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Endometriotic cells of endometriomas synthesize and secrete TGF-beta1, which accumulates in the surrounding ovarian tissue, disorganizing extracellular matrix and promoting fibrosis, eventually forming fibrosis and adhesion to adjacent ovarian tissue.
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Overexpression of miR-145 blocked TGF-beta1-induced myofibroblastic differentiation.
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The results confirmed that miR127 regulates the expression of TGFbeta1/Smad3. The potential pathological mechanism of the effect of miR127 may be based on the upregulation of the TGFbeta1/Smad3 signaling pathway.
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The result suggests that IL-37 induces pro-angiogenic responses through TGF-beta, which may act as the bridging molecule that mediates IL-37 binding to the TGF-beta receptor complex.
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TGF-b, IL-10, and Foxp3 mRNA levels were significantly higher in patients with breast cancer than in healthy controls (P < 0.05). In summary, our results suggest that nutritional status, especially BMI, may strongly affect systematic immune function in patients with breast cancer
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The TGF-beta1 gene -509C/T promoter polymorphism might contribute to an increased risk of colorectal cancer (CRC); in particular, males with the CC genotype have a greater risk for CRC development and progression. Colorectal cancer tissue expression of TGFB1 gene mRNA correlates with tumor progression and metastasis.
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The extent of calcification correlated positively with the flow velocity, as did the mRNA and protein levels of TGF-beta1, BMP2, and MSX2. These findings indicate that TGF-beta1/BMP2 signaling is involved in valve calcification induced by abnormal mechanical stimulation.
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Our data uncover the ZEB1-miR-190-SMAD2 axis and provide a mechanism to explain the TGF-beta network in breast cancer metastasis.
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MiR-128-3p overactivates the TGF-beta pathway in the non-small cell lung cancer cells.
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TT genotype for TGFbeta C-509T had an increased risk and CC genotype for TGFbeta T869C had a decreased risk of gastric cancer in south Indian population
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propose that a positive feedback mechanism between uPAR, plasmin and transforming growth factor beta1 (TGFbeta1) selects cells in the monolayer for matrix invasion
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TGFbeta1 induces epithelial to mesenchymal morphology transition in TGFbeta1 sensitive non-small cell lung cancer (NSCLC) lines but not in insensitive lines. TGFbeta1 not only increases the mesenchymal maker Vimentin expression, but also enhances NSCLC cell invasiveness. TGFbeta1 elevates both the expression level of cancer stem-like cell markers and anchorage-dependent colony formation ability in TGFbeta1 sensitive l...
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Despite the higher TGFbeta1 secretion it was not observed changes in the morphology or proliferation of epithelial cells when diabetes or hypertension was present
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The results strongly suggest that the integrated pathway of TGF-beta/Snail with TNFalpha/NF-kappaB may be the principal axis that links cancer cells to their microenvironment during the epithelial-mesenchymal transition process and results in poor prognosis in colorectal cancer patients.
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Although decreased TGF-beta1 and IL-35 plasma levels correlate positively with decreased vitamin D levels and negatively with severity of coronary artery disease, only TGF-beta1 has a significant association with vitamin D deficiency in CAD patients.
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Findings suggest that glucocorticoids might be a useful therapy for preventing tissue remodeling by blocking the epithelial-to-mesenchymal transition initiated by TGF-beta1-induced MAPK and Snail/Slug signaling pathways in chronic rhinosinusitis with nasal polyps.
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The present study highlights possible new molecular mechanisms involving progesterone, including inhibition of TGF-beta1-activated Smad signaling and TGF-beta1-regulated genes involved in bronchopulmonary dysplasia pathogenesis, which are likely to attenuate the development of BPD by inhibiting TGF-beta1-mediated airway remodeling.
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We concluded that TGF-ss1-509C/T polymorphism was significantly associated with LC susceptibility, while the codon 10T/C polymorphism seemed to have a limited role in predicting the occurrence of LC induced by HBV/HCV infection.
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In this review, regulatory interactions between fibulins and TGF-beta are discussed. Understanding biological roles of fibulins in TGF-beta regulation may introduce new insights into the pathogenesis of some human diseases. [review]
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TGFbeta1 gene SNP rs1982073 might be correlated with congenital heart disease (CHD) susceptibility, and the T allele might decrease the disease risk. However, TGFbeta1 gene polymorphism rs1800471 was not related to CHD risk.