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Molecular Targets in Preventing Pancreatic Cancer Progression
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Molecular Targets in Preventing Pancreatic Cancer Progression

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 December 2023) | Viewed by 5907

Special Issue Editor

Dr. Sijo Mathew

E-Mail Website
Guest Editor
Department of Pharmaceutical Sciences, School of Pharmacy, North Dakota State University, Fargo, ND 58105, USA
Interests: matrix proteins; integrin; pancreatic cancer

Special Issue Information

Dear Colleagues, 

Pancreatic cancer is the seventh leading cause of cancer mortality in the world and the third leading cause in the USA. The five-year survival rate for pancreatic cancer is 9%, which is the lowest of all cancers. In addition, it is typically diagnosed at an advanced stage with a very poor prognosis. The survival rate at the early stage of diagnosis is also under 31%. Majority of the pancreatic cancers are exocrine cancers. Advances in next-generation sequencing have revealed the very heterogeneous nature of pancreatic cancer, which develops resistance to conventional chemotherapy and radiotherapy. Another key component of chemotherapy resistance is the desmoplasia of the tumor microenvironment in pancreatic ductal adenoma (PDAC). Understanding the molecular details of PDAC is important to an effective treatment intervention. Pancreatic organoids and 3D culture studies have made significant contributions to the advancement of research into the mechanism and development of drugs in pancreatic cancer. Recent progress in targeted drug delivery is an important tool to help prevent PDAC's progression. Exosome-based diagnosis also contributes greatly to early detection efforts.

For this special issue, the research articles, methods and  reviews on molecular mechanism of pancreatic cancer, pancreatic organoids, exosomes, genetical approaches, in vitro, and in vivo on pancreatic cancer are invited. Besides, we’d like to gratefully acknowledge Dr. Anil Mathew Tharappel’s support in setting up, promoting, and developing this Special Issue.

Dr. Sijo Mathew
Guest Editor

Manuscript Submission Information

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.

Submitted manuscripts should not have been published previously, nor be under consideration for publication elsewhere (except conference proceedings papers). All manuscripts are thoroughly refereed through a single-blind peer-review process. A guide for authors and other relevant information for submission of manuscripts is available on the Instructions for Authors page. International Journal of Molecular Sciences is an international peer-reviewed open access semimonthly journal published by MDPI.

Please visit the Instructions for Authors page before submitting a manuscript. There is an Article Processing Charge (APC) for publication in this open access journal. For details about the APC please see here. Submitted papers should be well formatted and use good English. Authors may use MDPI's English editing service prior to publication or during author revisions.

Keywords

  • pancreatic cancer
  • molecular markers
  • pancreatic ductal adenocarcinoma
  • organoids
  • exosomes
  • drug delivery
  • diagnosis
  • desmoplasia
  • 3D culture
  • integrin
  • tumor microenvironment
  • hypoxia
  • PDX models

Published Papers (3 papers)

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Research

20 pages, 2710 KiB  
Article
Target-Specific Nanoparticle Polyplex Down-Regulates Mutant Kras to Prevent Pancreatic Carcinogenesis and Halt Tumor Progression
by Jill P. Smith, Wenqiang Chen, Narayan Shivapurkar, Monica Gerber, Robin D. Tucker, Bhaskar Kallakury, Siva Sai Krishna Dasa, Ruvanthi N. Kularatne and Stephan T. Stern
Int. J. Mol. Sci. 2023, 24(1), 752; https://doi.org/10.3390/ijms24010752 - 01 Jan 2023
Viewed by 1977
Abstract
Survival from pancreatic cancer is poor because most cancers are diagnosed in the late stages and there are no therapies to prevent the progression of precancerous pancreatic intraepithelial neoplasms (PanINs). Inhibiting mutant KRASG12D, the primary driver mutation in most human pancreatic [...] Read more.
Survival from pancreatic cancer is poor because most cancers are diagnosed in the late stages and there are no therapies to prevent the progression of precancerous pancreatic intraepithelial neoplasms (PanINs). Inhibiting mutant KRASG12D, the primary driver mutation in most human pancreatic cancers, has been challenging. The cholecystokinin-B receptor (CCK-BR) is absent in the normal pancreas but becomes expressed in high grade PanIN lesions and is over-expressed in pancreatic cancer making it a prime target for therapy. We developed a biodegradable nanoparticle polyplex (NP) that binds selectively to the CCK-BR on PanINs and pancreatic cancer to deliver gene therapy. PanIN progression was halted and the pancreas extracellular matrix rendered less carcinogenic in P48-Cre/LSL-KrasG12D/+ mice treated with the CCK-BR targeted NP loaded with siRNA to mutant Kras. The targeted NP also slowed proliferation, decreased metastases and improved survival in mice bearing large orthotopic pancreatic tumors. Safety and toxicity studies were performed in immune competent mice after short or long-term exposure and showed no off-target toxicity by histological or biochemical evaluation. Precision therapy with target-specific NPs provides a novel approach to slow progression of advanced pancreatic cancer and also prevents the development of pancreatic cancer in high-risk subjects without toxicity to other tissues. Full article
(This article belongs to the Special Issue Molecular Targets in Preventing Pancreatic Cancer Progression)
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19 pages, 4070 KiB  
Article
PAUF Induces Migration of Human Pancreatic Cancer Cells Exclusively via the TLR4/MyD88/NF-κB Signaling Pathway
by So Eun Youn, Fen Jiang, Hye Yun Won, Da Eun Hong, Tae Heung Kang, Yun-Yong Park and Sang Seok Koh
Int. J. Mol. Sci. 2022, 23(19), 11414; https://doi.org/10.3390/ijms231911414 - 27 Sep 2022
Cited by 4 | Viewed by 1875
Abstract
PAUF, a tumor-promoting protein secreted by cancer cells, exerts paracrine effects on immune cells through TLR4 receptors expressed on immune cell surfaces. This study aimed to investigate if PAUF elicits autocrine effects on pancreatic cancer (PC) cells through TLR4, a receptor that is [...] Read more.
PAUF, a tumor-promoting protein secreted by cancer cells, exerts paracrine effects on immune cells through TLR4 receptors expressed on immune cell surfaces. This study aimed to investigate if PAUF elicits autocrine effects on pancreatic cancer (PC) cells through TLR4, a receptor that is overexpressed on PC cells. In this study, TLR4 expression was detected in PC cells only, but not normal pancreatic cells. The migration of TLR4 high-expressing PC cells (i.e., BxPC-3) was reduced by a selective TLR4 inhibitor, in a dose-dependent manner. Using TLR4 overexpressed and knockout PC cell lines, we observed direct PAUF-TLR4 binding on the PC cell surfaces, and that PAUF-induced cancer migration may be mediated exclusively through the TLR4 receptor. Further experiments showed that PAUF signaling was passed down through the TLR4/MyD88 pathway without the involvement of the TLR4/TRIF pathway. TLR4 knockout also downregulated PC membrane PD-L1 expression, which was not influenced by PAUF. To the best of our knowledge, TLR4 is the first receptor identified on cancer cells that mediates PAUF’s migration-promoting effect. The results of this study enhanced our understanding of the mechanism of PAUF-induced tumor-promoting effects and suggests that TLR4 expression on cancer cells may be an important biomarker for anti-PAUF treatment. Full article
(This article belongs to the Special Issue Molecular Targets in Preventing Pancreatic Cancer Progression)
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19 pages, 6084 KiB  
Article
Prognostic Value, Immune Signature, and Molecular Mechanisms of the PHLDA Family in Pancreatic Adenocarcinoma
by Yunjie Duan, Yongxing Du, Zongting Gu, Xiaohao Zheng and Chengfeng Wang
Int. J. Mol. Sci. 2022, 23(18), 10316; https://doi.org/10.3390/ijms231810316 - 07 Sep 2022
Cited by 2 | Viewed by 1518
Abstract
Background: Increasing evidence supports the belief that the pleckstrin homology domain family A (PHLDA) family is associated with the development of a variety of cancers. However, the function of the PHLDA family members in PAAD is still unclear. Methods: Comprehensive bioinformatic analyses using [...] Read more.
Background: Increasing evidence supports the belief that the pleckstrin homology domain family A (PHLDA) family is associated with the development of a variety of cancers. However, the function of the PHLDA family members in PAAD is still unclear. Methods: Comprehensive bioinformatic analyses using R (version 3.6.3), Cytoscape (version 3.9.1), UALCAN, etc., were performed to study the clinicopathological characteristics, prognostic value, immune features, and functional mechanisms of the PHLDA family members in PAAD. Results: The PHLDA family members showed significantly elevated expression in PAAD compared with paracancerous or normal tissues. Their high expression or amplification were significantly correlated with worse clinicopathological characteristics and prognosis in PAAD patients. In addition, the role of the PHLDA family members in the immune regulation is diverse and complex. Mechanistically, TP53 mutations were significantly associated with the promoter methylation and expression levels of the PHLDA family members, which were activated in multiple oncogenic pathways, including the EMT, RAS/MAPK, and TSC/mTOR pathways. Moreover, we found that their expression levels were significantly correlated with the sensitivity of multiple traditional chemotherapeutic drugs and novel targeted MEK1/2 inhibitors. Conclusion: The PHLDA family members play an oncogenic role in the development of PAAD and might serve as new biomarkers or therapeutic targets. Full article
(This article belongs to the Special Issue Molecular Targets in Preventing Pancreatic Cancer Progression)
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