Involvement of the Interferon Signaling Pathways in Pancreatic Cancer Cells

Fujisawa, Mariko; Shibata, Toshikatsu; Sasaki, Reina; Masuzaki, Ryota; Matsumoto, Naoki; Nirei, Kazushige; Imazu, Hiroo; Kuroda, Kensuke; Sugitani, Masahiko; Takayama, Tadatoshi; Moriyama, Mitsuhiko

doi:10.21873/anticanres.14449

Cited by 15 publications

(11 citation statements)

References 45 publications

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“…Therefore, further studies will be conducted to fully uncover the role of combination use of GEM and DDP in PC. In addition, it has been recently reported that interferon signaling pathways are involved in the occurrence of PC and chronic pancreatitis ( 39 , 40 ). It is therefore hypothesized that interferon signaling pathways are important for the occurrence of PC and chronic pancreatitis and the relationship between NPTX1 and the interferon system in PC will be explored in a study.…”

Section: Discussionmentioning

confidence: 99%

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

Liu

et al. 2022

Oncol Lett

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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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Section: Discussionmentioning

confidence: 99%

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

Liu

et al. 2022

Oncol Lett

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“…Nanoparticles of SN-38 were recently reported to activate stimulator of interferon genes (STING) signaling pathway [31]. Interferon and the toll-like receptor 3 signaling pathway are potential pathways involved in the progression of pancreatic intraepithelial neoplasia to cancer and potential targets for pancreatic cancer treatment [32].…”

Section: Discussionmentioning

confidence: 99%

Efficacy and Safety of the Combination of Nano-Liposomal Irinotecan and 5-Fluorouracil/L-Leucovorin in Unresectable Advanced Pancreatic Cancer: A Real-World Study

et al. 2022

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Introduction: This retrospective study investigated the efficacy and safety of nano-liposomal irinotecan (nal-IRI) plus 5-fluorouracil/l-leucovorin (5-FU/l-LV) treatment in the second-line or later setting for advanced pancreatic cancer under real-world conditions. Methods: Between June 2020 and September 2021, a total of 44 patients with unresectable advanced pancreatic cancer treated with nal-IRI + 5-FU/l-LV in our affiliated hospitals were included. The prognosis, predictive factors (including systemic inflammation-based prognostic indicators), and adverse events were investigated. Results: The median age was 68 (interquartile range [IQR] 62-73) years old, and 22 patients (50.0%) were male. Concerning tumor factors, 9 patients (20.5%) had local advanced disease, and 35 patients (79.5%) had metastases. Twenty-five of the 44 patients were receiving second-line treatment, and 19 were receiving third-line or later treatment. The median overall survival (OS) and progression free survival (PFS) were 9.0 (range, 0.7-15.4) months and 4.4 (range, 0.6-15.4) months, respectively. The overall response rate (ORR) was 5.3%. The disease control rate (DCR) was 44.7%. Patients with a neutrophil-to-lymphocyte ratio (NLR) of >2.7 had a significant risk of a poor OS (HR=0.275, P=0.017). Adverse events were manageable, although gastrointestinal symptoms and neutropenia were observed. The most common grade ≥3 adverse event was neutropenia, which was reported in 20% of patients. Conclusions: Nal-IRI + 5-FU/l-LV therapy was considered to be a useful regimen as second-line or later treatment for unresectable advanced pancreatic cancer, even in clinical practice.

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“…Although it was also reported that Poly I:C can accelerate pancreatic carcinogenesis in KRAS-mutated mice [ 16 ] more recent evidence still supports its possible use as an adjuvant [ 37 , 105 , 106 ].…”

Section: Tlrs Agonistsmentioning

confidence: 99%

The Role of Toll-like Receptors (TLRs) Mediated Inflammation in Pancreatic Cancer Pathophysiology

Orlacchio

Mazzone

2021

IJMS

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Pancreatic cancer (PC) is one of the most lethal forms of cancer, characterized by its aggressiveness and metastatic potential. Despite significant improvements in PC treatment and management, the complexity of the molecular pathways underlying its development has severely limited the available therapeutic opportunities. Toll-like receptors (TLRs) play a pivotal role in inflammation and immune response, as they are involved in pathogen-associated molecular patterns (PAMPs) and danger-associated molecular patterns (DAMPs). Activation of TLRs initiates a signaling cascade, which in turn, leads to the transcription of several genes involved in inflammation and anti-microbial defense. TLRs are also deregulated in several cancers and can be used as prognostic markers and potential targets for cancer-targeted therapy. In this review we discuss the current knowledge about the role of TLRs in PC progression, focusing on the available TLRs-targeting compounds and their possible use in PC therapy.

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Involvement of the Interferon Signaling Pathways in Pancreatic Cancer Cells

Cited by 15 publications

References 45 publications

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

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

Efficacy and Safety of the Combination of Nano-Liposomal Irinotecan and 5-Fluorouracil/L-Leucovorin in Unresectable Advanced Pancreatic Cancer: A Real-World Study

The Role of Toll-like Receptors (TLRs) Mediated Inflammation in Pancreatic Cancer Pathophysiology

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