ArticleOncology letters2021
Pseudogene legumain promotes thyroid carcinoma progression via the microRNA-495/autophagy pathway.
Article in Oncology letters, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 4 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
4 citing papers in PubMed, 5 citations in OpenAlex.
- Review
- Assessment of circulating proteins in thyroid cancer: Proteome-wide Mendelian randomization and colocalization analysis.iScience · 2024Article
- The Mammalian Cysteine Protease Legumain in Health and Disease.International journal of molecular sciences · 2022Review
- Emerging role of competing endogenous RNA and associated noncoding RNAs in thyroid cancer.American journal of cancer research · 2022Review
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 at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
The pseudogene legumain (LGMN) has been reported to regulate cancer cell biology. However, the role of LGMN in thyroid carcinoma remains unknown. Herein, Cell Counting Kit 8 and Transwell assays were performed to evaluate cellular proliferation and invasion capacity, respectively. In addition, a tube formation assay was performed to assess HUVEC angiogenesis. The results showed that LGMN depletion attenuated cellular proliferation, invasion and tube formation ability, and that LGMN expression was dysregulated in thyroid carcinoma tumors. Furthermore, patients with high LGMN expression levels exhibited a lower overall survival rate than those with low expression levels. LGMN and microRNA (miR)-495 modulated the expression levels of autophagy-related gene 3 (ATG3) and p62. Finally, ATG3 overexpression rescued the LGMN-regulated thyroid carcinoma phenotype. In conclusion, LGMN was found to promote thyroid carcinoma progression via the miR-495/autophagy axis, thus providing novel insights for understanding the pathogenesis of thyroid carcinoma.
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.