ArticleOncotarget2018
TGF-β2-induced EMT is dampened by inhibition of autophagy and TNF-α treatment.
Article in Oncotarget, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 32 papers.
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
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Who cites it
32 citing papers in PubMed, 52 citations in OpenAlex.
- LncRNA YIYA drives pancreatic cancer proliferation under high-glucose conditions by reinforcing a RAS-PKM2-dependent Warburg phenotype.FEBS letters · 2026Article
- BRAF inhibition increases TGFβ2 production and stimulates metastasis in mice with endogenous BRAFProceedings of the National Academy of Sciences of the United States of America · 2025Article
- Phenomics Demonstrates Cytokines Additive Induction of Epithelial to Mesenchymal Transition.Journal of cellular physiology · 2025Article
- Autophagy: a necessary evil in cancer and inflammation.3 Biotech · 2024Review
- Human Chorionic Gonadotropin Regulates the Smad Signaling Pathway by Antagonizing TGF-β in Giant Cell Tumor of Bone.Recent patents on anti-cancer drug discovery · 2024Article
- Inhibition of anlotinib-induced autophagy attenuates invasion and migration by regulating epithelial-mesenchymal transition and cytoskeletal rearrangement through ATG5 in human osteosarcoma cells.Brazilian journal of medical and biological research = Revista brasileira de pesquisas medicas e biologica · 2024Article
- Influence of CCancers · 2023Article
- Autophagy, molecular chaperones, and unfolded protein response as promoters of tumor recurrence.Cancer metastasis reviews · 2023Review
- Heat treatment-induced autophagy promotes breast cancer cell invasion and metastasis via TGF-PeerJ · 2023Article
- Inhibition of autophagy by 3-methyladenine promotes migration and invasion of colon cancer cells through epithelial mesenchymal transformation.Translational cancer research · 2022Article
- Mig-6 Inhibits Autophagy in HCC Cell Lines by Modulating miR-193a-3p.International journal of medical sciences · 2022Article
- Progress of tumor-associated macrophages in the epithelial-mesenchymal transition of tumor.Frontiers in oncology · 2022Review
- Article
- KrasGenome biology · 2021Article
- The role of TGF-β2 in cartilage development and diseases.Bone & joint research · 2021Article
- TGFβ signaling networks in ovarian cancer progression and plasticity.Clinical & experimental metastasis · 2021Review
- Nuclear-Encoded lncRNAMolecular therapy. Nucleic acids · 2021Article
- Increased ATG5 Expression Predicts Poor Prognosis and Promotes EMT in Cervical Carcinoma.Frontiers in cell and developmental biology · 2021Article
- Duality of Interactions Between TGF-β and TNF-α During Tumor Formation.Frontiers in immunology · 2021Review
- Interleukin-6 Induced Proliferation Is Attenuated by Transforming Growth Factor-β-Induced Signaling in Human Hepatocellular Carcinoma Cells.Frontiers in oncology · 2021Article
Corrections and comments
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Authors and funding
5 authors at 2 institutions in 2 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Hepatocellular carcinoma (HCC) typically develops in a chronic inflammatory setting causal to release of a plethora of growth factors and cytokines. However, the molecular effect of these cytokines on HCC progression is poorly understood. In this study, we exposed HCC cells to TGF-β2 (Transforming Growth Factor-β2), which resulted in a significant elevation of EMT (Epithelial to Mesenchymal Transition) like features. Molecular analysis of EMT markers showed an increase at both RNA and protein levels upon TGF-β2 administration along with up-regulation of TGF-β-induced Smad signaling. Induction of EMT was associated with a simultaneous increase in reactive oxygen species (ROS) and cytostasis of TGF-β2-treated cells. Importantly, quenching of ROS resulted in a significant promotion of TGF-β2-induced EMT. Furthermore, cells treated with TGF-β2 also showed an enhanced autophagic flux. Interestingly, inhibition of autophagy by chloroquine-di-phosphate (CQDP) or siRNA-mediated ablation of ATG5 drastically inhibited TGF-β2-induced EMT. Autophagy inhibition significantly increased ROS levels promoting apoptosis. It was further observed that pro-inflammatory cytokine like, TNF-α (Tumor Necrosis Factor-α) can antagonize TGF-β2-induced response by down-regulating autophagy, increasing ROS levels and thus inhibiting EMT in HCC cells. This inhibitory effect of TNF-α is serum-independent. Transcriptomic analysis through RNA sequencing was further performed which validated that TGF-β2-induced autophagic genes are inhibited by TNF-α treatment suppressing EMT. Our study suggests that autophagy plays a pro-metastatic role facilitating EMT by regulating ROS levels in HCC cells and TNF-α can suppress EMT by inhibiting autophagy. We provide unique mechanistic insights into the role of TGF-β2 in HCC cells, along with appropriate cues to effectively control the disease.
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Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.