ArticleOncology reports2026
OLR1 promotes cell proliferation and invasion while represses apoptosis via regulating histone H3 lysine 18 lactylation‑mediated LEMD1 in papillary thyroid cancer.
Article in Oncology reports, 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Not yet cited in PubMed.
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Abstract
Oxidized low density lipoprotein receptor 1 (OLR1) regulates glycolytic metabolism, lactate production and carcinogenesis, but its role in papillary thyroid cancer (PTC) is still unclear. The present study aimed to investigate the effect of OLR1 modification on PTC cellular functions and its interaction with histone H3 lysine 18 lactylation (H3K18la) and downstream molecular mechanisms. Lectin‑like oxidized low‑density lipoprotein receptor‑1 (LOX‑1; OLR1 coding protein) and H3K18la expression was detected in twenty pairs of PTC and non‑tumor tissues by immunohistochemistry. Overexpressed OLR1 and small interfering (si)RNA were transfected into two PTC cell lines (TPC‑1 and IHH‑4 cells). After which, oxamate (to reduce lactate production) or LEM domain containing 1 (LEMD1) siRNA combined with OLR1 overexpression plasmid was used to treat PTC cell lines. Furthermore, PTC xenograft mice were constructed for
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