ArticleCell death & disease2022
ARHGEF3 regulates the stability of ACLY to promote the proliferation of lung cancer.
Article in Cell death & disease, 2022. 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, 15 citations in OpenAlex.
- Lung cancer metabolism: a dynamic and adaptive network.Cellular and molecular life sciences : CMLS · 2026Review
- Tumor-Intrinsic ARHGEF3 Enhances Antitumor Immunity by Promoting T-Cell Infiltration and Limiting Myeloid Cell-Mediated Immunosuppression.Advanced science (Weinheim, Baden-Wurttemberg, Germany) · 2026Article
- Asiatic Acid Ameliorates MNNG-Induced Chronic Atrophic Gastritis by Inhibiting the Activation of the HRAS/PI3K/AKT/GSK3β Signaling Axis.Phytotherapy research : PTR · 2026Article
- Targeted metabolism creates possibilities for lung cancer treatment in the precision tumor era.Respiratory research · 2026Review
- The Rho GTPase regulator ARHGEF3 orchestrates hair placode budding by coordinating cell fate and P-cadherin patterning in mice.PLoS biology · 2026Article
- ARHGEF3 coordinates adipocyte hypertrophy and differentiation through dual YAP-RhoA and PPARγ activation.Journal of advanced research · 2026Article
- The role of ubiquitination and deubiquitination in cancer lipid metabolism.Frontiers in oncology · 2025Review
- The role of acetylation and deacetylation in cancer metabolism.Clinical and translational medicine · 2025Review
- Interplay between acetylation and ubiquitination controls PSAT1 protein stability in lung adenocarcinoma.Communications biology · 2024Article
- ARHGEF3 Regulates Hair Follicle Morphogenesis.bioRxiv : the preprint server for biology · 2024Article
- Advances of E3 ligases in lung cancer.Biochemistry and biophysics reports · 2024Review
- Metabolic reprogramming in lung cancer and its clinical implication.Frontiers in pharmacology · 2024Review
- Ubiquitination Links DNA Damage and Repair Signaling to Cancer Metabolism.International journal of molecular sciences · 2023Review
Corrections and comments
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Authors and funding
7 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Rho GTPases play an essential role in many cellular processes, including cell cycle progress, cell motility, invasion, migration, and transformation. Several studies indicated that the dysregulation of Rho GTPase signaling is closely related to tumorigenesis. Rho GEFs considered being positive regulators of Rho GTPase, promoting the dissociation of Rho protein from GDP and binding to GTP, thus activating the downstream signaling pathway. Herein, we demonstrated that ARHGEF3, a member of the Rho GEFs family, played an important role in non-small cell lung cancer (NSCLC). We found that ARHGEF3 was highly expressed in non-small cell lung cancer and facilitated cancer cell proliferation of NSCLC cells in vitro and in vivo. Further studies demonstrated that ARHGEF3 enhanced the protein homeostasis of ATP-citrate lyase (ACLY) by reducing its acetylation on Lys17 and Lys86, leading to the dissociation between ACLY and its E3 ligase-NEDD4. Interestingly, this function of ARHGEF3 on the protein homeostasis of ACLY was independent of its GEF activity. Taken together, our findings uncover a novel function of ARHGEF3, suggesting that ARHGEF3 is a promising therapeutic target in non-small cell lung cancer.
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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.