Caspases interplay with kinases and phosphatases to determine cell fate

Akbari‐Birgani, Shiva; Khademy, Mitra; Mohseni-Dargah, Masoud; Madadi, Zahra; Mokhtar-Ahmadabadi, Roya; Davoodi-Monfared, Parviz

doi:10.1016/j.ejphar.2019.04.048

Cited by 5 publications

(2 citation statements)

References 146 publications

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“…This ability to promote cancer was suppressed when CRNDE was knocked down. In mitochondrial apoptosis-related pathways, anti-apoptotic gene Bcl-2 and pro-apoptotic Bax are two key in uencing genomic factors [ 20] .Caspases are essential components of the apoptotic mechanism, especially caspase-3 [ 21] . Following knockdown of CRNDE, Bcl-2 was drastically downregulated, with concomitant upregulation of Bax and caspase-3.…”

Section: Discussionmentioning

confidence: 99%

Long Non-coding RNA CRNDE Exacerbates NPC Advancement Mediated by the miR-545-5p/CCND2 Axis

Jiang

et al. 2021

Preprint

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Background: Previous studies indicated CRNDE to have a pivotal part within tumorigenesis. Notwithstanding, precise details on CRNDE activities within NPC are still uncertain. The investigation described in this article served to focus in greater depth on the mechanistics regarding CRNDE, together with all associated regulatory networks, on nasopharyngeal carcinoma (NPC) and its treatment possibilities.Methods：Quantitative real-time polymerase chain reaction (RT-qPCR) analyzed CRNDE, miR-545-5p and CCND2 expression within NPCs and representative cell lineages. CCK-8 cell counting-, EdU-, wound-healing- / transwell-assays analyzed cellular proliferation, migrative, together with invasive properties. Apoptosis / cell cycle progression were scrutinized through flow cytometry. Dual-luciferase reporter assays validated CRNDE / miR-545-5p / CCND2 interplay. Proteomic expression of apoptosis-related protein, EMT-related protein and CCND2 protein were evaluated through Western blotting. In addition, Ki67 expression was evaluated through immunohistochemical staining. The effect of CRNDE in vivo was assessed by nude murine xenograft model studies.Results: This study demonstrated up-regulated expression of CRNDE and CCND2 within NPC tissues /cell lines. Meanwhile, miR-545-5p was downregulated. CRNDE knockdown or miR-545-5p over-expression drastically reduced NPC proliferative, migrative and invasive properties, promoted apoptosis / altered cell cycle, and inhibited the expression of CCND2. However, miR-545-5p downregulation had opposing effects. All inhibiting functions generated by CRNDE downregulation upon NPC progression could be counterbalanced or synergistically exacerbated, depending on miR-545-5p downregulation or upregulation, respectively. Multiple-level investigations revealed CRNDE to serve as a sponge for miR-545-5p and can target CCND2 within NPCs.Conclusions：CRNDE increases CCND2 expression by competitive binding with miR-545-5p, thus accelerating the development of NPC. This provides potential therapeutic targets and prognostic markers against NPC.

show abstract

Section: Discussionmentioning

confidence: 99%

Long Non-coding RNA CRNDE Exacerbates NPC Advancement Mediated by the miR-545-5p/CCND2 Axis

Jiang

et al. 2021

Preprint

View full text Add to dashboard Cite

show abstract

“…In mitochondrial apoptosis-related pathways, anti-apoptotic gene Bcl-2 and pro-apoptotic Bax are two key influencing genomic factors [ 20 ]. Caspases are essential components of the apoptotic mechanism, especially caspase-3 [ 21 ]. Following knock-down of CRNDE, Bcl-2 was drastically down-regulated, with concomitant up-regulation of Bax and caspase-3.…”

Section: Discussionmentioning

confidence: 99%

Long non-coding RNA CRNDE exacerbates NPC advancement mediated by the miR-545-5p/CCND2 axis

Jiang

et al. 2021

Cancer Cell Int

View full text Add to dashboard Cite

Background Previous studies indicated CRNDE to have a pivotal part within tumorigenesis. Notwithstanding, precise details on CRNDE activities within NPC are still uncertain. The investigation described in this article served to focus in greater depth on the mechanistics regarding CRNDE, together with all associated regulatory networks, on nasopharyngeal carcinoma (NPC) and its treatment possibilities. Methods Quantitative real-time polymerase chain reaction (RT-qPCR) analyzed CRNDE, miR-545-5p and CCND2 expression within NPCs and representative cell lineages. CCK-8 cell counting-, EdU-, wound-healing-/transwell-assays analyzed cellular proliferation, migrative, together with invasive properties. Apoptosis/cell cycle progression were scrutinized through flow cytometry. Dual-luciferase reporter assays validated CRNDE/miR-545-5p/CCND2 interplay. Proteomic expression of apoptosis-related protein, EMT-related protein and CCND2 protein were evaluated through Western blotting. In addition, Ki67 expression was evaluated through immunohistochemical staining. The effect of CRNDE in vivo was assessed by nude murine xenograft model studies. Results This study demonstrated up-regulated expression of CRNDE and CCND2 within NPC tissues/cell lines. Meanwhile, miR-545-5p was down-regulated. CRNDE knock-down or miR-545-5p over-expression drastically reduced NPC proliferative, migrative and invasive properties, promoted apoptosis/altered cell cycle, and inhibited CCND2 expression. However, miR-545-5p down-regulation had opposing effects. All inhibiting functions generated by CRNDE down-regulation upon NPC progression could be counterbalanced or synergistically exacerbated, depending on miR-545-5p down-regulation or up-regulation, respectively. Multiple-level investigations revealed CRNDE to serve as a sponge for miR-545-5p, and can target CCND2 within NPCs. Conclusions CRNDE increases CCND2 expression by competitive binding with miR-545-5p, thus accelerating the development of NPC. This provides potential therapeutic targets and prognostic markers against NPC.

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