ArticleCell death & disease2023
TIM-4 orchestrates mitochondrial homeostasis to promote lung cancer progression via ANXA2/PI3K/AKT/OPA1 axis.
Article in Cell death & disease, 2023. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 35 papers, 1 of them a synthesis that pooled it.
What it found
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The trial behind it
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Who cites it
35 citing papers in PubMed, 1 synthesis or guideline pooled it, 39 citations in OpenAlex.
- NUSAP1 promotes gastric cancer radioresistance by inhibiting ubiquitination of ANXA2 and is suppressed by miR-129-5p.Journal of cancer research and clinical oncology · 2024Pooled it
- GJB2, a novel transcription target of HSF4, confers tumorigenic and metastatic phenotypes and sustains mitochondrial homeostasis in lung adenocarcinoma via the PI3K/AKT pathway.Cell adhesion & migration · 2026Article
- Reduced nerve growth factor (NGF) mediates arsenic-induced mitochondrial dynamics imbalance and neuronal damage both in vivo and in vitro.Journal of Zhejiang University. Science. B · 2026Article
- Review
- GSH-Responsive Nanoparticles Enhance Hepatocellular Carcinoma Immunotherapy Through Synergistic Effects of Cuproptosis and PI3K Inhibitor Combination.Advanced science (Weinheim, Baden-Wurttemberg, Germany) · 2026Article
- Caffeine Sodium Benzoate-Induced Macrophage M1 Polarization Promotes Endothelial Progenitor Cell Dysfunction by Inducing Mitochondrial Dysfunction Via Targeting let-7a-5p/OPA1 Axis.Applied biochemistry and biotechnology · 2026Article
- Infiltration of TIM4-positive intratumoral macrophages serves as an adverse prognostic factor in breast cancer.Breast cancer (Tokyo, Japan) · 2026Article
- Targeting the ANXA2-CD63-exosomal PD-L1 axis in hepatocellular carcinoma: A novel mechanism of immune evasion and its implications for precision immunotherapy.Neoplasia (New York, N.Y.) · 2026Article
- Mitochondrial metabolic-transcriptional axis drives adaptive drug tolerance across major lung cancer subtypes.Frontiers in genetics · 2026Review
- Oregano extract induces apoptosis and inhibits autophagy in HepG2 cells via the PI3K/AKT pathway.Frontiers in pharmacology · 2026Article
- PUM1 Promotes HCC Cell Proliferation and Inhibits Mitochondria‑mediated Apoptosis, Accompanied by Activation of the PI3K-AKT Pathway.Journal of hepatocellular carcinoma · 2026Article
- Relapse in childhood B-cell precursor acute lymphoblastic leukemia: insights from transcriptomic signatures of diagnostic bone marrow.Frontiers in oncology · 2026Review
- The symbiotic axis between the acidic tumor microenvironment and cancer stem cells: a driver of malignancy and therapeutic resistance.Frontiers in oncology · 2026Review
- AHSA1 promotes the progression of lung cancer by enhancing the expression of HSP90α.Histology and histopathology · 2026Article
- VSIG2 hinders gastric cancer progression by suppressing ANXA2-mediated NF-κB pathway activation.Acta biochimica et biophysica Sinica · 2025Article
- HSPB1/KDM1 A facilitates ANXA2 expression via hypomethylated DNA promoter to inhibit ferroptosis and enhance gemcitabine resistance in pancreatic cancer.Naunyn-Schmiedeberg's archives of pharmacology · 2025Article
- AI662270/GRP94 axis couples the unfolded protein response to mitochondrial dynamics during acute myocardial infarction.JCI insight · 2025Article
- Review
- Targeting Mitochondrial Quality Control for the Treatment of Triple-Negative Breast Cancer: From Molecular Mechanisms to Precision Therapy.Biomolecules · 2025Review
- S100 A16 promotes the progression of osteosarcoma by activating the PI3 K/AKT signaling pathway through ANXA2.Scientific reports · 2025Article
Corrections and comments
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Authors and funding
14 authors at 2 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Mitochondrial function and homeostasis are critical to the proliferation of lung cancer cells. T-cell immunoglobulin and mucin domain-containing molecule 4 (TIM-4) promotes the development and progression of lung cancer. However, the role of TIM-4 in mitochondria homeostasis in tumor cells remains completely unknown. In this study, we found that TIM-4 promoted growth and proliferation of lung cancer cells by the oxidative phosphorylation (OXPHOS) pathway. Consistently, inhibition of OXPHOS reversed TIM-4-induced proliferation of lung cancer cells. Notably, TIM-4 promoted mitochondrial fusion via enhancing L-OPA1 protein expression. Mechanistically, TIM-4 regulated protein of L-OPA1 through the PI3K/AKT pathway, and TIM-4 interacted with ANXA2 to promote the activation of PI3K/AKT signaling. Collectively, TIM-4 promotes oxidative phosphorylation of lung cancer cells to accelerate tumor progress via ANXA2/PI3K/AKT/OPA1 axis, which sheds significant new lights on the potential role of TIM-4 in regulating tumor cell metabolism.
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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.