scholarly journals CCL20 induces colorectal cancer neoplastic epithelial cell proliferation, migration, and further CCL20 production through autocrine HGF-c-Met and MSP-MSPR signaling pathways

Oncotarget ◽  
2021 ◽  
Author(s):  
Bisweswar Nandi ◽  
Jonathan Pastrana Del Valle ◽  
Mehmet K. Samur ◽  
Allison J. Gibbons ◽  
Rao H. Prabhala ◽  
...  
Keyword(s):  
Colorectal Cancer ◽  
Cell Proliferation ◽  
Epithelial Cell ◽  
Signaling Pathways ◽  
Epithelial Cell Proliferation ◽  
Neoplastic Epithelial Cell

scholarly journals Uterine ALK3 is essential during the window of implantation

2015 ◽  
Vol 113 (3) ◽  
pp. E387-E395 ◽  
Author(s):  
Diana Monsivais ◽  
Caterina Clementi ◽  
Jia Peng ◽  
Mary M. Titus ◽  
James P. Barrish ◽  
...  
Keyword(s):  
Cell Proliferation ◽  
Epithelial Cell ◽  
Signaling Pathways ◽  
Transforming Growth Factor ◽  
Apical Cell ◽  
Uterine Epithelium ◽  
Conditional Knockout ◽  
Epithelial Cell Proliferation ◽  
Uterine Receptivity ◽  
Uterine Epithelial Cell

The window of implantation is defined by the inhibition of uterine epithelial proliferation, structural epithelial cell remodeling, and attenuated estrogen (E2) response. These changes occur via paracrine signaling between the uterine epithelium and stroma. Because implantation defects are a major cause of infertility in women, identifying these signaling pathways will improve infertility interventions. Bone morphogenetic proteins (BMPs) are TGF-β family members that regulate the postimplantation and midgestation stages of pregnancy. In this study, we discovered that signaling via activin-like kinase 3 (ALK3/BMPR1A), a BMP type 1 receptor, is necessary for blastocyst attachment. Conditional knockout (cKO) of ALK3 in the uterus was obtained by producing Alk3flox/flox-Pgr-cre–positive females. Alk3 cKO mice are sterile and have defects in the luminal uterine epithelium, including increased microvilli density and maintenance of apical cell polarity. Moreover, Alk3 cKO mice exhibit an elevated uterine E2 response and unopposed epithelial cell proliferation during the window of implantation. We determined that dual transcriptional regulation of Kruppel-like factor 15 (Klf15), by both the transforming growth factor β (TGF-β) transcription factor SMAD family member 4 (SMAD4) and progesterone receptor (PR), is necessary to inhibit uterine epithelial cell proliferation, a key step for embryo implantation. Our findings present a convergence of BMP and steroid hormone signaling pathways in the regulation of uterine receptivity.

Differential effects of EPA and DHA on DSS-induced colitis in mice and possible mechanisms involved

2021 ◽  
Author(s):  
Zhuangwei Zhang ◽  
Zhe Xue ◽  
Haitao Yang ◽  
Feng Zhao ◽  
Chundi Liu ◽  
...  
Keyword(s):  
Cell Proliferation ◽  
Epithelial Cell ◽  
Tight Junction ◽  
Signaling Pathways ◽  
Intestinal Epithelial Cell ◽  
Intestinal Epithelial ◽  
Epithelial Cell Proliferation ◽  
Tight Junction Proteins ◽  
Inflammatory Signaling ◽  
Junction Proteins

EPA, superior to DHA, significantly attenuated DSS-induced colitis involved in promoting the expression of tight junction proteins, suppressing inflammatory signaling pathways and triggering intestinal epithelial cell proliferation.

Sign in / Sign up

Export Citation Format

Share Document