ArticleCell death and differentiation2017
RIP4 inhibits STAT3 signaling to sustain lung adenocarcinoma differentiation.
Article in Cell death and differentiation, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 26 papers.
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Who cites it
26 citing papers in PubMed, 30 citations in OpenAlex.
- RIPK4 is associated with altered bioenergetics and invasive in melanoma three-dimensional models.Scientific reports · 2026Article
- miR-575/RIPK4 axis modulates cell cycle progression and proliferation by inactivating the Wnt/β-catenin signaling pathway through inhibiting RUNX1 in colon cancer.Molecular and cellular biochemistry · 2024Article
- The involvement of RIPK4 in TNF-α-stimulated IL-6 and IL-8 production by melanoma cells.Journal of cancer research and clinical oncology · 2024Article
- Functions of the RIP kinase family members in the skin.Cellular and molecular life sciences : CMLS · 2023Review
- Vemurafenib and Dabrafenib Downregulates RIPK4 Level.Cancers · 2023Article
- Increased Expression of the Δ133p53β Isoform Enhances Brain Metastasis.International journal of molecular sciences · 2023Article
- Role of Receptor Interacting Protein (RIP) kinases in cancer.Genes & diseases · 2022Review
- Lysyl Oxidase Family Proteins: Prospective Therapeutic Targets in Cancer.International journal of molecular sciences · 2022Review
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- Knockdown of RNF183 suppressed proliferation of lung adenocarcinoma cellsCell cycle (Georgetown, Tex.) · 2022Article
- Depletion of RIPK4 parallels higher malignancy potential in cutaneous squamous cell carcinoma.PeerJ · 2022Article
- Deciphering the Functional Role of RIPK4 in Melanoma.International journal of molecular sciences · 2021Article
- Foot-and-Mouth Disease Virus Inhibits RIP2 Protein Expression to Promote Viral Replication.Virologica Sinica · 2021Article
- RIPK4 Suppresses the Invasion and Metastasis of Hepatocellular Carcinoma by Inhibiting the Phosphorylation of STAT3.Frontiers in molecular biosciences · 2021Article
- Overexpression of RIPK4 Predicts Poor Prognosis and Promotes Metastasis in Ovarian Cancer.BioMed research international · 2021Article
- Bioinformatics Analysis and Functional Verification of ADAMTS9-AS1/AS2 in Lung Adenocarcinoma.Frontiers in oncology · 2021Article
- Developing prognostic gene panel of survival time in lung adenocarcinoma patients using machine learning.Translational cancer research · 2020Article
- Insight Into the Function of RIPK4 in Keratinocyte Differentiation and Carcinogenesis.Frontiers in oncology · 2020Review
- Erchen Plus Huiyanzhuyu Decoction Inhibits the Growth of Laryngeal Carcinoma in a Mouse Model of Phlegm-Coagulation-Blood-Stasis Syndrome via the STAT3/Cyclin D1 Pathway.Evidence-based complementary and alternative medicine : eCAM · 2020Article
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7 authors at 4 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Loss of epithelial differentiation and extracellular matrix (ECM) remodeling are known to facilitate cancer progression and are associated with poor prognosis in patients with lung cancer. We have identified Receptor-interacting serine/threonine protein kinase 4 (RIP4) as a regulator of tumor differentiation in lung adenocarcinoma (AC). Bioinformatics analyses of human lung AC samples showed that poorly differentiated tumors express low levels of RIP4, whereas high levels are associated with better overall survival. In vitro, lung tumor cells expressing reduced RIP4 levels showed enhanced activation of STAT3 signaling and had a greater ability to invade through collagen. In contrast, overexpression of RIP4 inhibited STAT3 activation, which abrogated interleukin-6-dependent induction of lysyl oxidase, a collagen cross-linking enzyme. In an autochthonous mouse model of lung AC initiated by Kras(G12D) expression with loss of p53, Rip4 knockdown tumors progressed to a poorly differentiated state marked by an increase in Hmga2, reduced Ttf1, and enrichment of genes regulating extracellular remodeling and Jak-Stat signaling. Tail vein injections of cells overexpressing Rip4 showed a reduced potential to invade and form tumors, which was restored by co-expression of Stat3. Altogether, our work has identified that loss of RIP4 enhances STAT3 signaling in lung cancer cells, promoting the expression of ECM remodeling genes and cancer dedifferentiation.
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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.