ArticleJournal of nanobiotechnology2026
tLyP-1 peptide-modified MnO₂ co-delivering si-SLC16A1 and temozolomide synergistically suppresses glioblastoma via hypoxia modulation and metabolic stress.
Article in Journal of nanobiotechnology, 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Not yet cited in PubMed.
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
0 citing papers in PubMed.
No citing paper in PubMed yet.
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
Glioblastoma (GBM) is a highly lethal brain tumor with limited treatment efficacy due to therapy resistance and the blood-brain barrier (BBB). Here, we developed tLyP-1-modified polyethylene glycol (PEG)-coated hollow catalase-mimicking MnO₂-based nanocarriers (HM@si-SLC16A1/TMZ-tLyP-1, tLyP-NPs) for the targeted co-delivery of temozolomide (TMZ) and SLC16A1 siRNA (si-SLC16A1). These nanoparticles generate oxygen through H₂O₂ decomposition, alleviating tumor hypoxia and enhancing MRI imaging via Mn²⁺ release. In vitro, tLyP-NPs exhibited high siRNA loading efficiency, pH-responsive drug release, and effective SLC16A1 silencing, leading to reduced glioma cell viability and enhanced apoptosis under both normoxic and hypoxic conditions. tLyP-1 modification facilitated BBB penetration and glioma targeting, as evidenced by increased cellular uptake in a BMEC-C6 glioma co-culture model. In an orthotopic GBM rat model, the nanoparticles demonstrated superior tumor accumulation, prolonged T1-weighted MRI contrast, and enhanced therapeutic efficacy compared to non-modified formulations. Mechanistically, SLC16A1 silencing induced intracellular lactate accumulation, suppressed lactate-stimulated HCAR1/PI3K/AKT signaling, and promoted apoptosis in both in vitro and in vivo models. Histological analysis showed extensive tumor necrosis, increased apoptosis (Caspase-3, TUNEL), reduced proliferation (Ki67), and alleviated hypoxia (HIF-1α). Survival analysis revealed significantly prolonged survival without systemic toxicity. Collectively, tLyP-NPs represent a promising multifunctional nanoplatform that integrates BBB penetration, TME-responsive drug release, and synergistic chemo-gene therapy for GBM treatment.
Indexed as
Identifiers
What Socratic 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 Socratic graph.