GRB2 (Growth Factor Receptor Bound Protein 2)

The expression of ATP1A1, survivin, and SMAC did not differ by sex or diet, although an upregulation trend in both ATP1A1 and survivin was noted in the male-HFD group. There is sexual dimorphism in the response to HFD during the transition from senescence to the apoptosis-first apoptotic switch in MASH progression.

This deep learning model demonstrated excellent performance in multi-omics subtype predictions. In, conclusion, this study systematically elucidates the molecular heterogeneity of LUAD through a multi-omics integration strategy, establishes a clinically relevant molecular classification system, and provides a theoretical foundation for developing personalized treatment plans for LUAD.

Our study reveals that Toxoplasma uses defined motifs to co-opt host signaling hubs that control cell motility. Understanding how pathogens exploit the cytoskeleton not only sheds light on host-pathogen interactions but may also reveal broader principles of cell migration relevant to immunity, cancer, and development.

The results indicate that GRB2 and MYD88 may function as significant biomarkers for patient stratification and should be considered in the formulation of targeted therapies for gastric cancer. This study highlights the importance of GRB2 and MYD88 in the progression of gastric cancer and proposes their potential as therapeutic targets to enhance patient outcomes.

Subcutaneous xenograft nude mouse model showed that DDX42 significantly promoted tumour growth as compared to the control group and lifted the expression of GRB2, KI-67 and PCNA in vivo. In conclusion, our findings facilitate the acknowledgment of tumour initiation and mechanisms of treatment resistance in HCC, and targeting the axis of DDX42 and GRB2 may be promising strategies for synergy with radiotherapy or sorafenib for HCC patients.

Western blot analysis revealed a dose-dependent reduction in PIK3R2, GRB2, and MAPK1 expression in Gossypol-treated groups compared to controls (p < 0.05). Gossypol may exhibit anti-cervical cancer effects by modulating the PI3K/AKT signaling pathway.

GRB2 overexpression and shGRB2 reversed the effects of shSYNJ2 and overexpressed SYNJ2 on cell migration, invasion and angiogenesis and levels of metastasis-related proteins, respectively. In conclusion, SYNJ2 promotes GC cell metastasis and angiogenesis by up-regulating GRB2.

Collectively, the present study investigated the miRNA-mRNA regulatory network in HCC with HBV infection and showed that miRNA-93 positively regulated immune infiltration-related GRB2. Restoring GRB2 may be a candidate strategy for the treatment of HBV-related HCC.

circ_0026134 knockdown significantly delayed tumor growth in vivo (P < 0.05). Silencing circ_0026134 strengthens radiation treatment's anti-proliferation, anti-migration, invasion, and pro-apoptotic effects in hepatoma cells by negatively regulating the miR-1270/GRB2 pathway, thereby enhancing radiosensitivity.

These differences in tumor growth correlated with differential autophagy activity, indicating that autophagy effects might be related to the effects on tumorigenesis. Our data highlight a novel function of GRB2 as a BECN1 binding protein and a regulator of autophagy.

Additionally, we demonstrated that promoting MET degradation through deubiquitinase (USP8 or USP32) gene silence is another effective method for reversing drug resistance. Overall, our findings suggest that targeting MET receptor endocytosis and degradation is an attractive strategy for overcoming HGF-induced gefitinib resistance in EGFR-sensitive mutant lung adenocarcinoma.

RNF173 inhibits the invasion and metastasis of HCC by ubiquitinating and degrading GRB2, thereby suppressing the RAF/MEK/ERK signaling pathway. RNF173 is an independent risk factor for the survival and recurrence of HCC patients. RNF173 may serve as a novel prognostic molecule and potential therapeutic target for HCC. Video Abstract Graphical abstract Model of RNF173 on RAF/MEK/ERK signaling. RNF173 knockdown resulted in impaired ubiquitination and degradation of GRB2, leading to the activation of the RAF/MEK/ERK signaling pathway and promotion of invasion and metastasis in HCC cells.