ITGB4 (Integrin Subunit Beta 4)

ITGB4 is a key molecule influencing cisplatin sensitivity in p53 WT BC, and the combination of STAT3 inhibitors can enhance the antitumor effect of cisplatin.

In conclusion, this study innovatively identified the non-enzymatic function of QSOX2 in regulating OR in EGFR-mutant LUAD through the JUNB-ITGB4-FAK/AKT pathway. The QSOX2/JUNB-ITGB4 signaling axis represents a potential therapeutic target for overcoming OR and offers a novel strategy to improve outcomes in LUAD patients.

HF administration markedly disrupted the aggressive progression of tumor cell both in vitro and in vivo. In summary, our study not only establishes HF as a promising degrader of integrin β4 but also demonstrates the utility of natural product screening for discovering molecular glue degraders, providing a novel therapeutic strategy for targeting oncogenic transmembrane proteins.

Consistent with this, tumors with PTPRK mutations proliferated significantly more rapidly than their wild type counterparts in vivo. These findings suggest that PTPRK mutations contribute to DC development by dysregulating phosphorylation-mediated signaling pathways.

Tumor volumes and metastatic lesions were significantly reduced. This approach effectively reprograms TAMs, induces tumor cell apoptosis, and suppresses NSCLC metastasis, offering a novel nanomedicine-based strategy for enhancing anti-tumor immunity and improving therapeutic outcomes in NSCLC.

Intervening eIF6 suppresses non-NE transdifferentiation and enhances SCLC chemotherapy sensitivity in vitro and in vivo. These findings position the eIF6-CD104-FAK axis as a prognostic marker and therapeutic target, offering a potential strategy to mitigate SCLC resistance.

We established GC (Gemcitabine and Cisplatin)-resistant T24-R and UC3-R cell lines from T24 and UM-UC-3 (UC3) cells. Our results demonstrate that the FN1-ITGB4 axis drives chemoresistance in bladder cancer via FAK signaling. Targeting this axis represents a promising strategy to overcome chemoresistance.

Notably, suppression of CACNA1C induced transdifferentiation from stable/late-state cells to normal epithelium-like cells. This study provides novel insights into the EMT mechanism in ESCC, proposes an intervention strategy, and emphasizes the promising clinical application of pathological images in EMT assessment.

WTAP mediated the m6A methylation modification of ITGB4 to promote HCC progression and tumor stemness, providing a new idea for HCC therapy.

These findings indicate that Lenvatinib and Everolimus act synergistically to inhibit NEN proliferation and migration and to induce apoptosis in vitro, with robust synergistic activity also evident in vivo. This synergy appears to be mediated, at least in part, through the upregulation of ITGB4.

Our previous work established that the elevation of ITGB4 in BLCA was closely related to cisplatin resistance...Our research also discovered a positive correlation between ITGB4 and the ADCs drug target NECTIN4, and the overexpression of ITGB4 upregulates BLCA sensitivity to enfortumab vedotin treatment. It provides a basis for the treatment choice of advanced BLCA patients with immunotherapy resistance. Collectively, these results suggest that ITGB4 may be a promising therapeutic target for advanced BLCA.