Fibroblast subtypes in pancreatic cancer and pancreatitis: from mechanisms to therapeutic strategies DOI

Huizhen Huang,

Wanyi Lu,

Xiuli Zhang

et al.

Cellular Oncology, Journal Year: 2023, Volume and Issue: 47(2), P. 383 - 396

Published: Sept. 18, 2023

Language: Английский

Molecular profile of metastasis, cell plasticity and EMT in pancreatic cancer: a pre-clinical connection to aggressiveness and drug resistance DOI

Zhenli Guo,

Milad Ashrafizadeh, Wei Zhang

et al.

Cancer and Metastasis Reviews, Journal Year: 2023, Volume and Issue: 43(1), P. 29 - 53

Published: July 15, 2023

Language: Английский

Citations

46
Pancreatic cancer tumor microenvironment is a major therapeutic barrier and target DOI Creative Commons

Conner Hartupee,

Bolni Marius Nagalo, Chiswili Chabu

et al.

Frontiers in Immunology, Journal Year: 2024, Volume and Issue: 15

Published: Feb. 1, 2024

Pancreatic Ductal Adenocarcinoma (PDAC) is projected to become the 2nd leading cause of cancer-related deaths in United States. Limitations early detection and treatment barriers contribute lack substantial success this challenging-to-treat malignancy. Desmoplasia hallmark PDAC microenvironment that creates a physical immunologic barrier. Stromal support cells immunomodulatory face aberrant signaling by pancreatic cancer shifts complex balance proper repair mechanisms into state dysregulation. The product dysregulation desmoplastic environment encases malignant dense, hypoxic promotes further tumorigenesis, provides innate systemic resistance, suppresses anti-tumor immune invasion. This combined with immunoregulatory events allow it persist serve as primary focus review. barrier counterbalance tumor (TME) make an immunologically cold tumor. To convert hot tumor, could be considered alongside cells. We discuss network molecular cellular composition explore how they can targeted overcome immuno-therapeutic challenges.

Language: Английский

Citations

29
KRAS mutation: The booster of pancreatic ductal adenocarcinoma transformation and progression DOI Creative Commons
Zining Zhang, Heng Zhang, Xiang Liao

et al.

Frontiers in Cell and Developmental Biology, Journal Year: 2023, Volume and Issue: 11

Published: April 20, 2023

Pancreatic ductal adenocarcinoma (PDAC) is the most common type of pancreatic cancer. It has a poor response to conventional therapy and an extremely 5-year survival rate. PDAC driven by multiple oncogene mutations, with highest mutation frequency being observed in KRAS. The KRAS protein, which binds GTP, phosphokinase activity, further activates downstream effectors. contributes cancer cell proliferation, metabolic reprogramming, immune escape, resistance PDAC, acting as critical driver disease. Thus, positively associated poorer prognosis patients. This review focus on patterns emphases its role signal transduction, prognosis, hoping provide target strategies for PDAC.

Language: Английский

Citations

31
Immune-related gene SOX10 affects ferroptosis in pancreatic cancer and facilitates tumor progression by targeting CMTM7-mediated Wnt/β-catenin signaling pathway DOI Creative Commons

Guixing Jiang,

Bicheng Wu,

Kaikai Wang

et al.

European journal of medical research, Journal Year: 2025, Volume and Issue: 30(1)

Published: Jan. 4, 2025

SOX10 is crucially implicated in various cancer, yet the regulatory role pancreatic cancer (PC) remains enigmatic. Underlying molecular mechanisms of PC were explored our study.

Language: Английский

Citations

1
Exploring the biological mechanism and clinical value of perineural invasion in pancreatic cancer DOI
Hao Yuan, Yufeng Zhang, Fengyuan Liu

et al.

Cancer Letters, Journal Year: 2025, Volume and Issue: unknown, P. 217515 - 217515

Published: Jan. 1, 2025

Language: Английский

Citations

1
Pancreatic cancer and fibrosis: Targeting metabolic reprogramming and crosstalk of cancer-associated fibroblasts in the tumor microenvironment DOI Creative Commons
Xin Li, Jianbo Zhou, Xue Wang

et al.

Frontiers in Immunology, Journal Year: 2023, Volume and Issue: 14

Published: March 22, 2023

Pancreatic cancer is one of the most dangerous types today, notable for its low survival rate and fibrosis. Deciphering cellular composition intercellular interactions in tumor microenvironment (TME) a necessary prerequisite to combat pancreatic with precision. Cancer-associated fibroblasts (CAFs), as major producers extracellular matrix (ECM), play key role progression. CAFs display significant heterogeneity perform different roles Tumor cells turn into their slaves by inducing metabolic dysregulation, exacerbating fibrosis acquire drug resistance immune evasion. This article reviews impact reprogramming, effect obesity crosstalk on describes relevant therapies targeting reprogramming.

Language: Английский

Citations

15
Breaking the stromal barrier in pancreatic cancer: Advances and challenges DOI

Mohana Chakkera,

Jeremy B. Foote, Batoul Farran

et al.

Biochimica et Biophysica Acta (BBA) - Reviews on Cancer, Journal Year: 2023, Volume and Issue: 1879(1), P. 189065 - 189065

Published: Dec. 30, 2023

Language: Английский

Citations

14
Macroautophagy/autophagy promotes resistance to KRASG12D-targeted therapy through glutathione synthesis DOI Creative Commons
Leng Han,

Lingjun Meng,

Jiao Liu

et al.

Cancer Letters, Journal Year: 2024, Volume and Issue: 604, P. 217258 - 217258

Published: Sept. 13, 2024

Language: Английский

Citations

6
Glutamine Promotes Porcine Intestinal Epithelial Cell Proliferation through the Wnt/β-Catenin Pathway DOI

Yong-xia Fang,

En-Qing Lu,

Yujie Cheng

et al.

Journal of Agricultural and Food Chemistry, Journal Year: 2024, Volume and Issue: 72(13), P. 7155 - 7166

Published: March 25, 2024

Glutamine (Gln) is a critical nutrient required by neonatal mammals for intestinal growth, especially newborn piglets. However, the mechanisms underlying role of Gln in porcine epithelium development are not fully understood. The objective current study was to explore possible signaling pathway involved promotion epithelial cell (IPEC-J2) proliferation Gln. results showed that 1 mM promoted IPEC-J2 proliferation, and tandem mass tag proteomics revealed 973 differentially expressed proteins Gln-treated cells, 824 which were upregulated 149 downregulated. Moreover, gene set enrichment analysis indicated Wnt activated treatment. Western blotting further confirmed Wnt/β-catenin pathway. In addition, increased only cytosolic β-catenin but also nuclear protein expression. LF3 (a β-catenin/TCF4 interaction inhibitor) assay knockdown demonstrated Gln-mediated blocked. Furthermore, inhibition TCF4 expression suppressed Gln-induced proliferation. These findings Collectively, these positively regulated through data greatly enhance understanding mechanism regulates development.

Language: Английский

Citations

4
KIFC1 overexpression promotes pancreatic carcinoma progression via stabilizing BUB1 DOI Creative Commons
Xiaowei Fu,

Ao Cui,

Ying-Xue Yu

et al.

Research Square (Research Square), Journal Year: 2025, Volume and Issue: unknown

Published: Jan. 17, 2025

Abstract Pancreatic cancer (PC) is a highly lethal tumor of the gastrointestinal tract. New molecular targets are urgently needed for its treatment. Kinesin family member C1 (KIFC1) implicated in development and progression several types cancer. Previously, our studies indicated that KIFC1 overexpressed hepatocellular carcinoma activates malignant behavior through PI3K/AKT pathway. However, functional mechanisms PC have not been investigated. In this study, BUB1 were significantly upregulated patient samples, high expression was closely associated with phenotype poorer overall survival (OS) patients. Functional experiments showed knockdown inhibited cell growth vivo vitro, blocked cycle progression, hindered migration invasion. addition, reply induced behaviors dependent on BUB1. Mechanistically, regulates by competitively binding to reducing ubiquitination degradation. We shown first time regulatory mechanism between Therefore, shows promise as an attractive therapeutic target future.

Language: Английский

Citations

0