ArticleOncology letters2022
NPTX1 inhibits pancreatic cancer cell proliferation and migration and enhances chemotherapy sensitivity by targeting RBM10.
Article in Oncology letters, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 10 papers.
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Who cites it
10 citing papers in PubMed, 13 citations in OpenAlex.
- Integrative Proteomic Analysis Reveals VMG Oncolytic Virus-Induced Molecular Reprogramming in Pancreatic Ductal Adenocarcinoma.Research square · 2026Article
- The emerging role of exosomal circRNAs in modulating apoptotic pathways and overcoming cancer therapy resistance.Discover oncology · 2026Review
- The Emerging Role of FAM171A2 in Gynecological Malignancies: Bioinformatic Insights from UCEC and Ovarian Cancer.International journal of molecular sciences · 2025Article
- Bioinformatic prediction of key genes involved in pro-chondrogenic effect of fragmentated cartilage transplantation.Scientific reports · 2025Article
- Expression pattern, immune signature, and prognostic value of RBM10 in human cancers.Histology and histopathology · 2025Article
- RBM10 inhibits pancreatic cancer development by suppressing immune escape through PD-1 expression.Journal of Cancer · 2025Article
- Development and verification of lymphangiogenesis score for prediction of prognosis and immune landscape in gastric cancer.Frontiers in immunology · 2025Article
- Can DNA Methylation Profiling Classify Histologic Subtypes and Grades in Soft Tissue Sarcoma?Clinical orthopaedics and related research · 2024Article
- From Fruit Waste to Medical Insight: The Comprehensive Role of Watermelon Rind Extract on Renal Adenocarcinoma Cellular and Transcriptomic Dynamics.International journal of molecular sciences · 2023Article
- Exosome-delivered circRPS5 inhibits the progression of melanoma via regulating the miR-151a/NPTX1 axis.PloS one · 2023Article
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Authors and funding
4 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
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 overexpression. 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 experiments. 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.
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