NPTX1 inhibits pancreatic cancer cell proliferation and migration and enhances chemotherapy sensitivity by targeting RBM10

Abstract

Pancreatic cancer (PC), one of the deadliest diseases worldwide, has exhibited an increasing incidence rate in recent years. The present study aimed to explore the biological mechanism of PC. Therefore, the expression levels of neuronal pentraxin 1 (NPTX1) and RNA‑binding protein 10 (RBM10) were detected in PC cell lines using reverse transcription‑quantitative PCR (RT‑qPCR) and western blot analyses prior to or following NPTX1 and RBM10 overex‑ pression. Additionally, the proliferative ability of PANC‑1 and BxPC‑3 cells treated with or without gemcitabine (GEM) and cisplatin (DDP) was evaluated using Cell Counting Kit‑8 assay. Cell apoptosis and the expression levels of apoptosis‑related proteins were determined by TUNEL assay and western blot analysis, respectively. Furthermore, wound healing and Transwell assays were performed to measure the migration and invasion abilities of PANC‑1 and BxPC‑3 cells. The interaction between RBM10 and NPTX1 mRNA was detected by RNA binding protein immunoprecipitation (RIP) assay. Additionally, cells were treated with actinomycin D to verify the regulatory effect of RBM10 on NPTX1 expression. This effect was further confirmed by RT‑qPCR analysis. The results showed that NPTX1 was downregulated in PC cell lines. In addition, NPTX1 overexpression inhibited the proliferation and promoted apoptosis in PC cells. The results from the wound healing and Transwell assays revealed that the migration and invasion abilities of PANC‑1 and BxPC‑3 cells were reduced following NPTX1 overexpression. However, treatment of NPTX1‑overexpressing cells with GEM or DDP attenuated PC cell viability. In addition, the results of the RIP assay revealed that RBM10 could bind with NPTX1. Furthermore, RBM10 overexpression could regulate NPTX1 expression, as evidenced by actinomycin D experi‑ ments. Overall, the results of the present study suggested that NPTX1 could inhibit PC and enhance the sensitivity of PC cells to chemotherapy. Additionally, NPTX1 was found to interact with RBM10, indicating that NPTX1 could inhibit PC via targeting RBM10.