Reports on the roles of the secreted trefoil factor (TFF)1 and 3 in colorectal cancer (CRC) and their underlying mechanisms of action in tumorigenesis are not common and are controversial. In the present study, the mRNA expression and promoter methylation of TFF1 and TFF3 in cancer and adjacent normal tissues were investigated, and their association with other clinical factors and patient prognosis were evaluated. Moreover, the association between TFF3 and epithelial‑mesenchymal transition (EMT) was explored by overexpressing or inhibiting TFF3 expression. The results revealed that the mRNA level of TFF1 and TFF3 in the cancer tissues was significantly higher than that in the matched adjacent normal tissues (P=0.034 and P=0.007, respectively), and a higher expression of TFF3, but not TFF1, was predominantly associated with clinicopathological factors and a poorer prognosis. No correlation was observed between promoter methylation and the expression of TFF1 or TFF3. The overexpression of TFF3 promoted the proliferation, migration and invasiveness of HT29 cells, and induced an increase in the expression of Twist1, Snail and Vimentin, while causing a decrease in E‑cadherin expression. On the contrary, the knockdown of TFF3 resulted in opposite effects in the LoVo cells. On the whole, the findings of this study indicate that TFF3 may be a promising new factor for the estimation of the survival of patients with CRC, and may promote the malignant progression of CRC by activating the EMT process. Therefore, TFF3 may be a future potential therapeutic target for CRC.
Download full-text PDF |
Source |
---|---|
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC6741840 | PMC |
http://dx.doi.org/10.3892/ijo.2019.4854 | DOI Listing |
Int J Mol Sci
August 2023
Institute of Molecular Biology and Medicinal Chemistry, Otto-von-Guericke University Magdeburg, Leipziger Str. 44, 39120 Magdeburg, Germany.
Tff1 is a typical gastric peptide secreted together with the mucin, Muc5ac. -deficient () mice are well known for their prominent gastric phenotype and represent a recognized model for antral tumorigenesis. Notably, intestinal abnormalities have also been reported in the past in these animals.
View Article and Find Full Text PDFZhonghua Er Bi Yan Hou Tou Jing Wai Ke Za Zhi
August 2023
Department of Otorhinolaryngology Head and Neck Surgery, the First Affiliated Hospital of Nanchang University, Nanchang 330006, China Jiangxi Provincial Institute of Otorhinolaryngology Head and Neck Surgery, Nanchang 330006, China.
To study the effect of trefoil factor family (TFF) 3 on the expression of tight junctions (TJs) in the nasal mucosa epithelium of eosinophilic chronic rhinosinusitis (eCRS) and its mechanism. From September to December 2020, eligible patients from the Department of Otorhinolaryngology of the First Affiliated Hospital of Nanchang University were recruited, including 11 control patients and 37 patients with chronic rhinosinusitis with nasal polyps (CRSwNP), from whom nasal mucosa and nasal polyp tissue samples were collected. Immunohistochemistry (IHC) was used to detect the localization and expression intensity of TFFs (TFF1, TFF2 and TFF3) and TJs (occudin, claudin-1 and ZO-1) in nasal mucosa.
View Article and Find Full Text PDFIndian J Otolaryngol Head Neck Surg
April 2023
Department of Medical Pathology, Lokman Hekim University, Ankara, Turkey.
The trefoil factor family (TFF) is a relatively new family of peptides. In some studies, an association between trefoil factors and inflammatory diseases of the nasal and paranasal sinuses has been suggested. However, it is still not clear whether there is a relationship between trefoil peptides and inflammation of the respiratory tract.
View Article and Find Full Text PDFTransl Oncol
July 2023
Department of Comparative Biosciences, University of Illinois Urbana-Champaign, Urbana, IL, 61801, USA. Electronic address:
G0/G1 switch gene 2 (G0S2) is known to inhibit lipolysis by inhibiting adipose triglyceride lipase (ATGL). In this report, we dissect the role of G0S2 in ER+ versus ER- breast cancer. Overexpression of G0S2 in ER- cells increased cell proliferation, while G0S2 overexpression in ER+ cells decreased cell proliferation.
View Article and Find Full Text PDFOncol Lett
April 2023
Department of Gastrointestinal Surgery, Graduate School of Medicine, The University of Tokyo, Tokyo 113-8655, Japan.
Enter search terms and have AI summaries delivered each week - change queries or unsubscribe any time!