ArticleCell death & disease2024
Phosphorylation of INF2 by AMPK promotes mitochondrial fission and oncogenic function in endometrial cancer.
Article in Cell death & disease, 2024. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 24 papers.
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Who cites it
24 citing papers in PubMed, 18 citations in OpenAlex.
- Phosphorylation-dependent interaction between VAP proteins and INF2 influences ER morphology.Current biology : CB · 2026Article
- The dual role of AMPK in cancer metabolic reprogramming.Molecular biology reports · 2026Review
- An INF2-dependent actin-mediated step in inositol 1,4,5-trisphosphate receptor cluster formation and activity.Current biology : CB · 2026Article
- [Association between umbilical cord blood proteome and early infant neurodevelopmental risk].Beijing da xue xue bao. Yi xue ban = Journal of Peking University. Health sciences · 2026Article
- Review
- The SDF-1α/CXCR4 axis regulates chondrocyte mitochondrial dynamics via the ERK/AMPKα pathway.Cell communication and signaling : CCS · 2026Article
- Exon skipping as a potential diagnostic biomarker in colorectal cancer: an integrated epigenomic-transcriptomic analysis.Human genomics · 2026Article
- AMPK at the interface of nutrient sensing, metabolic flux and energy homeostasis.Nature metabolism · 2026Review
- Mechanical observables of cancer invasion: actin, adhesion, and metastatic plasticity.Frontiers in cell and developmental biology · 2026Review
- Exploring the Functional and Prognostic Significance of miR-217 in Uterine Corpus Endometrial Carcinoma.Current medicinal chemistry · 2026Article
- From organelles to therapy: rethinking combined hepatocellular-cholangiocarcinoma.Frontiers in cell and developmental biology · 2026Review
- Disulfidptosis-related genes signature predicts prognosis and immune microenvironment in colon cancer.Frontiers in molecular biosciences · 2026Article
- Glucose Deprivation-Induced Disulfidptosis via the SLC7A11-INF2 Axis: Pan-Cancer Prognostic Exploration and Therapeutic Validation.Advanced science (Weinheim, Baden-Wurttemberg, Germany) · 2025Article
- The AMPK Pathway: Molecular Rejuvenation of Metabolism and Mitochondria.Annual review of cell and developmental biology · 2025Review
- Mitochondrial metabolism and cancer therapeutic innovation.Signal transduction and targeted therapy · 2025Review
- EphA5 Expression Predicts Better Survival Despite an Association with Proliferative Activity in Endometrial Cancer.Journal of clinical medicine · 2025Article
- Targeting INF2 with DiosMetin 7-O-β-D-Glucuronide: a new stratagem for colorectal cancer therapy.BMC cancer · 2025Article
- Expression of AMPK and PLIN2 in the regulation of lipid metabolism and oxidative stress in bitches with open cervix pyometra.BMC veterinary research · 2025Article
- Remodeling the tumor microenvironment: regulatory effects of β-sitosterol and luteolin on the immunosuppressive milieu in endometrial carcinoma and implications for combinatorial immunotherapy.Frontiers in immunology · 2025Review
- Revisiting IGF2BP1 in Endometrial Cancer: Ethnic-Specific Prognostic Implications and Association with Caspase-3 and pSTAT3.Journal of Cancer · 2025Article
Corrections and comments
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Authors and funding
6 authors at 2 institutions in 2 countries.
Funding
Abstract
Mitochondria are highly dynamic organelles capable of altering their sizes and shapes to maintain metabolic balance through coordinated fission and fusion processes. In various cancer types, mitochondrial hyperfragmentation has been frequently observed, contributing to the progression of cancer toward metastasis. Inverted formin 2 (INF2), which resides in the endoplasmic reticulum (ER), has been found to accelerate actin polymerization and drive mitochondrial fission. In this study, we demonstrate that INF2 expression is significantly upregulated in endometrial cancer (EC) and is associated with a poor prognosis in EC patients. INF2 promotes anchorage-dependent and independent EC cell growth in part by facilitating mitochondrial fission. Furthermore, in conditions of energy stress, AMP-activated protein kinase (AMPK) phosphorylates INF2 at Ser1077, leading to increased localization of INF2 to the ER and enhanced recruitment of the dynamin-related protein 1 (DRP1) to mitochondria. This AMPK-mediated phosphorylation of INF2 at Ser1077 facilitates mitochondrial division and promotes EC cell growth. Pathological examination using immunohistochemical analyses revealed a positive correlation between AMPK activity and phosphorylated INF2 (Ser1077) in EC specimens. Collectively, our findings uncover novel molecular mechanisms involving the AMPK-INF2 axis, which regulates mitochondrial dynamics and malignant cell growth in EC.
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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.