ArticleAmerican journal of translational research2021
Knockdown of TRIM11 suppresses cell progression and apoptosis of cervical cancer cells via PI3K/AKT pathway.
Article in American journal of translational research, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 6 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
6 citing papers in PubMed, 10 citations in OpenAlex.
- TRIM11 is upregulated in esophageal cancer and promotes tumor progression through modulation of the β-catenin signaling pathway.Functional & integrative genomics · 2026Article
- Intricate confrontation: Research progress and application potential of TRIM family proteins in tumor immune escape.Journal of advanced research · 2023Review
- TRIM family contribute to tumorigenesis, cancer development, and drug resistance.Experimental hematology & oncology · 2022Review
- Cancer-Associated Dysregulation of Sumo Regulators: Proteases and Ligases.International journal of molecular sciences · 2022Review
- The Role of SUMO E3 Ligases in Signaling Pathway of Cancer Cells.International journal of molecular sciences · 2022Review
- TRIM11 Posttranscriptionally Modulated by miR-5193 Facilitates Tumor Growth and Metastasis of Prostate Cancer.Technology in cancer research & treatmentArticle
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
6 authors at 5 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
objectiveTo detect the expression pattern of TRIM11 in CC and to investigate the effect of TRIM11 knockdown on CC progression.
methodsFirst, the expression pattern and function of TRIM11 in CC were inferred by GEPIA database. The expression of TRIM11 in CC tissues and cells was verified by RT-qPCR and Western blot assays. TRIM11 shRNA was transfected into CC cells. The effect of TRIM11 knockdown on CC cell proliferation and cell apoptosis was assessed by CCK-8 assay, clone formation test and flow cytometry (FCM). Furthermore, the effect of TRIM11 knockdown on cell migration and invasion was measured by Transwell assay. The apoptosis-related proteins (Bax, Bcl-2 and Cleaved caspase 3) and PI3K/AKT pathway-related proteins (PI3K, p-PI3K, AKT and p-Akt) were examined by Western blot assay.
resultsTRIM11 was found to be dramatically upregulated in CC tissues and cells. Besides this, TRIM11 was closely related to FIGO stage, infiltration depth and metastasis. Moreover, high expression of TRIM11 was found to be associated with poor prognosis of CC patients. Functional experiments showed that knockdown of TRIM11 obviously suppressed CC cell proliferation, migration and invasion, while accelerated cell apoptosis. In addition, the PI3K inhibitor (LY294002) was used to assess the connection between PI3K/AKT pathway and TRIM11 in CC cells. We found that TRIM11 overexpression suppressed the phosphorylation of PI3K and AKT in CC cells.
conclusionHence, TRIM11 regulates CC cell progression by modulating PI3K/AKT pathway. The results suggested that TRIM11 might be a possible target for the diagnosis and prognosis of CC patients.
Indexed as
Identifiers
34650700PMC8507035W3206234733What 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.