CCNG2 (Cyclin G2)

In this study, we identified three diagnostic biomarkers for HSCC (NRG1, CCNG2, and CHSY1) and established their corresponding ceRNA network via bioinformatic analysis, providing novel insights into the screening and treatment of HSCC.

Taken together, these findings suggests the identification of two common pathways induced by AR-antagonists and SAL, used in bipolar androgen therapy, to mediate growth inhibition and induction of cellular senescence in CRPC.

The Editor sincerely apologizes to the readership for any incovenience caused, and we thank the reader for bringing this matter to our attention. [Oncology Reports 40: 2067‑2078, 2018; DOI: 10.3892/or.2018.6636].

In summary, PAGln can effectively inhibit the proliferation, migration, and invasion of PCa by upregulating CCNG2 and suppressing the Wnt/β-catenin signaling pathway. These findings suggest that PAGln may serve as a promising therapeutic agent for prostate cancer.

Yet, these effects were blocked by further silencing of PATZ1. In summary, this research demonstrates that SMURF1 activates β-catenin signaling by suppressing the PATZ1/CCNG2 axis, thereby promoting the progression of ESCC.

We identified a binding site of miR-1246 in the 3'UTR of cyclin G2 (CCNG2) and demonstrated direct binding by a luciferase reporter assay.Increased expression of CCNG2 has been associated with cancer metastasis and poor patient outcomes in other malignancies. Our study demonstrates that intercellular communication contributes to the transfer of properties, such as increased invasive capacity, between heterogeneous melanoma cells via EV-transported miRNAs.

The data provide evidence of the tumor suppressive activity of SAL and a novel signaling by the AR-BHLHE40-CCNG2 axis for androgen-induced cellular senescence, linking circadian rhythm factor to androgen signaling as a novel tumor suppressive pathway.

HQ-transformed cells' exosomal miR-1246 targets CCNG2, regulating TK6 cell cycle arrest, highlighting its potential as a biomarker for HQ-induced malignant transformation.

The networks of miRNAs with their confirmed targets improved comprehension of miRNA-mediated therapeutic responses to trastuzumab and might be proposed for more characterization of miRNA functions. Moreover, these data indicated that miR-195-5p, miR-34c-3p, and miR-1246 could be possible biomarkers for prognosis and early detection of the trastuzumab-resistant group from the sensitive group of HER2-positive breast cancer patients.

Treatment of the CLL cell line MEC1 and primary CLL patient samples with DUB inhibitors including PR-619 (pan-DUBi), P5091 (USP7i) and HBX19818 (USP7i) alone reduces the phosphorylation of AKTS437 and FOXO1T24, indicating that DUBs play a role in inhibiting FOXO1 activity. Additionally, FOXO1 activity studies demonstrated significant activation of FOXO1 upon ibrutinib treatment, which was further enhanced in the USP7 KD and combination with USP7i. These studies suggest that selective DUBs play a role in BCR-mediated signalling to aid in the promotion of CLL cell survival and chemo-resistance through FOXO1 inhibition, and targeting these DUBs enhance FOXO1 activity leading to cell cycle arrest and apoptosis.