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1.
J Clin Lab Anal ; 36(2): e24220, 2022 Feb.
Artigo em Inglês | MEDLINE | ID: mdl-35007362

RESUMO

BACKGROUND: Prostate cancer (PCa) is a genetically heterogeneous disease with highly molecular aberrations. It has been revealed that a newly discovered class of non-coding RNAs called circular RNAs (circRNAs) play key roles in dictating tumor behaviors and phenotypes of the prostate tumors. In the current study, our aim was to determine the expression profiles of circHIAT1 and circCDR1AS in PCa compared with benign prostatic hyperplasia (BPH) tissues, as well as their clinicopathological relevance. METHODS: The 50 prostate tissues including 25 PCa tissues and 25 BPH samples were collected for analyzing the expression levels of target circRNAs by quantitative real-time PCR (qRT-PCR). RESULTS: The results revealed that expression of circCDR1AS was significantly elevated in PCa compared with the BPH (p < 0.05). We also observed that PCa patients over the age of 60 had a higher expression of the circCDR1AS than patients under the age of 60 (p = 0.017). Moreover, a lower expression level of circHIAT1 was found in the PCa than BPH tissues (p < 0.05), and finally, the findings indicated that the area under the curve (AUC) of circCDR1AS was 0.848, with 92% sensitivity and 76% specificity, as well as an AUC of 0.828, with the 80% sensitivity and 76% specificity for circHIAT1. CONCLUSION: These observations suggest that the abnormal expression of circCDR1AS and circHIAT1 can be regarded as two different types of molecular pathology with potential biomarker values for PCa, although further studies are needed.


Assuntos
Neoplasias da Próstata/metabolismo , Proteínas Proto-Oncogênicas c-akt/metabolismo , RNA Circular/metabolismo , Área Sob a Curva , Biomarcadores Tumorais , Humanos , Masculino , Próstata/metabolismo , Hiperplasia Prostática/genética , Hiperplasia Prostática/metabolismo , Neoplasias da Próstata/genética , Reação em Cadeia da Polimerase em Tempo Real , Receptores Androgênicos , Transdução de Sinais
2.
Infect Genet Evol ; 122: 105613, 2024 Aug.
Artigo em Inglês | MEDLINE | ID: mdl-38844190

RESUMO

The appearance of SARS-CoV-2 in 2019 triggered a significant economic and health crisis worldwide, with heterogeneous molecular mechanisms that contribute to its development are not yet fully understood. Although substantial progress has been made in elucidating the mechanisms behind SARS-CoV-2 infection and therapy, it continues to rank among the top three global causes of mortality due to infectious illnesses. Non-coding RNAs (ncRNAs), being integral components across nearly all biological processes, demonstrate effective importance in viral pathogenesis. Regarding viral infections, ncRNAs have demonstrated their ability to modulate host reactions, viral replication, and host-pathogen interactions. However, the complex interactions of different types of ncRNAs in the progression of COVID-19 remains understudied. In recent years, a novel mechanism of post-transcriptional gene regulation known as "competing endogenous RNA (ceRNA)" has been proposed. Long non-coding RNAs (lncRNAs), circular RNAs (circRNAs), and viral ncRNAs function as ceRNAs, influencing the expression of associated genes by sequestering shared microRNAs. Recent research on SARS-CoV-2 has revealed that disruptions in specific ceRNA regulatory networks (ceRNETs) contribute to the abnormal expression of key infection-related genes and the establishment of distinctive infection characteristics. These findings present new opportunities to delve deeper into the underlying mechanisms of SARS-CoV-2 pathogenesis, offering potential biomarkers and therapeutic targets. This progress paves the way for a more comprehensive understanding of ceRNETs, shedding light on the intricate mechanisms involved. Further exploration of these mechanisms holds promise for enhancing our ability to prevent viral infections and develop effective antiviral treatments.


Assuntos
COVID-19 , Redes Reguladoras de Genes , SARS-CoV-2 , Humanos , COVID-19/virologia , COVID-19/genética , SARS-CoV-2/genética , RNA Viral/genética , Interações Hospedeiro-Patógeno/genética , MicroRNAs/genética , RNA Circular/genética , RNA não Traduzido/genética , RNA Longo não Codificante/genética
3.
Mol Neurobiol ; 2023 Oct 24.
Artigo em Inglês | MEDLINE | ID: mdl-37874482

RESUMO

It has been more than three years since COVID-19 impacted the lives of millions of people, many of whom suffer from long-term effects known as long-haulers. Notwithstanding multiorgan complaints in long-haulers, signs and symptoms associated with cognitive characteristics commonly known as "brain fog" occur in COVID patients over 50, women, obesity, and asthma at excessive. Brain fog is a set of symptoms that include cognitive impairment, inability to concentrate and multitask, and short-term and long-term memory loss. Of course, brain fog contributes to high levels of anxiety and stress, necessitating an empathetic response to this group of COVID patients. Although the etiology of brain fog in COVID-19 is currently unknown, regarding the mechanisms of pathogenesis, the following hypotheses exist: activation of astrocytes and microglia to release pro-inflammatory cytokines, aggregation of tau protein, and COVID-19 entry in the brain can trigger an autoimmune reaction. There are currently no specific tests to detect brain fog or any specific cognitive rehabilitation methods. However, a healthy lifestyle can help reduce symptoms to some extent, and symptom-based clinical management is also well suited to minimize brain fog side effects in COVID-19 patients. Therefore, this review discusses mechanisms of SARS-CoV-2 pathogenesis that may contribute to brain fog, as well as some approaches to providing therapies that may help COVID-19 patients avoid annoying brain fog symptoms.

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