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Reprogramming the Tumor Microenvironment in Pancreatic Cancer
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Reprogramming the Tumor Microenvironment in 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: closed (31 October 2024) | Viewed by 5336

Special Issue Editor

Dr. Mi Kyung Park

E-Mail Website
Guest Editor
1. Department of Cancer Biomedical Science, Graduate School of Cancer Science and Policy National Cance Center, Goyang 10408, Republic of Korea
2. Department of Bio-Healthcare, Hwasung Medi-Science University, Hwaseong-si 18274, Republic of Korea
Interests: molecular mechanism; tumor microenvironment; epithelial-to-mesenchymal transition (EMT); post-translational modification (PTM); autophagy; potential therapeutic approaches; preclinical mouse models for cancers; breast cancer; liver cancer; lung cancer; pancreatic cancer; cancer progression and metastasis
Special Issues, Collections and Topics in MDPI journals

Special Issue Information

Dear Colleagues,

Pancreatic cancer constitutes a highly aggressive and deadly form of cancer that is resistant to conventional treatments. The tumor microenvironment (TME) plays a crucial role in disease progression, treatment response, and patient outcomes. Recent studies have shown that various components of the TME, such as cancer-associated fibroblasts, immune cells, extracellular matrix, and signaling molecules, actively contribute to pancreatic cancer development, invasion, and metastasis. Therefore, there is a growing interest in reprogramming the TME as a promising therapeutic approach to improve treatment outcomes and patient survival.

This Special Issue focuses on the latest advances in reprogramming the TME in pancreatic cancer, including the identification of novel therapeutic targets, the development of targeted therapeutics, and the evaluation of preclinical and clinical outcomes. The topics covered in this Issue include the role of TME components in pancreatic cancer progression, the molecular mechanisms underlying TME–T-cell interactions, the design and effectiveness of TME-targeted immunotherapy, emerging strategies for TME reprogramming, and the clinical translation of TME-based therapeutics. Overall, this Special Issue provides a comprehensive overview of the current state of the art and future prospects of TME reprogramming in pancreatic cancer.

Dr. Mi Kyung Park
Guest Editor

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Published Papers (2 papers)

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Research

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18 pages, 2549 KiB  
Article
TANK Binding Kinase 1 Promotes BACH1 Degradation through Both Phosphorylation-Dependent and -Independent Mechanisms without Relying on Heme and FBXO22
by Liang Liu, Mitsuyo Matsumoto, Miki Watanabe-Matsui, Tadashi Nakagawa, Yuko Nagasawa, Jingyao Pang, Bert K. K. Callens, Akihiko Muto, Kyoko Ochiai, Hirotaka Takekawa, Mahabub Alam, Hironari Nishizawa, Mikako Shirouzu, Hiroki Shima, Keiko Nakayama and Kazuhiko Igarashi
Int. J. Mol. Sci. 2024, 25(8), 4141; https://doi.org/10.3390/ijms25084141 - 9 Apr 2024
Viewed by 1655
Abstract
BTB and CNC homology 1 (BACH1) represses the expression of genes involved in the metabolism of iron, heme and reactive oxygen species. While BACH1 is rapidly degraded when it is bound to heme, it remains unclear how BACH1 degradation is regulated under other [...] Read more.
BTB and CNC homology 1 (BACH1) represses the expression of genes involved in the metabolism of iron, heme and reactive oxygen species. While BACH1 is rapidly degraded when it is bound to heme, it remains unclear how BACH1 degradation is regulated under other conditions. We found that FBXO22, a ubiquitin ligase previously reported to promote BACH1 degradation, polyubiquitinated BACH1 only in the presence of heme in a highly purified reconstitution assay. In parallel to this regulatory mechanism, TANK binding kinase 1 (TBK1), a protein kinase that activates innate immune response and regulates iron metabolism via ferritinophagy, was found to promote BACH1 degradation when overexpressed in 293T cells. While TBK1 phosphorylated BACH1 at multiple serine and threonine residues, BACH1 degradation was observed with not only the wild-type TBK1 but also catalytically impaired TBK1. The BACH1 degradation in response to catalytically impaired TBK1 was not dependent on FBXO22 but involved both autophagy-lysosome and ubiquitin-proteasome pathways judging from its suppression by using inhibitors of lysosome and proteasome. Chemical inhibition of TBK1 in hepatoma Hepa1 cells showed that TBK1 was not required for the heme-induced BACH1 degradation. Its inhibition in Namalwa B lymphoma cells increased endogenous BACH1 protein. These results suggest that TBK1 promotes BACH1 degradation in parallel to the FBXO22- and heme-dependent pathway, placing BACH1 as a downstream effector of TBK1 in iron metabolism or innate immune response. Full article
(This article belongs to the Special Issue Reprogramming the Tumor Microenvironment in Pancreatic Cancer)
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Review

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34 pages, 2305 KiB  
Review
Y-Box Binding Protein 1: Unraveling the Multifaceted Role in Cancer Development and Therapeutic Potential
by Ngoc Thi Minh Dinh, Tuan Minh Nguyen, Mi Kyung Park and Chang Hoon Lee
Int. J. Mol. Sci. 2024, 25(2), 717; https://doi.org/10.3390/ijms25020717 - 5 Jan 2024
Cited by 3 | Viewed by 3263
Abstract
Y-box binding protein 1 (YBX1), a member of the Cold Shock Domain protein family, is overexpressed in various human cancers and is recognized as an oncogenic gene associated with poor prognosis. YBX1’s functional diversity arises from its capacity to interact with a broad [...] Read more.
Y-box binding protein 1 (YBX1), a member of the Cold Shock Domain protein family, is overexpressed in various human cancers and is recognized as an oncogenic gene associated with poor prognosis. YBX1’s functional diversity arises from its capacity to interact with a broad range of DNA and RNA molecules, implicating its involvement in diverse cellular processes. Independent investigations have unveiled specific facets of YBX1’s contribution to cancer development. This comprehensive review elucidates YBX1’s multifaceted role in cancer across cancer hallmarks, both in cancer cell itself and the tumor microenvironment. Based on this, we proposed YBX1 as a potential target for cancer treatment. Notably, ongoing clinical trials addressing YBX1 as a target in breast cancer and lung cancer have showcased its promise for cancer therapy. The ramp up in in vitro research on targeting YBX1 compounds also underscores its growing appeal. Moreover, the emerging role of YBX1 as a neural input is also proposed where the high level of YBX1 was strongly associated with nerve cancer and neurodegenerative diseases. This review also summarized the up-to-date advanced research on the involvement of YBX1 in pancreatic cancer. Full article
(This article belongs to the Special Issue Reprogramming the Tumor Microenvironment in Pancreatic Cancer)
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