Non-coding RNAs (ncRNAs) are emerging as important regulators in various pathological conditions, including human cancers. NcRNAs exert potentially crucial effects on cell cycle progression, proliferation, and invasion in cancer cells by targeting various cell cycle-related proteins at transcriptional and post-transcriptional levels. As one of the key cell cycle regulatory proteins, p21 is involved in various processes, including the cellular response to DNA damage, cell growth, invasion, metastasis, apoptosis, and senescence. P21 has been shown to have either a tumor-suppressive or oncogenic effect depending on the cellular localization and posttranslational modifications. P21 exerts a significant regulatory effect on both G1/S and G2/M checkpoints by regulating the function of cyclin-dependent kinase enzymes (CDKs) or interacting with proliferating cell nuclear antigen (PCNA). P21 has an important effect on the cellular response to DNA damage by separating DNA replication enzymes from PCNA and inhibiting DNA synthesis resulting in G1 phase arrest. Furthermore, p21 has been shown to negatively regulate the G2/M checkpoint through the inactivation of cyclin-CDK complexes. In response to any cell damage caused by genotoxic agents, p21 exerts its regulatory effects by nuclear preservation of cyclin B1-CDK1 and preventing their activation. Notably, several ncRNAs, including lncRNAs and miRNAs, have been shown to be involved in tumor initiation and progression through the regulation of the p21 signaling axis. In this review, we discuss the miRNA/lncRNA-dependent mechanisms that regulate p21 and their effects on gastrointestinal tumorigenesis. A better understanding of the regulatory effects of ncRNAs on the p21 signaling may help to discover novel therapeutic targets in gastrointestinal cancer.
Non-coding RNAs (ncRNAs) are emerging as important regulators in various pathological conditions including tumorigenesis, metastasis, and drug resistance in human cancers. Oncogenic or tumor suppressor ncRNAs exert prominent effects on cell proliferation, migration and invasion in cancer cells through modulating various signaling pathways including Wnt/β-catenin. Upregulation of the oncogenic Wnt/β-catenin pathway was reported to be implicated in multiple human cancers including breast, liver, colorectal, and urothelial cancers. Therefore, identifying interactions between ncRNAs and canonical Wnt signaling components may represent novel therapeutic targets for better treatment and management of cancer. In this review, we summarized the recent findings about miRNA/lncRNA-dependent mechanisms that regulate Wnt/β-catenin signaling involved in tumorigenesis and metastasis of urinary tract cancers.
Background: Cervical cancer is one of the most prevalent gynecologic cancers associated with high morbidity and mortality worldwide. There is mounting evidence indicating an association between the 9p21 locus genetic variants with susceptibility to various human malignancies. In this current study, we aimed to evaluate the potential relationship between the rs1333049 genetic variant in chromosome 9p21 and the risk of cervical carcinogenesis. background: Cervical cancer is one of the most prevalent gynecological cancers associated with high morbidity and mortality worldwide. There is mounting evidence indicating an association between the 9p21 locus genetic variants with susceptibility to various human malignancies. Method: The possible correlation between rs1333049 polymorphism and susceptibility to cervical cancer was investigated in 221 patients with or without cancer. DNAs were isolated and genotyped using a TaqMan-based real-time RT-PCR method. Result: The rs1333049 genetic variant was found to be correlated with an elevated risk of cervical neoplasia using recessive and additive genetic models (p<0.001). method: The possible correlation between rs1333049 polymorphism and susceptibility to cervical cancer was investigated in 221 patients with, or without cancer. DNAs were isolated and genotyped using a TaqMan-based real-time RT-PCR method. Conclusion: CDKN2A/B genetic variant (rs1333049) was significantly associated with an elevated risk of cancer, suggesting its potential as a novel predictive marker for cervical carcinogenesis. other: .
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