissue (GSE32879 and GSE76297) and two microarrays containing methylation data of cholangiocarcinoma tissue (GSE38860 and GSE49656) were downloaded from the Gene Expression Omnibus database (GEO; https://www.ncbi.nlm.nih.gov/geo/ ) [ 23 ]. The data were normalized according to the description provided by the uploaders, which is available in the database.…”

“…Total RNA was extracted from the various cell groups using TRIzol reagent (Invitrogen, California, USA), and each RNA sample (400 ng) was reverse transcribed into cDNA using a PrimeScript RT Reagent Kit (Takara, Dalian, China), as directed by the manufacturer. The relative levels of targeted gene mRNA transcripts to the control GAPDH were measured by quantitative real-time PCR using ChamQ Universal SYBR qPCR Master Mix (Vazyme, Nanjing, China) and specific primers in the iQ5 quantitative PCR detection system (Bio-Rad, Richmond, CA, USA) [ 23 ]. The sequences of the primers were as follows: SFRP1-F, 5’-GAGCCGGTCATGCAGTTCTT-3’ and SFRP1-R, 5’-CGTTGTCACAGGGAGGACAC-3’; H2A.Z-F, 5’-GGCAGGAAATGCATCAAAAG-3’ and H2A.Z-R, 5’-TGGATGTGTGGAATGACACC-3’; GAPDH-F, 5’-TTTGTCAAGCTCATTTCCTGG-3’ and GAPDH-R, 5’-TGATGGTACATGACAAGGTGC-3’.…”

Keratin 8 Is an Inflammation-Induced and Prognosis-Related Marker for Pancreatic Adenocarcinoma

“…(2) The marker should be used for the diagnosis of PDAC. (3) The marker should indicate the prognosis of PDAC patients. Here, we assessed differentially expressed genes (DEGs) by bioinformatic methods with the expression profiles available online for a caerulein-induced mouse model and human PDAC tissue based on the etiology of PDAC.…”

“…The overall 5-year survival rate of PDAC is approximately 9% [ 1 ]. Although the incidence rate is relatively low, the mortality rate of PDAC is high due to its absence of early symptoms, high invasive ability, and delayed diagnosis [ 2 , 3 ]. Surgical treatment is the best treatment for PDAC patients in the early stages.…”