Article3 Biotech2025
POGZ targeted by LINC01355/miR-27b-3p retards thyroid cancer progression via interplaying with MAD2L2.
Article in 3 Biotech, 2025. 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
Despite the high morbidity of thyroid cancer (THCA), the underlying molecular pathology remains elusive. That autism-associated protein POGZ has recently been involved in tumorigenesis intrigues us exploring its relevant molecular regulatory network in THCA. Clinical characteristics and intermolecular relationships were dissected by bioinformatics. Interaction between POGZ and MAD2L2 was examined by Co-IP assay. Targeting relationships between miR-27b-3p and POGZ/LINC01355 was verified by sequence prediction and dual-luciferase reporter detection. Cellular effects of genes were assessed by CCK-8 assay, clone formation assay, and Transwell assay, and further confirmed by a tumor-bearing nude mice model. Our results demonstrated a decrease in POGZ expression in THCA tissues and cell lines, and an interaction between POGZ and MAD2L2 protein. POGZ inhibited both the proliferation and motility of THCA cells, with these effects being reversed upon MAD2L2 silencing. LINC01355 exhibited low expression level and a positive correlation with POGZ in THCA. Both miR-27b-3p and LINC01355 were identified as regulators of POGZ through targeting. Elevated miR-27b-3p suppressed POGZ expression. LINC01355 promoted POGZ and counteracted the inhibitory effects of miR-27b-3p. Furthermore, miR-27b-3p increased the proliferation and motility of THCA cells, an effect that was blocked by LINC01355. At the animal level, POGZ, LINC01355, and MAD2L2 all attenuated tumor growth in THCA. Collectively, POGZ restrains THCA growth by interacting with MAD2L2 protein, and POGZ modulation involves a complex interplay orchestrated by LINC01355-targeted miR-27b-3p. By reporting the first POGZ-focused ceRNA network involving noncoding RNA in THCA, our study paves the way for exploring POGZ-related pathways and developing new therapeutic strategies in cancer. Supplementary Information: The online version contains supplementary material available at 10.1007/s13205-025-04231-7.
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.