ArticleExperimental cell research2010
The C/EBPbeta isoform, liver-inhibitory protein (LIP), induces autophagy in breast cancer cell lines.
Article in Experimental cell research, 2010. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 13 papers.
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Who cites it
13 citing papers in PubMed, 30 citations in OpenAlex.
- Transcriptional and epigenetic regulation of autophagy: mechanisms, disease relevance and therapeutic opportunities.Signal transduction and targeted therapy · 2026Review
- Peritumoral adipose tissue promotes lipolysis and white adipocytes browning by paracrine action.Frontiers in endocrinology · 2023Article
- Pre-activation of autophagy impacts response to olaparib in prostate cancer cells.Communications biology · 2022Article
- Analysis of core genes for colorectal cancer prognosis based on immune and stromal scores.PeerJ · 2021Article
- Metformin Regulates the Expression of CD133 Through the AMPK-CEBPβ Pathway in Hepatocellular Carcinoma Cell Lines.Neoplasia (New York, N.Y.) · 2019Article
- Human transposons are an abundant supply of transcription factor binding sites and promoter activities in breast cancer cell lines.Mobile DNA · 2019Article
- Primate-specific oestrogen-responsive long non-coding RNAs regulate proliferation and viability of human breast cancer cells.Open biology · 2016Article
- Degradation of polyomavirus JC T-antigen by stress involves the LIP isoform of C/EBP.Cell cycle (Georgetown, Tex.) · 2015Article
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- Mechanisms of autophagy and apoptosis: Recent developments in breast cancer cells.World journal of biological chemistry · 2011Article
- Tetradecylthioacetic acid inhibits proliferation of human SW620 colon cancer cells--gene expression profiling implies endoplasmic reticulum stress.Lipids in health and disease · 2011Article
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Authors and funding
2 authors at 1 institution in 1 country.
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Abstract
Autophagy is a process involving the bulk degradation of cellular components in the cytoplasm via the lysosomal degradation pathway. Autophagy manifests a protective role in stressful conditions such as nutrient or growth factor depletion; however, extensive degradation of regulatory molecules or organelles essential for survival can lead to the demise of the cell, or autophagy-mediated cell death. The role of autophagy in cancer is complex with roles in both tumor suppression and tumor promotion proposed. Here we report that an isoform of the C/EBPbeta transcription factor, liver-enriched inhibitory protein (LIP), induces cell death in human breast cancer cells and stimulates autophagy. Overexpression of LIP is incompatible with cell growth and when cell cycle analysis was performed, a DNA profile of cells undergoing apoptosis was not observed. Instead, LIP expressing cells appeared to have large autophagic vesicles when examined via electron microscopy. Autophagy was further assessed in LIP expressing cells by monitoring the development of acidic vesicular organelles and conversion of LC3 from the cytoplasmic form to the membrane-bound form. Our work shows that C/EBPbeta isoform, LIP, is another member of the group of transcription factors, including E2F1 and p53, which are capable of playing a role in autophagy.
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Registered trials
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