SMAD9 (SMAD Family Member 9)

This multi-omics analysis reveals that the development of sessile serrated adenomas and conventional adenomas (CA) is associated with distinct epithelial origins, with serrated lesions linked to SSC cells and CA linked to ASC cells. These lesion-specific molecular features provide a mechanistic basis for improving preoperative detection and for developing adjunct molecular tools for high-risk polyp assessment.

However, its genetic characteristics remain unclear. The role of SMAD9 mutations is not yet fully understood, but identifying such mutations may deepen our understanding of genetic associations in colorectal polyposis syndromes.

Functional enrichment revealed activation of NOTCH, MAPK, PI3K, and TGF-β signaling and enrichment of early and late estrogen-response programs, uncovering a noncanonical role of SMAD9 in TGF-β signaling. Together, these findings delineate the transcriptional and hormonal circuitry underlying thyroid tumorigenesis, providing a regulatory framework for biomarker-driven therapies based on network activity states.

Kyoto Encyclopedia of Genes and Genomes analysis revealed pathways related to morphine addiction and protein digestion/absorption...Sensitivity to chemotherapeutics, such as AZD6482, ABT-263, A-770041, and BMS-536924, was observed in LUAD. Reverse transcription-quantitative polymerase chain reaction validation results demonstrated that KRT8 and S100A16 were significantly upregulated in tumor tissues, while COL4A3 and SMAD9 expression was downregulated, which was consistent with the TCGA-LUAD database analysis. In conclusion, 6 genes (KRT8, S100A16, COL4A3, SMAD9, MAP3K8, and CCDC146) were identified as potential biomarkers, offering valuable insights into LUAD pathogenesis and therapeutic strategies.

Lathyrol can repress the expression of key proteins in the TGF-β/Smad signaling pathway, impede signal transduction, arrest the cell cycle progression of Renca cells, and subsequently inhibit the proliferation of RCC cells. Future studies are needed to further explore the mechanism of lathyrol in RCC treatment.

HSPA6, NOTCH3, PKP2, SMAD9, and GPD1L were five novel biomarkers for CRC and LUAD clinical diagnosis or treatment. HSPA6 and SMAD9 might take part in the progression of CRC and LUAD via protein binding function.

P3, N=170, Terminated, St Vincent's Hospital Melbourne Pty Ltd | Active, not recruiting --> Terminated

Poor survival was associated with high genes expression, including CDKN2A, MEX3A, RPL39L, VARS, GSPT1, SNRPE, SSR1, and TIA1 in breast and colon cancer but not with lung cancer; and poor survival was associated with low genes expression, including PPARGC1B, EIF4E3, and SMAD9 in breast, colon, and lung cancer. This study highlights the significant contribution of PPARGC1B, EIF4E3, and SMAD9 out of 11 RBP genes as prognostic predictors in patients with breast, colon, and lung cancers and their potential application in personalized therapy.

MEK inhibitors have emerged as promising therapeutic agents for targeting most EP-TF risk genes in NB. Our novel prognostic model shows significant potential for predicting and evaluating the overall survival of NB patients, offering insights into therapeutic targets.

Additionally, protein-protein interaction (PPI) network analysis was conducted to evaluate the potential druggability of these identified genes. The culmination of our efforts led to the identification of five genes (tier 1) with the most compelling evidence, including SECISBP2L, PRCD, SMAD9, C2orf91, and HSD17B13, and eight genes (tier 2) with convincing evidence for their potential as therapeutic targets.

Understanding these mechanisms may help develop targeted treatments that may improve health outcomes of Kenyan women diagnosed with breast cancer. Longitudinal studies with larger cohorts will be needed to validate our results.

Mechanistically, SMAD9 is ubiquitinated by ASB2, and the regulatory effect of CHPF on SMAD9 activity was exerted via its mediation of ASB2. Collectively, CHPF functioned as a promising prognostic biomarker and tumor-promoter of CRC by regulating the ASB2-mediated ubiquitination of SMAD9.