Nuclear Factor κB Signaling and Its Related Non-coding RNAs in Cancer Therapy

Liu, Xiaomin; Shao, Yang; Zhou, Jinbao; Qian, Guangren; Ma, Zhongliang

doi:10.1016/j.omtn.2019.11.007

Cited by 34 publications

(16 citation statements)

References 120 publications

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“…NF-κB is considered to be closely related to the inflammatory response, cancer development, cellular proliferation, apoptosis, etc. [ 87 ]. NF-κB transcription factor is expressed in glial cells in the spinal cord, and its main function is to mediate a variety of mechanisms, such as immune response, injury response, and astrogliosis [ 88 ].…”

Section: Discussionmentioning

confidence: 99%

Exosomes derived from miR-26a-modified MSCs promote axonal regeneration via the PTEN/AKT/mTOR pathway following spinal cord injury

Chen

Tian

et al. 2021

Stem Cell Res Ther

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Background Exosomes derived from the bone marrow mesenchymal stem cell (MSC) have shown great potential in spinal cord injury (SCI) treatment. This research was designed to investigate the therapeutic effects of miR-26a-modified MSC-derived exosomes (Exos-26a) following SCI. Methods Bioinformatics and data mining were performed to explore the role of miR-26a in SCI. Exosomes were isolated from miR-26a-modified MSC culture medium by ultracentrifugation. A series of experiments, including assessment of Basso, Beattie and Bresnahan scale, histological evaluation, motor-evoked potential recording, diffusion tensor imaging, and western blotting, were performed to determine the therapeutic influence and the underlying molecular mechanisms of Exos-26a in SCI rats. Results Exos-26a was shown to promote axonal regeneration. Furthermore, we found that exosomes derived from miR-26a-modified MSC could improve neurogenesis and attenuate glial scarring through PTEN/AKT/mTOR signaling cascades. Conclusions Exosomes derived from miR-26a-modified MSC could activate the PTEN-AKT-mTOR pathway to promote axonal regeneration and neurogenesis and attenuate glia scarring in SCI and thus present great potential for SCI treatment. Graphical abstract

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Section: Discussionmentioning

confidence: 99%

Exosomes derived from miR-26a-modified MSCs promote axonal regeneration via the PTEN/AKT/mTOR pathway following spinal cord injury

Chen

Tian

et al. 2021

Stem Cell Res Ther

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“…In normal condition, IκB arrests NF‐κB in the cytoplasm. Upon activation, the arrested NF‐κB is released and translocated into the nucleus to modulate target expression [12]. Besides protein‐encoding genes, human genome also encodes more noncoding RNAs.…”

Section: Introductionmentioning

confidence: 99%

Long noncoding RNA LINC01578 drives colon cancer metastasis through a positive feedback loop with the NF‐κB/YY1 axis

et al. 2020

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Metastasis accounts for poor prognosis of cancers and related deaths. Accumulating evidence has shown that long noncoding RNAs (lncRNAs) play critical roles in several types of cancer. However, which lncRNAs contribute to metastasis of colon cancer is still largely unknown. In this study, we found that lncRNA LINC01578 was correlated with metastasis and poor prognosis of colon cancer. LINC01578 was upregulated in colon cancer, associated with metastasis, advanced clinical stages, poor overall survival, disease-specific survival, and disease-free survival. Gain-of-function and loss-of-function assays revealed that LINC01578 enhanced colon cancer cell viability and mobility in vitro and colon cancer liver metastasis in vivo. Mechanistically, nuclear factor kappa B (NF-jB) and Yin Yang 1 (YY1) directly bound to the LINC01578 promoter, enhanced its activity, and activated LINC01578 expression. LINC01578 was shown to be a chromatin-bound lncRNA, which directly bound NFKBIB promoter. Furthermore, LINC01578 interacted with and recruited EZH2 to NFKBIB promoter and further repressed NFKBIB expression, thereby activating NF-jB signaling. Through activation of NF-jB, LINC01578 further upregulated YY1 expression. Through activation of the NF-jB/YY1 axis, LINC01578 in turn enhanced its own promoter activity, suggesting that LINC01578 and NF-jB/YY1 formed a positive feedback loop. Blocking NF-jB signaling abolished the oncogenic roles of LINC01578 in colon cancer. Furthermore, the expression levels of LINC01578, NFKBIB, and YY1 were correlated in clinical tissues. Collectively, this study demonstrated that LINC01578 promoted colon cancer metastasis via forming a positive feedback loop with NF-jB/YY1 and suggested that LINC01578 represents a potential prognostic biomarker and therapeutic target for colon cancer metastasis.

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“…Three different modes are involved in the activation of NF- κ B [ 18 ]. In the canonical NF- κ B activation pathway, the with NF- κ B inhibitor (I κ B) being phosphorylated and degraded, the NF- κ B dimer (p65/p50) will enter the nucleus, acting as a transcriptional activator [ 19 ].…”

Section: Nf- κ B Signalingmentioning

confidence: 99%

Modulation of the Wound Healing through Noncoding RNA Interplay and GSK-3β/NF-κB Signaling Interaction

Wang

2021

International Journal of Genomics

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Diabetic foot ulcers are seriously endangering the physical and mental health of patients. Due to the long duration of inflammation, the treatment of nonhealing wounds in diabetes is one of the most prominent healthcare problems in the world. The nuclear factor kappa B (NF-κB) signaling pathway, a classical pathway that triggers inflammatory response, is regulated by many regulators, such as glycogen synthase kinase 3 beta (GSK-3β). Noncoding RNAs, a large class of molecules that regulate gene expression at the posttranscriptional or posttranslational level, play an important role in various stages of wound healing, especially in the stage of inflammation. Herein, we summarized the roles of noncoding RNAs in the NF-κB/GSK-3β signaling, which might provide new ideas for the treatment of diabetic wound healing.

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Nuclear Factor κB Signaling and Its Related Non-coding RNAs in Cancer Therapy

Cited by 34 publications

References 120 publications

Exosomes derived from miR-26a-modified MSCs promote axonal regeneration via the PTEN/AKT/mTOR pathway following spinal cord injury

Exosomes derived from miR-26a-modified MSCs promote axonal regeneration via the PTEN/AKT/mTOR pathway following spinal cord injury

Long noncoding RNA LINC01578 drives colon cancer metastasis through a positive feedback loop with the NF‐κB/YY1 axis

Modulation of the Wound Healing through Noncoding RNA Interplay and GSK-3β/NF-κB Signaling Interaction

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