Mechanistically, USP30-AS1 acts as a competing endogenous RNA (ceRNA) by sponging miR-3646, which leads to the derepression of Frizzled-7 (FZD7) and subsequent activation of the Wnt/β-catenin signaling pathway. These findings identify USP30-AS1 as a critical promoter of stemness, chemoresistance, and metastasis in BCSCs via the miR-3646/FZD7/Wnt axis, suggesting it is a potential therapeutic target for breast cancer intervention.
24 days ago
Journal
|
CTNNB1 (Catenin (cadherin-associated protein), beta 1) • CD44 (CD44 Molecule) • POU5F1 (POU Class 5 Homeobox 1) • ALDH1A1 (Aldehyde Dehydrogenase 1 Family Member A1) • FZD7 (Frizzled Class Receptor 7) • USP30-AS1 (USP30 Antisense RNA 1)
This promotes epigenetic up-regulation of c-Myc by reducing H3K27 trimethylation. Together, these findings demonstrate the critical role of USP30-AS1 in breast cancer progression through HnRNPF/p21 and EZH2/c-Myc/p21 axes, highlighting its potential as a therapeutic target for breast cancer treatment.
This study established a PANR-associated lncRNA prognostic model with robust predictive accuracy for SKCM survival. The risk stratification system correlates with immune dysregulation, therapy response, and pathway activation, offering a potential tool for personalized prognosis and treatment strategies.
4 months ago
Journal
|
KRAS (KRAS proto-oncogene GTPase) • HLA-DQB1 (Major Histocompatibility Complex, Class II, DQ Beta 1) • USP30-AS1 (USP30 Antisense RNA 1)
Elevated ELFN1-AS1 expression was associated with breast cancer that lacked P53 mutation. These changes suggest their promise as biomarkers for distinguishing between cancerous and noncancerous tissues.
Notably, overexpression of MYBBP1A alleviated the stimulatory effect of USP30-AS1 knockdown on NF-κB activation. Collectively, these findings suggest that USP30-AS1 acts as a suppressor of colorectal cancer cell growth by modulating the MYBBP1A/NF-κB signaling pathway, thereby highlighting USP30-AS1 as a potential novel therapeutic target for colorectal cancer treatment.
Moreover, the model has certain relevance in the immune cells and functions between high and low risk groups, and simultaneously, the signature has the role of guiding the option of immunotherapy and chemotherapeutic drugs. Altogether, our study established a tight connection between m7G-associated lncRNAs and ovarian cancer, with potential that the prognostic patterns contribute to steering the prognosis of ovarian cancer patients, measuring the efficacy of immunotherapeutic approaches, and detecting effective chemotherapeutic agents.
Moreover, USP30-AS1 was found to modulate the expression of ubiquitin-specific peptidase 30 (USP30) by sponging microRNA-2467-3p (miR-2467-3p) and recruiting the FUS RNA binding protein (FUS), thereby stabilizing β-catenin and activating the Wnt/β-catenin signaling pathway. These findings suggest that USP30-AS1 enhances CC cell growth and migration through the miR-2467-3p/FUS/USP30 axis, highlighting its potential as a biomarker for CC.
Our study constructed a risk assessment model by irlncRNA pairs regardless of expression levels, which contributed to predicting the efficacy of immunotherapy in TNBC. Furthermore, the lncRNA USP30-AS1 in the model was positively correlated with the expression of PD-L1 and provided a potential therapeutic target for TNBC.
Tumor metastasis and risk scores alone were good prognostic indicators, and a combination of the two variables can better predict the prognosis of osteosarcoma. We identified four lncRNAs, AC015819.1, AC015911.3, AL365361.1, and USP30-AS1, as potential biomarkers for osteosarcoma prognosis.
Conventional chemotherapeutics, such as docetaxel and paclitaxel, showed greater efficacy in BC patients classified as high-risk. The silencing of C6orf99 markedly decreased the proliferation, migration, and invasion capacities in MCF-7 cells. Our study identified a signature of metabolism-related lncRNAs that predicts outcomes in BC patients and could assist in tailoring personalized prevention and treatment plans.
Additionally, the findings offer significant insights into the plausible role of lncRNAs in modulating immune activities, thus adding to our understanding of the disease biology. Additional investigations are necessary to unravel the molecular mechanisms underpinning these connections and validate the results seen in independent cohorts and experimental models.