ADAM12 (ADAM Metallopeptidase Domain 12)

TIMPs display contrasting expression profiles and distinct pathway associations in breast cancer. TIMP1 emerges as the only consistently overexpressed inhibitor, while TIMP4 appears as a promising prognostic marker with unique MMP correlations that may influence tumor behaviors.

ADAM12 overexpression triggered the PI3K-AKT-mTOR pathway, enhanced the development and lung metastasis of bladder cancer xenografts, and markedly increased the invasion, migration, and proliferation of bladder cancer cells. The above results indicate that ADAM12, as a matrix-driven factor, links matrix remodeling, PI3K-AKT signaling pathway and bladder cancer immunosuppression, and has good prognostic and therapeutic stratification potential, providing new ideas for precision targeted intervention and treatment of bladder cancer.

Its ablation elicits IFN-I-responsive programs, reconfigures myofibroblast population structures into progenitor-like states, revitalizes T cell-based immune responses, and induces tumor rejection across various murine models. Further combined with human genomics data analysis, our findings position ADAM12 as a potential target for fibroblasts, paving the way for actionable therapeutic interventions.

Conclusion HB-EGF expression is a characteristic feature of SIP. ADAM12 and HIF-1α may contribute to the distinctive upregulation of HB-EGF observed in SIP.

Collectively, the present findings suggested that ADAM12 is involved in PC progression and may facilitate the shedding of HB-EGF, thereby inducing EMT through the EGFR pathway. These results suggest that targeting the ADAM12/HB-EGF/EGFR signaling pathway could represent a potential therapeutic strategy, warranting further in vivo and in vitro investigations to elucidate the underlying mechanisms.

ADAM12 might be a valuable prognostic biomarker and a promising candidate for tumor immunotherapy.

Our study successfully developed a predictive model based on 9 recurrence-related genes, enabling accurate stratification of glioma patients into high- and low-risk recurrence groups. Furthermore, we identified apoptosis, particularly the extrinsic apoptotic pathway involving FADD and CASP8, as a critical mechanism associated with glioma recurrence. These findings provide valuable insights into the molecular basis of glioma recurrence and may facilitate the development of targeted therapeutic strategies.

Telotristat ethyl affects the expression of genes associated with the ECM and interferes with SI-NET-fibroblast crosstalk. Further analysis is required; however, this study represents an important step in understanding the mechanisms of telotristat ethyl when treating SI-NET patients.

Furthermore, administration of Compound C, an AMPK inhibitor, reversed the suppressive effects of CLDN1 knockdown on cell proliferation, EMT, and lipid metabolism, indicating the AMPK signaling pathway is involved in CLDN1-mediated EMT and lipid metabolism in CRC cells. These findings suggest that CLDN1 plays a significant role in EMT and lipid metabolism of CRC cells and can be utilized as a therapeutic target for CRC.

N-cadherin and ADAM12 showed statistically significant associations with PSA (p = 0.038 and p = 0.013, respectively) but not with other clinical variables. These findings support the involvement of EMT-related markers in PC and suggest their potential utility in biological characterization, although further studies are required to determine their prognostic value.

MiR-181d-3p deficiency reversed the regulatory role of Circ_0046336 in biological behaviors of OSCC cells. Circ_0046336 silencing promoted E-cadherin expression and inhibited N-cadherin and Vimentin expressions, but such effects were reversed by miR-181d-3p downregulation.ConclusionCirc_0046336 acts as a ceRNA to regulate apoptosis, migration, invasion and EMT of OSCC cells via miR-181d-3p/ADAM12 axis.

In addition to providing novel biomarkers for diagnosis that can be detected non-invasively, the secretion levels of hub genes-associated proteins were found in plasma, serum, and oral epithelium. The drug repositioning analysis revealed vorinostat, meclocycline sulfosalicylate, and trichostatin A, which exhibited significant binding affinities to the hub genes compared to their inhibitors via molecular docking analysis.