Noncoding RNAs (ncRNAs) are the dominant product of eukaryotic transcription. These products range from short microRNAs (miRNAs) to long intergenic noncoding RNAs (lincRNAs). Circular RNAs composed of exonic sequences represent an understudied form of ncRNA that was discovered more than 20 years ago. Using a TaqMan-based reverse transcriptase polymerase chain reaction assay, we analyzed the relationship between cir-ITCH expression and colorectal cancer (CRC) in a total of 45 CRCs and paired adjacent non-tumor tissue samples. We found that cir-ITCH expression was typically down-regulated in CRC compared to the peritumoral tissue. This result, as well as several follow-up experiments, showed that cir-ITCH could increase the level of ITCH, which is involved in the inhibition of the Wnt/β-catenin pathway. Therefore, our results showed that cir-ITCH plays a role in CRC by regulating the Wnt/β-catenin pathway.

Download full-text PDF

Source
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC4482251PMC
http://journals.plos.org/plosone/article?id=10.1371/journal.pone.0131225PLOS

Publication Analysis

Top Keywords

wnt/β-catenin pathway
12
cir-itch plays
8
colorectal cancer
8
regulating wnt/β-catenin
8
noncoding rnas
8
cir-itch expression
8
cir-itch
5
plays inhibitory
4
inhibitory role
4
role colorectal
4

Similar Publications

Introduction: Melanoma (MM), the deadliest form of skin cancer, originates from melanocytes. Despite advances in immunotherapy that have somewhat improved the prognosis for MM patients, high levels of resistance to treatment continue to result in poor clinical outcomes. Identifying novel biomarkers and therapeutic targets is critical for improving the prognosis and treatment of MM.

View Article and Find Full Text PDF

Introduction: The Wnt/planar cell polarity (PCP) signaling pathway is pivotal in regulating various biological processes such as early embryonic development, neural crest cell migration, and cancer invasion. Despite advances in understanding the role of Wnt/PCP pathway dysregulation in tumorigenesis, numerous unanswered questions remain. Our study focused on VANGL2, a core PCP gene, to elucidate its potential mechanistic involvement in cancer development.

View Article and Find Full Text PDF

Advances and challenges in molecular understanding, early detection, and targeted treatment of liver cancer.

World J Hepatol

January 2025

Shenzhen Branch, Guangdong Laboratory of Lingnan Modern Agriculture, Genome Analysis Laboratory of the Ministry of Agriculture and Rural Affairs, Agricultural Genomics Institute at Shenzhen, Chinese Academy of Agricultural Sciences, Shenzhen 518000, Guangdong Province, China.

In this review, we explore the application of next-generation sequencing in liver cancer research, highlighting its potential in modern oncology. Liver cancer, particularly hepatocellular carcinoma, is driven by a complex interplay of genetic, epigenetic, and environmental factors. Key genetic alterations, such as mutations in , , and , alongside epigenetic modifications such as DNA methylation and histone remodeling, disrupt regulatory pathways and promote tumorigenesis.

View Article and Find Full Text PDF

Age-induced abnormalities in bone metabolism disrupt the equilibrium between bone resorption and formation. This largely stems from disturbances in bone homeostasis, in which signaling pathways exert a significant regulatory influence. Aging compromises the functionality of the bone marrow mesenchymal stem cells (BMSCs), ultimately resulting in tissue dysfunction and pathological aging.

View Article and Find Full Text PDF

Objectives: The osteogenic potential of periodontal ligament stem cells (PDLSCs) is crucial for periodontal tissue regeneration. Prolonged and excessive oxidative stress (OS) impairs the osteogenic function of PDLSCs. Recently, Semaphorin 3A (Sema3A) has been reported to have multiple roles in bone protection.

View Article and Find Full Text PDF

Want AI Summaries of new PubMed Abstracts delivered to your In-box?

Enter search terms and have AI summaries delivered each week - change queries or unsubscribe any time!