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IJMS
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Molecular and Cellular Mechanisms of Pancreatic Cancer
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Molecular and Cellular Mechanisms of Pancreatic Cancer

A special issue of International Journal of Molecular Sciences (ISSN 1422-0067). This special issue belongs to the section "Molecular Oncology".

Deadline for manuscript submissions: 20 June 2025 | Viewed by 5340

Special Issue Editor

Dr. Sanith Cheriyamundath

E-Mail Website
Guest Editor
Rutgers Cancer Institute of New Jersey, Rutgers University, New Brunswick, NJ 08901, USA
Interests: cancer biology; molecular oncology; PDAC; micro-environment; cancer-associated fibroblast; metastasis; novel therapy

Special Issue Information

Dear Colleagues,

Pancreatic ductal adenocarcinoma (PDAC) is among the most lethal human cancers, with only a five-year overall survival rate in 11% of patients. This poor survival rate is due to the inability to detect PDAC at an early stage and the lack of effective treatment. Mutations are one of the key drivers of PDAC. KRAS, TP53, CDKN2A, SMAD4, and BRCA mutations are frequently observed in PDAC. Additionally, in more than 85% of cases, PDAC is triggered by KRAS mutations such as G12D, G12V, G12R, and G12C. At present, chemotherapy represents the main strategic treatment for unresectable tumors, and its efficacy is limited compared to novel chemotherapy regimens such as FOLFIRINOX and gemcitabine plus nab-paclitaxel. Resistance towards treatments is common for chemotherapy and radiotherapy, and PDAC remains recalcitrant to numerous immune checkpoint therapy agents, such as anti-PD- 1, anti-PD-L1, and anti-CTLA4. The presence of extensive desmoplasia and immunosuppressive conditions in the PDAC stroma is one of the underlying reasons for treatment resistance and failure. Understanding the molecular and cellular mechanisms of PDAC progression and metastasis, and the interaction of cancer cells with stromal cells, will help to improve our knowledge of the biology of PDAC progression, and will aid in developing therapeutic strategies for PDAC and improving its prognosis.

In this Special Issue of IJMS, we invite authors to contribute original research and review articles focusing on elucidating the fundamental molecular and cellular mechanisms underlying the biology of PDAC.

Dr. Sanith Cheriyamundath
Guest Editor

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Manuscripts should be submitted online at www.mdpi.com by registering and logging in to this website. Once you are registered, click here to go to the submission form. Manuscripts can be submitted until the deadline. All submissions that pass pre-check are peer-reviewed. Accepted papers will be published continuously in the journal (as soon as accepted) and will be listed together on the special issue website. Research articles, review articles as well as short communications are invited. For planned papers, a title and short abstract (about 100 words) can be sent to the Editorial Office for announcement on this website.

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Keywords

  • PDAC
  • metastasis
  • tumor microenvironment
  • cancer-associated fibroblasts
  • KRAS
  • immune cells
  • inhibitors
  • resistance
  • signaling pathways
  • EMT

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Published Papers (2 papers)

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Research

14 pages, 3522 KiB  
Article
Pancreatic Adenocarcinoma Up-Regulated Factor (PAUF) Transforms Human Monocytes into Alternative M2 Macrophages with Immunosuppressive Action
by Yeon Jeong Kim, Sitansu Sekhar Nanda, Fen Jiang, Seung Yeon Pyo, Jin-Yeong Han, Sang Seok Koh and Tae Heung Kang
Int. J. Mol. Sci. 2024, 25(21), 11545; https://doi.org/10.3390/ijms252111545 - 27 Oct 2024
Viewed by 1697
Abstract
Tumor-associated macrophages (TAMs) in the tumor microenvironment (TME) promote immune evasion, cancer cell proliferation, and metastasis. Ongoing research is focused on finding ways to prevent tumor growth by inhibiting TAM polarization, which has shown a correlation with unfavorable prognosis in clinical studies. Pancreatic [...] Read more.
Tumor-associated macrophages (TAMs) in the tumor microenvironment (TME) promote immune evasion, cancer cell proliferation, and metastasis. Ongoing research is focused on finding ways to prevent tumor growth by inhibiting TAM polarization, which has shown a correlation with unfavorable prognosis in clinical studies. Pancreatic adenocarcinoma up-regulated factor (PAUF) is a protein secreted from pancreatic cancer (PC) and acts as a TME modulator that affects the TME by acting on not only cancer cells but also stromal cells and immune cells. Tumor cells can evade the immune system by PAUF binding to Toll-like receptor (TLR) in monocytes, as this research shows. In this study, the examination centered around the recruitment of human monocytes by PAUF and the subsequent differentiation into macrophages. In an in vitro chemotaxis assay, PAUF induced chemotactic migration of TLR2-mediated monocytes. In addition, PAUF induced differentiation of monocytes into M2 macrophages, which was verified based on expressing surface markers and cytokines and morphological analysis. The inhibition of T cell proliferation and function was observed in differentiated M2 macrophages. To conclude, these findings indicate that PAUF functions as a promoter of cancer progression by regulating the recruitment and differentiation of macrophages within TMEs, ultimately causing immunosuppression. Full article
(This article belongs to the Special Issue Molecular and Cellular Mechanisms of Pancreatic Cancer)
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16 pages, 3151 KiB  
Article
Decoding Metabolic Symbiosis between Pancreatic Cancer Cells and Cancer-Associated Fibroblasts Using Cultured Tumor Microenvironment
by Yuma Nihashi, Xiaoyu Song, Masamichi Yamamoto, Daiki Setoyama and Yasuyuki S. Kida
Int. J. Mol. Sci. 2023, 24(13), 11015; https://doi.org/10.3390/ijms241311015 - 3 Jul 2023
Cited by 3 | Viewed by 2441
Abstract
Pancreatic ductal adenocarcinoma (PDAC) is a highly aggressive cancer with a poor prognosis, largely due to its unique tumor microenvironment (TME) and dense fibrotic stroma. Cancer-associated fibroblasts (CAFs) play a crucial role in promoting tumor growth and metastasis, contributing to the metabolic adaptation [...] Read more.
Pancreatic ductal adenocarcinoma (PDAC) is a highly aggressive cancer with a poor prognosis, largely due to its unique tumor microenvironment (TME) and dense fibrotic stroma. Cancer-associated fibroblasts (CAFs) play a crucial role in promoting tumor growth and metastasis, contributing to the metabolic adaptation of PDAC cells. However, the metabolic interactions between PDAC cells and CAFs are not well-understood. In this study, an in vitro co-culture model was used to investigate these metabolic interactions. Metabolomic analysis was performed under monoculture conditions of Capan−1 PDAC cells and CAF precursor cells, as well as co-culture conditions of PDAC cells and differentiated inflammatory CAF (iCAF). Co-cultured Capan−1 cells displayed significant metabolic changes, such as increased 2-oxoglutaric acid and lauric acid and decreased amino acids. The metabolic profiles of co-cultured Capan−1 and CAFs revealed differences in intracellular metabolites. Analysis of extracellular metabolites in the culture supernatant showed distinct differences between Capan−1 and CAF precursors, with the co-culture supernatant exhibiting the most significant changes. A comparison of the culture supernatants of Capan−1 and CAF precursors revealed different metabolic processes while co-culturing the two cell types demonstrated potential metabolic interactions. In conclusion, this study emphasizes the importance of metabolic interactions between cancer cells and CAFs in tumor progression and highlights the role of TME in metabolic reprogramming. Full article
(This article belongs to the Special Issue Molecular and Cellular Mechanisms of Pancreatic Cancer)
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