MIEN1 (Migration And Invasion Enhancer 1)

Our findings emphasize the involvement of MIEN1in diverse signaling pathways responsible for CRC migration, with its deletion leading to the disruption of several biological processes, particularly actin cytoskeleton rearrangement, which is crucial for metastasis. Therefore, targeting MIEN1 may be an effective therapeutic strategy against CRC.

CTCF+ TANs represent a novel TAN subtype that drives CRC progression and immunosuppression via the CTCF-MIEN1-IL-1β axis. These findings highlight the potential of targeting CTCF+ TANs to overcome immunotherapy resistance and improve patient outcomes.

While MPD ERR significantly increases the complexity of perioperative management following MIEN, it does not affect long-term metabolic outcomes and patient QoL.

PDDRNet-MH achieved consistently high accuracy, with perfect prediction scores for gemcitabine and vinorelbine (Area Under the Receiver Operating Characteristic Curve [AUC-ROC] = 1.00; Area Under the Precision-Recall Curve [AUC-PR] = 1.00) and near-perfect scores for methotrexate and zoledronate (AUC-ROC = 0.95; AUC-PR = 0.99), demonstrating its ability to robustly distinguish sensitive from resistant patients. Biologically, PDDRNet-MH accurately prioritized established clinical biomarkers, including HER2 (ERBB2) for lapatinib and BRCA1/2 for doxorubicin and cyclophosphamide. Beyond known associations, the model identified additional genes within the HER2 amplicon on chromosome 17q12, including STARD3, MIEN1, and PPP1R1B, whose amplification was significantly associated with elevated drug response scores, suggesting potential roles in HER2-targeted therapy. These findings highlight the ability of PDDRNet-MH to recover and extend clinically relevant drug-biomarker associations, supporting its utility in guiding precision oncology.

MiR-136 demonstrates promising potential as a novel biomarker and therapeutic target in various human cancers. Further research is needed to fully elucidate its complex roles in cancer development, progression, and drug resistance, particularly regarding its potential in immunotherapy.

Mechanistically, MIEN1 activates the IL-6/JAK2/STAT3 signaling pathway, which drives the proliferation, invasion, and migration of gastric cancer cells. This study demonstrates that MIEN1 contributes to the malignant behavior of gastric cancer through the IL-6/JAK2/STAT3 pathway, suggesting that MIEN1 could serve as a valuable therapeutic target for gastric cancer.

Our results show differences in important clinicopathological features between HER2-low and both HER2-positive and negative tumors. Given this unique phenotype, it is crucial to evaluate the potential advantages of ADC therapies for this emerging subtype of breast cancer.

In contrast, miR-136-5p expression in GC tissues shows a negative correlation. A previously unexplored therapeutic target for GC involves the CRNDE/miR-136-5p/MIEN1 signal transduction cascade.

The association between TEXLs and UCEC was methodically elucidated by our investigation. A stable pTEXLs risk prediction model and a diagnosis model for UCEC were also established.

D-LA3IK remained stable in mouse plasma for 24 h with 75% remaining, exhibiting superior pharmacokinetic properties over D/L-RP-7. In summary, our findings mark the first report of short peptides based on MIEN1 protein sequence capable of inhibiting cancer signaling pathways, effectively impeding cancer progression both in vitro and in vivo.

The novel immune-related risk scoring system has some advantages in predicting the prognosis and treatment response of cervical cancer patients treated with radiotherapy. Moreover, it might provide novel clues for providing targeted immune therapy to these patients.

ExportNetworkToCytoscape determined that MIEN1 and GRB7 are tightly connected to ERBB2., Finally, 14 single-cell intestinal gastric cancer samples were investigated, and it was shown that the TFAP2A transcription factor regulon was highly expressed in ERBB2 group, as was the EMT score. Overall, our data provide comprehensive molecular characteristics of ERBB2-Amp type gastric cancer, which offers additional information to improve HER2-targeted gastric cancer treatment.