-
Splicing type of ING4 affects the translocation of ING4 proteins into the nucleus.
-
Both CELSR2 and ING4 display increased cytoplasmic staining in breast cancer cells compared to benign epithelium, suggesting a possible role of both genes in the pathogenesis of human mammary neoplasia.
-
These results demonstrated that overexpression of ING4 can induce the apoptosis of melanoma cells and CD3+ T cells through signaling pathways such as the Fas/FasL pathway, and that ING4 gene therapy for melanoma treatment is a novel approach.
-
Inhibitor of growth 4 upregulation plus radiotherapy induced synergistic tumor suppression in SPC-A1 xenografts implanted in athymic nude mice. Thus, the restoration of inhibitor of growth 4 function might provide a potential strategy for non-small cell lung cancer radiosensitization.
-
Results found that ING4 expression was significantly reduced in CRC tissues and associated with increased lymph node metastasis, advanced TNM stage and poor overall survival. Also, ING4 suppressed CRC angiogenesis by inhibition of Sp1 expression and transcriptional activity through destabilization and ubiquitin degradation and down-regulation of Sp1 downstream pro-angiogenic factors MMP-2 and COX-2.
-
Low ING4 expression is associated with malignant phenotype and temozolomide chemoresistance in glioblastomas.
-
ING4 directly binds the Miz1 promoter and is required to induce Miz1 mRNA and protein expression during luminal cell differentiation.
-
The oncogenic role of miR-330 in Hepatocellular Carcinoma Cells is linked to downregulation of ING4.
-
ING4 binds double-stranded DNA through its central region with micromolar affinity.
-
results indicate that the combination of ING4 and PTEN may provide an effective therapeutic strategy for HCC
-
ING4 can facilitate cancer cell sensitivity to chemotherapy and radiotherapy. Although ING4 loss is observed for many types of cancers, increasing evidences show that ING4 can be used for gene therapy. In this review, the recent progress of ING4 regulating tumorigenesis is discussed
-
ING4 inhibits CRC invasion and metastasis probably via a switch from mesenchymal marker N-cadherin to epithelial marker E-cadherin through downregulation of Snail1 epithelial-mesenchymal transition (EMT)-inducing transcription factor (EMT-TF).
-
Data show that Ras protein regulates inhibitor of growth protein 4 (ING4)-thymine-DNA glycosylase (TDG)-Fas protein axis to promote apoptosis resistance in pancreatic cancer.
-
MiR-761 directly targeted ING4 and TIMP2.
-
Data suggest a close connection between aberrant ING4 expression and the carcinogenesis of human bladder cells.
-
This review summarizes the recent published literature that investigates the role of ING4 in regulating tumorigenesis and progression, and explores its potential for cancer treatment. [review]
-
SCF(JFK) as a bona fide E3 ligase for ING4 and unraveled the JFK-ING4-NF-kappaB axis as an important player in the development and progression of breast cancer
-
work suggests that ING4 can suppress osteosarcoma progression through signaling pathways such as mitochondria pathway and NF-kappaB signaling pathway and ING4 gene therapy is a promising approach to treating osteosarcoma.
-
The enhanced antitumor activity generated by Ad.RGD-ING4-PTEN was closely associated with activation of the intrinsic and extrinsic apoptotic pathways and additive inhibition of tumor angiogenesis both in vitro and in vivo.
-
The low expression level of ING4 protein was correlated with high-risk gastrointestinal stromal tumors.
