scholarly journals Sox2 Cooperates with Inflammation-Mediated Stat3 Activation in the Malignant Transformation of Foregut Basal Progenitor Cells

2013 ◽  
Vol 12 (3) ◽  
pp. 304-315 ◽  
Author(s):  
Kuancan Liu ◽  
Ming Jiang ◽  
Yun Lu ◽  
Hao Chen ◽  
Jun Sun ◽  
...  
Keyword(s):  
Progenitor Cells ◽  
Malignant Transformation ◽  
Basal Progenitor

Ablation of cdk4 and cdk6 affects proliferation of basal progenitor cells in the developing dorsal and ventral forebrain

2018 ◽  
Vol 78 (7) ◽  
pp. 660-670 ◽  
Author(s):  
Alice Grison ◽  
Carine Gaiser ◽  
Andrea Bieder ◽  
Constanze Baranek ◽  
Suzana Atanasoski
Keyword(s):  
Progenitor Cells ◽  
Basal Progenitor

scholarly journals HIV induces airway basal progenitor cells to adopt an inflammatory phenotype

2021 ◽  
Vol 11 (1) ◽  
Author(s):  
Nancy P. Y. Chung ◽  
K. M. Faisal Khan ◽  
Robert J. Kaner ◽  
Sarah L. O’Beirne ◽  
Ronald G. Crystal
Keyword(s):  
Progenitor Cells ◽  
Inflammatory Mediators ◽  
Lung Inflammation ◽  
Mapk Signaling ◽  
Gm Csf ◽  
Basal Progenitor ◽  
Inflammatory Phenotype ◽  
Mapk Signaling Pathways ◽  
Chronic Hiv Infection

AbstractDespite the introduction of anti-retroviral therapy, chronic HIV infection is associated with an increased incidence of other comorbidities such as COPD. Based on the knowledge that binding of HIV to human airway basal stem/progenitor cells (BC) induces a destructive phenotype by increased MMP-9 expression through MAPK signaling pathways, we hypothesized that HIV induces the BC to express inflammatory mediators that contribute to the pathogenesis of emphysema. Our data demonstrate that airway BC isolated from HAART-treated HIV+ nonsmokers spontaneously release inflammatory mediators IL-8, IL-1β, ICAM-1 and GM-CSF. Similarly, exposure of normal BC to HIV in vitro up-regulates expression of the same inflammatory mediators. These HIV-BC derived mediators induce migration of alveolar macrophages (AM) and neutrophils and stimulate AM proliferation. This HIV-induced inflammatory phenotype likely contributes to lung inflammation in HIV+ individuals and provides explanation for the increased incidence of COPD in HIV+ individuals.

Basal progenitor cells bridge the development, malignant cancers, and multiple diseases of esophagus

2017 ◽  
Vol 233 (5) ◽  
pp. 3855-3866
Author(s):  
Baoshun Lin ◽  
Fuan Xie ◽  
Zhangwu Xiao ◽  
Xiaoqian Hong ◽  
Liming Tian ◽  
...  
Keyword(s):  
Progenitor Cells ◽  
Basal Progenitor

Interruption of Klf5 acetylation in basal progenitor cells promotes luminal commitment by activating Notch signaling

2021 ◽  
Author(s):  
Baotong Zhang ◽  
Siyuan Xia ◽  
Mingcheng Liu ◽  
Xiawei Li ◽  
Shimin Shuai ◽  
...  
Keyword(s):  
Notch Signaling ◽  
Progenitor Cells ◽  
Basal Progenitor

scholarly journals Anatomic Origin of Osteochondrogenic Progenitors Impacts Sensitivity to EWS-FLI1-Induced Transformation

Cancers ◽  
2019 ◽  
Vol 11 (3) ◽  
pp. 313 ◽  
Author(s):  
Elise Pfaltzgraff ◽  
April Apfelbaum ◽  
Andrew Kassa ◽  
Jane Song ◽  
Wei Jiang ◽  
...  
Keyword(s):  
Gene Expression ◽  
Cell Proliferation ◽  
Progenitor Cells ◽  
Malignant Transformation ◽  
Ewing Sarcoma ◽  
Hox Genes ◽  
High Expression ◽  
Wild Type ◽  
Superficial Zone ◽  
The Impact

Ewing sarcomas predominantly arise in pelvic and stylopod bones (i.e., femur and humerus), likely as a consequence of EWS-FLI1 oncogene-induced transformation of mesenchymal stem/progenitor cells (MSCs). MSCs located in the embryonic superficial zone cells (eSZ) of limbs express anatomically distinct posterior Hox genes. Significantly, high expression of posterior HOXD genes, especially HOXD13, is a hallmark of Ewing sarcoma. These data drove our hypothesis that Hox genes in posterior skeleton MSCs contribute to Ewing sarcoma tumorigenesis. We isolated eSZ cells from stylopod and zeugopod (i.e., tibia/fibula, radius/ulna) bones, from wild-type and Hoxd13 mutant embryos, and tested the impact of EWS-FLI1 transduction on cell proliferation, gene expression, and tumorigenicity. Our data demonstrate that both stylopod and zeugopod eSZ cells tolerate EWS-FLI1 but that stylopod eSZ cells are relatively more susceptible, demonstrating changes in proliferation and gene expression consistent with initiation of malignant transformation. Significantly, loss of Hoxd13 had no impact, showing that it is dispensable for the initiation of EWS-FLI1-induced transformation in mouse MSCs. These findings show that MSCs from anatomically distinct sites are differentially susceptible to EWS-FLI1-induced transformation, supporting the premise that the dominant presentation of Ewing sarcoma in pelvic and stylopod bones is attributable to anatomically-defined differences in MSCs.

Sign in / Sign up

Export Citation Format

Share Document