In particular, increase in the invasion ability of MSCs by TGF-β1 and decrease in p53, which plays a key role in cancer development, is an important discovery.
Multivariable logistic regression of cancer status in an over-dominant TGFB1rs1800469/TGFBR1 rs11568785 model demonstrated a 3.03-fold reduction in cervical cancer odds.
The differential modulation of important cellular pathways like TGF-β1 and STAT1 can explain the sensitivity of tissues to HPV cancer progression.<b>IMPORTANCE</b> Although the high-risk human papillomavirus 16 infects anogenital and oropharyngeal sites, the cervical epithelium has a unique vulnerability to progression of cancer.
The plasma expression levels of snaR and TGF-β1 were positively correlated in patients with HCC; however, not in healthy controls. snaR overexpression significantly promoted cancer cell migration and invasion, and additionally increased TGF-β1 expression.
The TG-interacting factor 1 (TGIF1) gene, which encodes a nuclear transcriptional corepressor of the TGFβ1/Smad signaling pathway, has been implicated in the pathogenesis of various types of human cancer; however, its role in pancreatic ductal adenocarcinoma (PDAC) has yet to be elucidated.
The observations in this study identify an important regulatory mechanism of fascin-1 in BLCA, and the TGF-β1/ZEB1-AS1/miR-200b/FSCN1 axis may serve as a potential target for cancer therapeutic purposes.
Tumor cell epithelial-mesenchymal transition (EMT), which can be induced by transforming growth factor β1 (TGFβ1), has been regarded as a significant contributor to cancer invasion and migration.
Studies have demonstrated that transforming growth factor beta-1 (TGF-β1) exhibits oncogenic activity in different types of cancer, including ovarian cancer (OC).
GASL1 overexpression and knockdown cancer cell lines were constructed and the effects on transforming growth factor β1 (TGF-β1) expression and cell proliferation were explored by Western blot and CCK-8 assay, respectively.
Transforming growth factor-β1 (TGF-β1) is one of very few cytokines produced in a latent form, requiring activation to exert any of its vastly diverse effects on development, immunity, and cancer.
Down-regulation of lncRNA snaR effectively distinguished HPV-negative CSCC patients from healthy controls. lncRNA snaR was further down-regulated in patients with distant recurrence (DR) but not in patients with local-recurrence or without recurrence. lncRNA snaR overexpression decreased TGF-β1 expression in CSCC cells, while exogenous TGF-β1 treatment showed no significant effects on lncRNA snaR expression. lncRNA snaR overexpression inhibited cancer cell migration and invasion, while TGF-β1 treatment attenuated the inhibitory effect of lncRNA snaR overexpression on cancer cell migration and invasion.
Moreover, TGFβ1 was able to enhance the mRNA expression of Oct4, Nanog and Sox2 and drastically increased anchorage-independent colony formation in TGFβ1-sensitive NSCLC cells, suggesting the acquisition of cancer stem-like properties.
Markers relevant for bulk cancer cell migration were regulated differently when compared with EMT: Twist expressed in primary tumour, invasion front, and metastasis was not associated with TGFβ1 and canonical Wnt, as Slug, Snail, and Smads were negative and β-Catenin expressed membraneously.
Here, we used genetic engineering to generate a stable SMAD3-silencing human NK cell line, NK-92-S3KD, whose cancer-killing activity and cytokine production were significantly enhanced under TGFβ1-rich condition compared with the parental cell line.