TGFB1I1 (Transforming growth factor beta 1 induced transcript 1)

This integrative multi-cohort study uncovered common transcriptional and immune signatures underlying SjD, MALT lymphoma, and thyroid cancer. The identification of shared hub genes, particularly PLA2G7 and TGFB1I1, provides novel insight into the immune-driven transition from chronic inflammation to malignancy and offers promising biomarkers for cross-disease diagnosis and immunotherapeutic stratification. Key Points • Key genes (PLA2G7 and TGFB1I1) affecting the occurrence of Sjögren's syndrome, mucosa-associated lymphoid tissue lymphoma, and thyroid cancer are identified for the first time. • Bioinformatics methods were employed to simultaneously study three diseases for the first time.

The current study may identify novel lncRNAs implicated in BC metastasis; still, additional research is required to determine the potential functions of these lncRNAs in BC metastasis.

Western blotting confirmed biotinylation and enrichment of FAK and vinculin, known interactors of Hic-5 and paxillin, as well as several potentially unique proximity interactors of Hic-5 and paxillin, including septin 7 and ponsin, respectively. Further investigation into the functional relationship between the unique interactors and Hic-5 or paxillin may yield novel insights into their distinct roles in cell migration.

The EMT markers also decreased upon TGFB1I1 knockdown. In this study, we identified that TGFB1I1 regulates UC cell proliferation and viability and induces the EMT to facilitate cell migration in vitro, leading to its essential role in promoting tumor aggressiveness in both UTUC and UBUC.

Twenty-seven BLCA samples from the local hospital proved that the risk model was associated with the malignant degree (P < 0.05). At last, the human macrophage THP-1 and U937 cells were treated with HO to mimic the senescent process in macrophage, and the expressions of these molecules in the model were detected (all P < 0.05).Overall, a macrophage cell senescence-related gene signature was constructed to predict the prognosis, immunotherapeutic response, and chemotherapy sensitivity in BLCA, which provides novel insights to uncover the underlying mechanisms of macrophage senescence.

Our rewiring analysis highlighted the impact of β-catenin and SMAD signaling as also some transcript factors like TGFB1I1 in prostate cancer progression. Altogether, we developed a miRNA-mRNA co-expression bipartite network to identify the hidden aspects of the prostate cancer mechanism, which traditional analysis -like differential expression- was not detect it.

In addition, risk score were positively correlated with multiple immunotherapy biomarkers. Our study revealed that a novel model based on senescence-related genes could serve as a reliable predictor of survival for patients with BCa.

CONCLUSIONS This study identified 4 differentially-expressed LIM genes - LMO3, FHL1, TGFB1I1, and NEBL - and revealed they were involved in the mucosa-adenoma-carcinoma sequence via regulating cancer-related pathways, influencing epigenetic field, or affecting immune infiltration. Our findings provide new insights into the roles of LIM proteins in the course of mucosa-adenoma-carcinoma.

Multiple gene set enrichment analysis of individual genes showed strong correlations with stromal and immune interactions, indicating that these nine genes may be related to carcinogenesis, invasion, and metastasis of bladder cancer. These findings provide useful insight into the molecular mechanisms of bladder cancer development, and suggest candidate biomarkers for prognosis and treatment.

In human ovaries (n = 15, < 150 days gestation) many of the same genes as in bovine (FBN3, GATA4, HMGA2, FSHR, DENND1A and LHCGR but not TOX3 or FSHB) were expressed and correlated with each other. With so many relationships between PCOS candidate genes during development of the fetal ovary, including TGFβ and androgen signalling, we suggest that future studies should determine if perturbations of these genes in the fetal ovary can lead to PCOS in later life.