ArticleCancer cell international2021
Downregulation of miR-29c promotes muscle wasting by modulating the activity of leukemia inhibitory factor in lung cancer cachexia.
Article in Cancer cell international, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 11 papers.
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Who cites it
11 citing papers in PubMed, 18 citations in OpenAlex.
- Review
- Circulating miRNAs Signature as a Predictor of Cachexia in Chronic Heart Failure: Diagnostic and Prognostic Implications.Journal of cardiovascular translational research · 2025Article
- Article
- A novel approach in the identification of microRNAs in malignant pleural effusion for lung cancer diagnosis.Oncology reviews · 2025Review
- Mechanism of exercise-derived circulating exosomes as a target for sarcopenia management.Frontiers in physiology · 2025Review
- Exploring heterogeneity: a dive into preclinical models of cancer cachexia.American journal of physiology. Cell physiology · 2024Review
- Epigenetics of Skeletal Muscle Atrophy.International journal of molecular sciences · 2024Review
- Oncostatin M signaling drives cancer-associated skeletal muscle wasting.Cell reports. Medicine · 2024Article
- Muscle and Bone Defects in Metastatic Disease.Current osteoporosis reports · 2022Review
- Three Pathways of Cancer Cachexia: Inflammation, Changes in Adipose Tissue and Loss of Muscle Mass-The Role of miRNAs.Journal of personalized medicine · 2022Review
- The Molecular Basis and Therapeutic Potential of Leukemia Inhibitory Factor in Cancer Cachexia.Cancers · 2022Review
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Authors and funding
13 authors at 4 institutions in 1 country.
Funding
Abstract
backgroundCancer cachexia is a wasting disorder characterized by significant weight loss, and is attributed to skeletal muscle weakness. In the process of cancer development, microRNAs act as oncogenes or tumor suppressors. Moreover, they are implicated in muscle development and wasting. This study sought to explore the mechanisms and correlation between miR-29c and muscle wasting in lung cancer cachexia.
methodsData for expression analysis were retrieved from the Cancer Genome Atlas (TCGA) database. qRT-PCR analyses were performed to explore the expression levels of miR-29c and Leukemia Inhibitory Factor (LIF). Lewis lung carcinoma (LLC) cell line was used to establish a cachexia model to explore the functions of miR-29c and LIF in lung cancer cachexia. Furthermore, in vitro (in C2C12 myotubes) and in vivo (in LLC tumor-bearing mice) experiments were performed to explore the mechanisms of miR-29c and LIF in lung cachexia.
resultsAnalysis of the lung cancer cachexia model showed that miR-29c was down-regulated, and its expression was negatively correlated with muscle catabolic activity. Overexpression of miR-29c mitigated the cachectic phenotype. Mechanistic studies showed that LIF was a direct target gene of miR-29c, and LIF was upregulated in vitro and in vivo. Analysis showed that LIF promoted muscle wasting through the JAK/STAT and MAP-kinase pathways.
conclusionsThe findings indicated that miR-29c was negatively correlated with the cachectic phenotype, and the miR-29c-LIF axis is a potential therapeutic target for cancer cachexia.
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