ArticleDiscover oncology2024
The role of autophagy related 12 (ATG12) in the progression of hepatocellular carcinoma and its prognostic value.
Article in Discover oncology, 2024. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 1 paper.
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
1 citing paper in PubMed.
- Autophagy as a potential therapeutic target in regulating improper cellular proliferation.Frontiers in pharmacology · 2025Review
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
4 authors.
Funding
Abstract
The aim of our research was to explore the character of autophagy related 12 (ATG12) in the development of hepatocellular carcinoma (HCC). A total of 145 HCC tissues as well as paired adjacent normal tissues were collected, then immunohistochemistry was conducted to access the expression of ATG12. HCC cells were transfected with pcDNA ATG12 or si-ATG12 to overexpress ATG12 or downregulate ATG12. The vitality of HCC cells was accessed using CCK-8 assay, and the ability of invasion of them was tested through Transwell assay. The apoptotic rate of HCC cells was calculated by flow cytometry. The expression of ATG12 was lower in HCC tissues than that in normal tissues, and HCC patients with high ATG12 level survived longer. Overexpressed of ATG12 restrained vitality and invasion of HCC cells, while elevated apoptotic rate of HCC cells. Silence of ATG12 expression yielded opposite results to overexpression of ATG12 in HCC cells. In conclusion, ATG12 is low expressed in HCC, which attenuated the growth and invasion of HCC, while induced the apoptosis of HCC cells. Current research suggested that ATG12 might be a potential target for the diagnosis and treatment of HCC.
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.