ArticleAdvanced science (Weinheim, Baden-Wurttemberg, Germany)2026
Lactylated SPTAN1 Accelerates Hepatocellular Carcinoma Progression by Promoting NOTCH1/HES1 Activation and Immunosuppression.
Article in Advanced science (Weinheim, Baden-Wurttemberg, Germany), 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 9 papers.
What it found
Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.
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.
The trial behind it
Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.
Who cites it
9 citing papers in PubMed.
- Lipid metabolic reprogramming of tumor-associated macrophages drives resistance to immune checkpoint blockade in lung cancer: a narrative review of mechanisms and therapeutic strategies.Translational lung cancer research · 2026Review
- Lactate metabolism and protein lactylation in inflammatory and tumor microenvironments.Molecular biomedicine · 2026Review
- G6PC Downregulation Promotes Renal Calcium Oxalate Stone Formation via Lactate-Induced SNAIL1 K206 Lactylation and Epithelial-Mesenchymal Transition.Advanced science (Weinheim, Baden-Wurttemberg, Germany) · 2026Article
- Post-Translational Modifications in Cancer-Associated CD8⁺ T-Cell Exhaustion: Mechanisms and Therapeutic Opportunities.International journal of biological sciences · 2026Review
- Lactate and lactylation in sepsis: regulation of immune-metabolic crosstalk and organ injury.Frontiers in immunology · 2026Review
- Aminoacyl-tRNA synthetases in tumor immunity: canonical translation, source-resolved immune circuits and therapeutic opportunities.Frontiers in immunology · 2026Review
- Lactylated SPTAN1 Accelerates Hepatocellular Carcinoma Progression by Promoting NOTCH1/HES1 Activation and Immunosuppression.Advanced science (Weinheim, Baden-Wurttemberg, Germany) · 2026Article
- Unveiling the hidden regulators: how post-translational modifications influence the progression and treatment of hepatocellular carcinoma.Frontiers in oncology · 2026Review
- The immunoecology of occult hepatitis B virus infection: genetic remodeling and the immune-mediated microcosm.Frontiers in immunology · 2026Review
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
9 authors.
Funding
Abstract
Nonerythrocytic alphaII-spectrin (SPTAN1) is crucial for neuronal functions, yet its role in oncogenic processes remains inadequately characterized. This study investigates the lactylation (kla) modification of SPTAN1 (SPTAN1-kla) and its mechanistic contributions to hepatitis B virus (HBV)-related hepatocellular carcinoma (HCC). Results indicate that SPTAN1 undergoes lactylation at lysine residues K1952 and K1957 specifically in HBV-positive HCC tissues. Alanyl-tRNA synthetase 1 (AARS1) mediates SPTAN1-kla formation, while histone deacetylase 1 (HDAC1) acts as a delactylase. HBV infection enhances lactate production by inducing the expression of HK2, promoting SPTAN1-kla formation, and disrupting the liquid-liquid phase separation (LLPS) of cytoplasmic SPTAN1, thereby facilitating its nuclear translocation. Within the nucleus, SPTAN1-kla interacts with core-binding factor β (CBFB) to activate NOTCH1/HES1 signaling, thereby promoting HCC cell proliferation. Furthermore, SPTAN1-kla activates the COX2/mPGES1 pathway through NOTCH1/HES1 signaling, thereby enhancing the biosynthesis of prostaglandin E2 (PGE2) and increasing the infiltration of exhausted CD8⁺ T cells. Therapeutic targeting of SPTAN1-kla using specific inhibitory peptides significantly attenuates HCC tumor growth in preclinical models. Our research identifies SPTAN1-kla as a novel oncogenic driver in HBV-related HCC, functioning via metabolic reprogramming and immune modulation. These findings position SPTAN1-kla as a promising therapeutic target for developing precision interventions against HBV-related HCC.
Indexed as
Identifiers
What OpenQuestion holds
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.