ArticleAmerican journal of translational research2025
Downregulated TRAF3IP2-AS1 promotes hepatocellular carcinoma progression through the miR-374a-5p/SEL1L1/RPL6 axis to enhance DNA damage repair.
Article in American journal of translational research, 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
9 authors.
Funding
No grant is acknowledged in the PubMed record.
Abstract
objectivesExcessive activity in the DNA damage repair (DDR) pathway causes genomic instability, leading to the development of hepatocellular carcinoma (HCC), the most common form of liver cancer. The long non-coding RNA (lncRNA) tumor necrosis factor receptor-associated factor 3 interacting protein 2 antisense RNA 1 (TRAF3IP2-AS1) acts as a tumor suppressor. MicroRNA (miR)-374a-5p is a target miRNA for TRAF3IP2-AS1, while SEL1L ERAD E3 ligase adaptor subunit (SEL1L) acts as a target gene of miR-374a-5p. Moreover, DDR-participating molecule ribosomal protein L6 (RPL6) interacts with SEL1L. In this study, we aimed to explore the role and mechanism of TRAF3IP3-AS1 in HCC.
methodsIn vitro HCC cell lines were cultured. In vivo, a mouse in situ HCC model was constructed using a liver injection of HepG2 cells. Additionally, clinical HCC and adjacent tissues were used to verify the pathway.
resultsOxidative stress downregulated TRAF3IP2-AS1 in HCC cells. TRAF3IP2-AS1 downregulated the proliferation, migration, and invasion of HCC cells by inhibiting miR-374a-5p levels. SEL1L was a target gene of miR-374a-5p in HCC cells. Mir-374a-5p facilitated the proliferation, migration, and invasion of HCC cells by inhibiting SEL1L. TRAF3IP2-AS1 and miR-374a-5p regulated the interaction between SEL1L and RPL6 as well as RPL6 ubiquitin degradation in HCC cells in an opposite manner. DDR was upregulated in HCC cells through the TRAF3IP2-AS1/miR-374a-5p/SEL1L1/RPL6 pathway. Downregulated SEL1L promoted the proliferation, migration, and invasion of HCC cells by upregulating RPL6 expression. Furthermore, the TRAF3IP2-AS1/miR-374a-5p/SEL1L/RPL6 pathway exacerbated the progression of HCC in mice. This pathway also promoted the proliferation, migration, and invasion of in vivo HCC cells by enhancing DDR.
conclusionsTRAF3IP2-AS1/miR-374a-5p/SEL1L/RPL6 pathway in HCC cells promoted DDR and HCC progression. Our data identify the role and mechanism of TRAF3IP2-AS1 in HCC and imply treatment targets for 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.