Perspectives on miRNAs directly targeting BDNF for cancer diagnosis and treatment (Review)

Xie, Ziteng; Xu, Xinhua; Cao, Wenbo; He, Luyun; Kou, Chen; He, Jiajia; Guo, Yongfeng; Yue, Mingjin; Mo, Saijun

doi:10.3892/ijo.2023.5478

Cited by 1 publication

(2 citation statements)

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“…BDNF plays a crucial role in neural development, synaptic adaptability, and cell survival. It has notable effects on neurotransmission and is associated with various brain disorders and cancer progression 35,84 …”

Section: Discussionmentioning

confidence: 99%

“…It has notable effects on neurotransmission and is associated with various brain disorders and cancer progression. 35,84 Our research emphasizes the impact of chronic morphine treatment on reducing BDNF levels, especially in neural cell lines, and explores the potential of combined treatments (CAB + Mdivi-1) to counteract this reduction. This discovery is consistent with previous studies that suggest long-term morphine usage can affect BDNF expression in the ventral tegmental area (VTA), 85 thereby influencing the rewarding effects of the drug.…”

Section: Bdnf and Morphine's Effects On Neural Plasticitymentioning

confidence: 99%

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Exploring neuroadaptive cellular pathways in chronic morphine exposure: An in‐vitro analysis of cabergoline and Mdivi‐1 co‐treatment effects on the autophagy–apoptosis axis

Makvand,

Mirtorabi,

Campbell

et al. 2024

J of Cellular Biochemistry

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The complex impacts of prolonged morphine exposure continue to be a significant focus in the expanding area of addiction studies. This research investigates the effectiveness of a combined treatment using Cabergoline and Mdivi‐1 to counteract the neuroadaptive changes caused by in vitro morphine treatment. The impact of Methadone, Cabergoline, and a combination of Cabergoline and Mdivi‐1 on the cellular and molecular responses associated with Morphine‐induced changes was studied in human Neuroblastoma (SK‐N‐MC) and Glioblastoma (U87‐MG) cell lines that were exposed to prolong Morphine treatment. Cabergoline and Mdivi‐1 combined treatment effectively influenced the molecular alterations associated with neuroadaptation in chronic morphine‐exposed neural cells. This combination therapy normalized autophagy and reduced oxidative stress by enhancing total‐antioxidant capacity, mitigating apoptosis, restoring BDNF expression, and balancing apoptotic elements. Our research outlines morphine's dual role in modulating mitochondrial dynamics via the dysregulation of the autophagy–apoptosis axis. This emphasizes the significant involvement of DRP1 activity in neurological adaptation processes, as well as disturbances in the dopaminergic pathway during in vitro chronic exposure to morphine in neural cells. This study proposes a novel approach by recommending the potential effectiveness of combining Cabergoline and Mdivi‐1 to modulate the neuroadaptations caused by morphine. Additionally, we identified BDNF and PCNA in neural cells as potential neuroprotective markers for assessing the effectiveness of drugs against opioid toxicity, emphasizing the need for further validation. The study uncovers diverse effects observed in pretreated morphine glioblastoma cells under treatment with Cabergoline and methadone. This highlights the potential for new treatments in the DRD2 pathway and underscores the importance of investigating the interplay between autophagy and apoptosis to advance research in managing cancer‐related pain. The study necessitates an in‐depth investigation into the relationship between autophagy and apoptosis, with a specific emphasis on protein interactions and the dynamics of cell signaling.

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Section: Discussionmentioning

confidence: 99%