ArticleTranslational cancer research2026
Mechanism of miR-188-5p enhancing radioresistance in nasopharyngeal carcinoma by targeting PTEN to activate the PI3K/Akt signaling pathway.
Article in Translational cancer research, 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
7 authors.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Background: Radiotherapy resistance remains a critical obstacle in nasopharyngeal carcinoma (NPC) treatment, yet the underlying mechanisms are not fully understood. Although miR-188-5p has been implicated in the malignant progression of various tumors, its role in NPC radioresistance requires further investigation. This study aims to explore whether miR-188-5p mediates radioresistance by targeting PTEN to activate the PI3K/AKT signaling pathway and induce epithelial-mesenchymal transition (EMT). Methods: Radioresistant NPC cell lines C666-1R were established. Cell proliferation and radioresistance were evaluated using Cell Counting Kit-8 (CCK-8) and colony forming assays. C666-1R cells were transfected with miR-188-5p inhibitor/mimic and sh-PTEN, followed by 4 Gy irradiation. Quantitative real-time polymerase chain reaction (qRT-PCR), western blotting, Transwell assay, wound healing assay, flow cytometry, and dual-luciferase reporter assay were performed to assess the effects of miR-188-5p on cell proliferation, invasion, migration, apoptosis, and the PTEN/PI3K/AKT pathway. Results: Radioresistant NPC cell lines were successfully established and validated. miR-188-5p was highly expressed in NPC tissues and NPC cell lines, particularly in the radioresistant C666-1R cells. Inhibition of miR-188-5p enhanced radiosensitivity, as evidenced by reduced cell viability, invasion, migration, and increased apoptosis. Dual-luciferase reporter assay confirmed that miR-188-5p directly bound to the 3'-UTR of PTEN and suppressed its expression. Rescue experiments demonstrated that PTEN knockdown reversed the miR-188-5p inhibition-induced suppression of PI3K/AKT activity and EMT phenotype, restoring p-PI3K, p-AKT, N-cadherin, and Vimentin levels while downregulating E-cadherin. These findings indicate that miR-188-5p activates the PI3K/AKT pathway and promotes EMT by directly targeting PTEN, thereby mediating NPC radioresistance. Conclusions: miR-188-5p enhances radioresistance in NPC cells by suppressing PTEN expression, relieving its negative regulation of the PI3K/AKT signaling pathway, activating this pathway, and inducing EMT. Thus, inhibiting miR-188-5p may represent a promising strategy to overcome radioresistance in NPC.
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.