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GENE:

SMAD7 (SMAD Family Member 7)

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Other names: SMAD7, SMAD Family Member 7, Mothers Against Decapentaplegic Homolog 7, Mothers Against DPP Homolog 8, MAD Homolog 8, HSMAD7, MADH7, MADH8, MAD (Mothers Against Decapentaplegic, Drosophila) Homolog 7, MAD, Mothers Against Decapentaplegic Homolog 7 (Drosophila), Mothers Against Decapentaplegic, Drosophila, Homolog Of, 7 , SMAD, Mothers Against DPP Homolog 7 (Drosophila), Mothers Against Decapentaplegic Homolog 8, SMAD, Mothers Against DPP Homolog 7, Mothers Against DPP Homolog 7, MAD Homolog 7, SMAD 7, CRCS3, Smad7
8d
AANG: A natural compound formulation for targeting macrophage-myofibroblast transition in non-small-cell lung carcinoma. (PubMed, Phytomedicine)
More encouragingly, this optimized AANG can effectively block MMT-derived cancer progression on mouse cancer models with syngeneic lung cancer LLC and human NSCLC xenograft A549 without side-effect in vivo. Thus, AANG may represent the first natural compound formulation for blocking MMT-derived pro-tumoral CAF formation in the clinical NSCLC.
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TGFB1 (Transforming Growth Factor Beta 1) • SMAD7 (SMAD Family Member 7) • SMAD3 (SMAD Family Member 3)
11d
YTHDF2 promotes arsenic carcinogenesis through m6A-dependent SMAD7 decay and PRR5 escape from decay. (PubMed, Int J Biol Macromol)
Functionally, YTHDF2 promoted malignant phenotypes in keratinocytes and exacerbated arsenic-induced skin lesions in mice, accompanied by activation of the PRR5-mTORC2-AKT axis and enhancement SMAD2/3 signaling. This study advances our understanding of how opposing m6A regulatory axes shape YTHDF2 engagement and mRNA decay outputs, thereby promoting arsenic carcinogenesis by regulating oncogenic and tumor-suppressive signaling.
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FTO (Alpha-Ketoglutarate-Dependent Dioxygenase FTO) • SMAD7 (SMAD Family Member 7) • METTL3 (Methyltransferase Like 3) • YTHDF2 (YTH N6-Methyladenosine RNA Binding Protein 2)
17d
Beyond glycemic control: the cardiac and hepatic benefits of SGLT2 and DPP-4 inhibitors in mitigating chronic cadmium-induced inflammation, oxidative/nitrative stress, apoptosis and fibrosis. (PubMed, Front Physiol)
This study aims to contrast the protective effects of "Canagliflozin; Cana" versus "Sitagliptin; Sita" in countering the chronic Cd-induced cardiac and hepatic damage. Both medications showed comparable cardio-hepatic protective effects. Yet, Cana outperformed Sita as a potentially effective therapy to counteract the negative consequences of chronic Cd-induced cardiac and hepatic pathologies.
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NOTCH1 (Notch 1) • TNFA (Tumor Necrosis Factor-Alpha) • IL10 (Interleukin 10) • NFKB1 (Nuclear factor of kappa light polypeptide gene enhancer in B-cells 1) • CASP3 (Caspase 3) • SMAD7 (SMAD Family Member 7) • SMAD3 (SMAD Family Member 3)
20d
IFN-γ and TNF-α Impair Lung Development by Upregulating SMAD7 to Inhibit TGF-β Signaling Pathway and ECM Dysregulation. (PubMed, Inflammation)
Mechanistically, IFN-γ and TNF-α synergistically promoted SMAD7 overexpression, which competitively bound to SMAD2/3 and suppressed TGF-β signaling, ultimately leading to ECM dysregulation. These data delineate a novel inflammatory axis impairing lung development, highlighting SMAD7 and TGF-β pathways as promising intervention targets.
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IFNG (Interferon, gamma) • TNFA (Tumor Necrosis Factor-Alpha) • FN1 (Fibronectin 1) • TGFB1 (Transforming Growth Factor Beta 1) • COL1A1 (Collagen Type I Alpha 1 Chain) • COL3A1 (Collagen Type III Alpha 1 Chain) • SMAD7 (SMAD Family Member 7) • NECTIN1 (Nectin Cell Adhesion Molecule 1)
1m
TGFβ pathway represses hepatic ribosome biogenesis and protein synthesis by regulating p70S6K-S6RP proteins. (PubMed, Cell Mol Biol Lett)
Collectively, our data reveal a SMAD-dependent regulatory role of TGFβ-superfamily signaling on hepatocytes that is tightly connected with hepatic growth to ensure proper energy homeostasis and metabolism. This is a critical regeneration parameter, which is closely related to the restoration of hepatic mass, especially following liver injury and fibrosis.
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TP53 (Tumor protein P53) • MYC (V-myc avian myelocytomatosis viral oncogene homolog) • mTOR (Mechanistic target of rapamycin kinase) • TGFB1 (Transforming Growth Factor Beta 1) • SMAD7 (SMAD Family Member 7) • SMAD3 (SMAD Family Member 3)
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sirolimus
1m
Cross-Regional Transcriptome Data Reveal Transcriptional Abnormalities Associated with Lung Adenocarcinoma. (PubMed, Rep Biochem Mol Biol)
Our findings suggest that the expression levels of serglycin, ILK, ESD, and PLPD1 may play a significant role in the development of LAC. This information can be valuable for identifying potential treatment targets for lung cancer.
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CD123 (Interleukin 3 Receptor Subunit Alpha) • SPARC (Secreted Protein Acidic And Cysteine Rich) • VIM (Vimentin) • IL3RA (Interleukin 3 Receptor Subunit Alpha) • KRT19 (Keratin 19) • AQP1 (Aquaporin 1) • BST1 (Bone Marrow Stromal Cell Antigen 1) • COL3A1 (Collagen Type III Alpha 1 Chain) • SMAD7 (SMAD Family Member 7) • TAGLN (Transgelin) • ADH1B (Alcohol Dehydrogenase 1B (Class I), Beta Polypeptide) • AIMP2 (Aminoacyl TRNA Synthetase Complex Interacting Multifunctional Protein 2) • AKAP12 (A-Kinase Anchoring Protein 12) • RGS2 (Regulator Of G Protein Signaling 2) • NCOA1 (Nuclear Receptor Coactivator 1)
1m
Smad7 drives cisplatin resistance in ovarian cancer via a PRMT5-dependent mechanism. (PubMed, Tissue Cell)
In conclusion, our work identifies Smad7 as a critical driver of cisplatin resistance in vivo and delineates a novel in vitro mechanism whereby PRMT5 promotes oncogenic signaling through R57 methylation of Smad7. This PRMT5-Smad7 axis presents a promising therapeutic target for overcoming cisplatin resistance in ovarian cancer.
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CDH1 (Cadherin 1) • CDH2 (Cadherin 2) • MMP9 (Matrix metallopeptidase 9) • SMAD7 (SMAD Family Member 7)
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cisplatin
2ms
ERα inhibits the progression of hepatocellular carcinoma by regulating the circRNA/miRNA/SMADs network. (PubMed, Adv Clin Exp Med)
ERα can function as aTF, modulating the expression of various circRNAs with differential expression in HCC. Through this regulation, it modulates the circRNA/miRNA/SMADs network, thereby inhibiting the progression of HCC.
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ER (Estrogen receptor) • MIR96 (MicroRNA 96) • SMAD7 (SMAD Family Member 7)
2ms
Bulk RNA-seq deconvolution heterogeneity across paired pancreatic cancer human samples. (PubMed, Front Genet)
Any potential difference in observed expression values across the paired samples could be related to the different cell type proportions across the samples. The sample size was small, and each study used different sequencing technologies, so any interpretation should be confirmed with additional studies.
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KRAS (KRAS proto-oncogene GTPase) • TP53 (Tumor protein P53) • CDKN2A (Cyclin Dependent Kinase Inhibitor 2A) • SMAD4 (SMAD family member 4) • CTNNB1 (Catenin (cadherin-associated protein), beta 1) • SMAD7 (SMAD Family Member 7) • SMAD3 (SMAD Family Member 3) • TCF7 (Transcription Factor 7)
3ms
Integrated Bioinformatics Analysis of Differentially Expressed RNA-Binding Proteins in Human Gliomas. (PubMed, Cell Mol Neurobiol)
Further, RBPs like RPS8, RPL5, RPS3A, EEF1A1, and EIF4E1B were found to be strongly correlated with patients' overall survival. Taken together, our analyses identified several candidate RBPs which might serve as potential targets for oncological measures against gliomas.
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IGF2BP1 (Insulin Like Growth Factor 2 MRNA Binding Protein 1) • RPS6 (Ribosomal Protein S6) • YBX1 (Y-Box Binding Protein 1) • CPEB1 (Cytoplasmic Polyadenylation Element Binding Protein 1) • EEF1A1 (Eukaryotic Translation Elongation Factor 1 Alpha 1) • RPL5 (Ribosomal Protein L5) • SMAD7 (SMAD Family Member 7) • PABPC1 (Poly(A) Binding Protein Cytoplasmic 1)
3ms
Construction of the cancer cell continuum reveals hybrid EMT state driving lung adenocarcinoma aggression. (PubMed, Cancer Gene Ther)
Furthermore, we developed a risk stratification model based on EMT continuum signatures, providing a novel tool for prognostic assessment. Our findings contribute to a comprehensive understanding of EMT-driven tumor evolution and open new avenues for prognostic stratification and targeted therapies in LUAD.
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FOXA1 (Forkhead Box A1) • TGFB1 (Transforming Growth Factor Beta 1) • FOXA2 (Forkhead Box A2) • SMAD7 (SMAD Family Member 7) • TCF7 (Transcription Factor 7)
3ms
IGF2BP3 regulates EMP1 stability in an m6A-dependent manner and activates the TGF-β pathway to promote pancreatic cancer invasion. (PubMed, Cell Death Dis)
In conclusions, IGF2BP3 functions as an invasion driver that induces PDAC development via the EMP1/TGF-β axis. And IGF2BP3/EMP1 axis may be involved in regulating microenvironmental remodeling in pancreatic cancer.
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TGFB1 (Transforming Growth Factor Beta 1) • SMAD7 (SMAD Family Member 7) • IGF2BP3 (Insulin Like Growth Factor 2 MRNA Binding Protein 3) • SMAD3 (SMAD Family Member 3)