PRIM1 promotes the proliferation of hepatocellular carcinoma cells in vitro and in vivo

Abstract

PRIM1 plays an important role during oncogenesis, however it has never been reported in liver cancer, and thus our objective is to explore the role of PRIM1 in liver cancer. We selected RNAseq data of 50 paired liver cancer samples from the Cancer Gene Atlas (TCGA), and then bioinformatics methods and Mann-Whitney U test were used to analyze the correlation between PRIM1 and the clinical pathological stage of liver cancer. Quantitative polymerase chain reaction (QPCR) was used to detect mRNA expression of PRIM1 in BEL-7404, BCL-7402, HepG2 and SMMC-7721 cell lines. LV-PRIM1-RNAi was transfected into BEL-7404 and SMMC-7721 cells by lentivirus, and then Celigo imaging cytometer, Caspase3/7 Assay, flow cytometry and MTT assay were used to detect the proliferation and apoptosis of BEL-7404 and SMMC-7721 cells with ≥50% gene reduction rate after lentivirus transfection detected by QPCR. BEL-7404 and SMMC-7721 carrying PRIM1 gene were used for oncogenesis in vitro to observe the weight and fluorescence intensity of the tumor. Bioinformatics method was used to obtain the information about PRIM1 gene, and the correlation between PRIM1 and clinical pathological stage of liver cancer was analyzed by Mann-Whitney U test. QPCR results showed that PRIM1 was expressed in BEL-7404, BCL-7402, HepG2 and SMMC-7721 cell lines, which was highest in BCL-7404 cell line. Celigo imaging cytometer, Caspase3/7 Assay, flow cytometry and MTT assay showed that the proliferative ability of BEL-7404 and SMMC-7721 were decreased after LV-PRIM1-RNAi transfection. Furthermore, the weight and the fluorescence intensity of the tumors in vitro formed by LV-PRIM1-RNAi cells on SCID mice were decreased. So, interference of PRIM1 expression can inhibit the proliferation of BEL-7404 and SMMC-7721 cells, as well as induce the apoptosis of liver cancer cells.

YAP/TEAD-induced PRIM1 contributes to the progression and poor prognosis of gastric carcinoma

“…In the present study, knockdown of PRIM1 resulted in an increase in Cdc25, Cyclin B, and Cdc2, arresting the cell cycle in G2/M phase, along with a decrease in S-phase cells and an increase in sub-G1 phase cells (apoptotic cells). Knocking down PRIM1 in cancer cell lines increased apoptosis in our and other studies [ 31 , 32 ]. Therefore, our results revealed that PRIM1 was a tumor-promoting regulator that induced the malignant behavior of gastric carcinoma.…”

Cell-cycle and apoptosis related and proteomics-based signaling pathways of human hepatoma Huh-7 cells treated by three currently used multi-RTK inhibitors

“…PRIM1 containing two subunits synthesizes the RNA primer for the discontinuous DNA replication ( Lee et al, 2019 ). Silencing of PRIM1 gene expression in human hepatic carcinoma cells significantly inhibits the cell proliferation and increases the cell apoptosis ( Jiang et al, 2020 ). The relationship between DNA replication and MCM3 or MCM4 has been described above.…”

DNA primase subunit 1 deteriorated progression of hepatocellular carcinoma by activating AKT/mTOR signaling and UBE2C-mediated P53 ubiquitination

“…Besides, PRIM1 was also identified as a predictor that indicated poor survival of tumor patients. Though recent studies described the abnormal expression features of PRIM1 [ 15 ], the mechanisms underlying its oncogenic roles have not been elucidated.…”