ArticleTranslational cancer research2021
Regulation of dynamin-related protein 1 (DRP1) levels modulates myoblast atrophy induced by C26 colon cancer-conditioned medium.
Article in Translational cancer research, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 3 papers.
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3 citing papers in PubMed, 3 citations in OpenAlex.
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- Transcriptome Analysis of the Inhibitory Effects of 20(S)-Protopanaxadiol on NCI-H1299 Non-Small Cell Lung Cancer Cells.Molecules (Basel, Switzerland) · 2023Article
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7 authors at 5 institutions in 1 country.
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No grant is acknowledged in the PubMed record.
Abstract
backgroundCancer associated-cachexia, which involves progressive skeletal muscle loss, is induced by multiple factors. However, the underlying mechanism remains unclear. Dynamin-related protein 1 (DRP1), a major modulator of mitochondrial fission, has been reported to participate in muscle turnover. This study aimed to explore the role of DRP1 in muscle during the process of cancer associated-cachexia (CAC) via an in vitro model and the mechanisms involved.
methodsC26 colon cancer cell-conditioned medium (CM) was used to incubate with C2C12 myotubes to simulate cachexia. Myotubes were then transduced with lentiviral vectors of DRP1-small interfering RNA (siRNA), DRP1 overexpression plasmid, or a control plasmid to regulate the DRP1 levels, and their diameters were assessed using a biological microscope. Furthermore, transcriptome sequencing was performed to screen the pathways involved, and real-time polymerase chain reaction (RT-PCR) was used for verification.
resultsThe cachexia model was successfully established with a decreased myotube diameter and increased DRP1 expression. DRP1 knockdown significantly ameliorated myotube wasting during cachexia, while DRP1 overexpression intensified this phenomenon. Transcriptome sequencing indicated that DRP1 knockdown was associated with the activation of ribosomal biogenesis. However, PCR results showed that compared to the control, one of the ribosomal biogenesis marker's (Ubf) level was decreased by C26 CM, and DRP1 knockdown did not significantly restore its level.
conclusionsDuring C26 CM-induced cachexia, DRP1 was activated, while the regulation of DRP1 levels was able to modulate the atrophy of C2C12 myotubes. The underlying mechanism of the alleviated muscle atrophy induced by DRP1 knockdown was likely associated with increased ribosomal activity.
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