Expansion and Maintenance of CD133-Expressing Pancreatic Ductal Epithelial Cells by Inhibition of TGF-β Signaling

Zhang, Fangfang; Ma, Dongshen; Liu, Tingsheng; Liu, Yu Hong; Guo, Jiamin; Song, Jing; Wu, Qiong; Pan, Yi; Zhang, Yanfeng; Guo, Cui; Teng, Chun‐Bo

doi:10.1089/scd.2019.0087

Cited by 4 publications

(3 citation statements)

References 53 publications

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“…Co-expression of acinar markers and duct markers is used to detect ADM ( Figure 2 ). The co-expression of various digestive enzymes is not completely lost in acinar cells during ADM and there is a concomitant upregulated expression of the duct markers including Sox9 [ 33 ], Hnf1b [ 3 , 34 ], Hnf6 [ 35 ], Pdx1 [ 36 ], CA19–9 [ 37 ], CAII [ 38 ], CD133 [ 39 ], and osteopontin [ 40 ] (see Figure 1 ).…”

Section: Definition Of Acinar-to-ductal Metaplasia (Adm) and Transcri...mentioning

confidence: 99%

“…during ADM and there is a concomitant upregulated expression of the duct markers including Sox9 [33], Hnf1b [3,34], Hnf6 [35], Pdx1 [36], CA19-9 [37], CAII [38], CD133 [39], and osteopontin [40] (see Figure 1). The transcription factors Hnf1b, Hnf6, Pdx1 and Sox9 are known to play critical roles in the development and differentiation of pancreatic cells [41,42].…”

Section: Definition Of Acinar-to-ductal Metaplasia (Adm) and Transcri...mentioning

confidence: 99%

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Acinar-to-Ductal Metaplasia (ADM): On the Road to Pancreatic Intraepithelial Neoplasia (PanIN) and Pancreatic Cancer

Marstrand-Daucé,

Lorenzo,

Chassac

et al. 2023

IJMS

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Adult pancreatic acinar cells show high plasticity allowing them to change in their differentiation commitment. Pancreatic acinar-to-ductal metaplasia (ADM) is a cellular process in which the differentiated pancreatic acinar cells transform into duct-like cells. This process can occur as a result of cellular injury or inflammation in the pancreas. While ADM is a reversible process allowing pancreatic acinar regeneration, persistent inflammation or injury can lead to the development of pancreatic intraepithelial neoplasia (PanIN), which is a common precancerous lesion that precedes pancreatic ductal adenocarcinoma (PDAC). Several factors can contribute to the development of ADM and PanIN, including environmental factors such as obesity, chronic inflammation and genetic mutations. ADM is driven by extrinsic and intrinsic signaling. Here, we review the current knowledge on the cellular and molecular biology of ADM. Understanding the cellular and molecular mechanisms underlying ADM is critical for the development of new therapeutic strategies for pancreatitis and PDAC. Identifying the intermediate states and key molecules that regulate ADM initiation, maintenance and progression may help the development of novel preventive strategies for PDAC.

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Section: Definition Of Acinar-to-ductal Metaplasia (Adm) and Transcri...mentioning

confidence: 99%

Section: Definition Of Acinar-to-ductal Metaplasia (Adm) and Transcri...mentioning

confidence: 99%

Acinar-to-Ductal Metaplasia (ADM): On the Road to Pancreatic Intraepithelial Neoplasia (PanIN) and Pancreatic Cancer

Marstrand-Daucé,

Lorenzo,

Chassac

et al. 2023

IJMS

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“…Characteristic markers of ductal lineage are upregulated, including cytokeratins, carbonic anhydrase II (CAII), mucin, cystic fibrosis transmembrane receptor (CFTR), and transcription factors such as SOX9, HNF6, and HNF1β [58][59][60][61][62]. Murine pancreatic ducts are also selectively labeled by CD133, Dolichos biflorus agglutinin, and osteopontin [63][64][65]. Thus, the identity and evolution of PDM is regulated by a variety of signaling pathways and their cross-interactions.…”

Section: Molecular Pathologymentioning

confidence: 99%

Clinical significance of pancreatic ductal metaplasia

Jiang

Fang

Xie

2022

The Journal of Pathology

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Pancreatic ductal metaplasia (PDM) is the stepwise replacement of differentiated somatic cells with ductal or ductallike cells in the pancreas. PDM is usually triggered by cellular and environmental insults. PDM development may involve all cell lineages of the pancreas, and acinar cells with the highest plasticity are the major source of PDM. Pancreatic progenitor cells are also involved as cells of origin or transitional intermediates. PDM is heterogeneous at the histological, cellular, and molecular levels and only certain subsets of PDM develop further into pancreatic intraepithelial neoplasia (PanIN) and then pancreatic ductal adenocarcinoma (PDAC). The formation and evolution of PDM is regulated at the cellular and molecular levels through a complex network of signaling pathways. The key molecular mechanisms that drive PDM formation and its progression into PanIN/PDAC remain unclear, but represent key targets for reversing or inhibiting PDM. Alternatively, PDM could be a source of pancreas regeneration, including both exocrine and endocrine components. Cellular aging and apoptosis are obstacles to PDM-to-PanIN progression or pancreas regeneration. Functional identification of the cellular and molecular events driving senescence and apoptosis in PDM and its progression would help not only to restrict the development of PDM into PanIN/PDAC, but may also facilitate pancreatic regeneration. This review systematically assesses recent advances in the understanding of PDM physiology and pathology, with a focus on its implications for enhancing regeneration and prevention of cancer.

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Molecular signaling in pancreatic ductal metaplasia: emerging biomarkers for detection and intervention of early pancreatic cancer

Xie

2022

Cell Oncol.

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Expansion and Maintenance of CD133-Expressing Pancreatic Ductal Epithelial Cells by Inhibition of TGF-β Signaling

Cited by 4 publications

References 53 publications

Acinar-to-Ductal Metaplasia (ADM): On the Road to Pancreatic Intraepithelial Neoplasia (PanIN) and Pancreatic Cancer

Acinar-to-Ductal Metaplasia (ADM): On the Road to Pancreatic Intraepithelial Neoplasia (PanIN) and Pancreatic Cancer

Clinical significance of pancreatic ductal metaplasia

Molecular signaling in pancreatic ductal metaplasia: emerging biomarkers for detection and intervention of early pancreatic cancer

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