ArticleOncotarget2016
Knockdown of TRIM65 inhibits lung cancer cell proliferation, migration and invasion: A therapeutic target in human lung cancer.
Article in Oncotarget, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. It has been retracted, and should not be counted. Cited by 16 papers.
What it found
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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
16 citing papers in PubMed, 29 citations in OpenAlex.
- The Magic and Mystery of TRIM65 in Diseases.Current medicinal chemistry · 2025Review
- Retraction Note: Silencing of Histone Deacetylase 9 Expression in Podocytes Attenuates Kidney Injury in Diabetic Nephropathy.Scientific reports · 2024Article
- Intricate confrontation: Research progress and application potential of TRIM family proteins in tumor immune escape.Journal of advanced research · 2023Review
- Transposable element-mediated rearrangements are prevalent in human genomes.Nature communications · 2022Article
- Machine learning and bioinformatics to identify 8 autophagy-related biomarkers and construct gene regulatory networks in dilated cardiomyopathy.Scientific reports · 2022Article
- TRIM65 Promotes Malignant Cell Behaviors in Triple-Negative Breast Cancer by Impairing the Stability of LATS1 Protein.Oxidative medicine and cellular longevity · 2022Article
- Autophagy Regulation by Crosstalk between miRNAs and Ubiquitination System.International journal of molecular sciences · 2021Review
- LncRNA LINC00963 promotes colorectal cancer cell proliferation and metastasis by regulating miR‑1281 and TRIM65.Molecular medicine reports · 2021Article
- The population genomics of adaptive loss of function.Heredity · 2021Review
- TRIM Proteins in Colorectal Cancer: TRIM8 as a Promising Therapeutic Target in Chemo Resistance.Biomedicines · 2021Review
- The Tripartite Nexus: Autophagy, Cancer, and Tripartite Motif-Containing Protein Family Members.Frontiers in pharmacology · 2020Review
- Investigation of the Genome-Wide Genetic and Epigenetic Networks for Drug Discovery Based on Systems Biology Approaches in Colorectal Cancer.Frontiers in genetics · 2020Article
- Prognosis of clear cell renal cell carcinoma (ccRCC) based on a six-lncRNA-based risk score: an investigation based on RNA-sequencing data.Journal of translational medicine · 2019Article
- Knockdown of TRIM65 inhibits autophagy and cisplatin resistance in A549/DDP cells by regulating miR-138-5p/ATG7.Cell death & disease · 2019Article
- TRIM15 Exerts Anti-Tumor Effects Through Suppressing Cancer Cell Invasion in Gastric Adenocarcinoma.Medical science monitor : international medical journal of experimental and clinical research · 2018Article
- DNA Methylation Profiling Reveals the Change of Inflammation-AssociatedFrontiers in aging neuroscience · 2018Article
Corrections and comments
- Retraction · 2024-05-16Duplication of/in Image ·
- Retracted
Authors and funding
11 authors at 2 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Lung cancer is the most commonly diagnosed type of cancer worldwide. Although TRIM65 is an important protein involved in white matter lesion, the role of TRIM65 in human cancer remains less understood. Here, we reported that TRIM65 was significantly overexpressed in lung cancer tissues compared with adjacent normal lung tissues. Furthermore, TRIM65 expression was closely related to overall survival of patients with lung cancer. Knock down of TRIM65 in two lung cancer cell lines, SPC-A-1 and NCI-H358, resulted in a significant reduction in cell proliferation, migration, invasion and adhesion and a dramatic increase in G0-G1 phase arrest and apoptosis. In vivo tumorigenesis experiment also revealed that depletion of TRIM65 expression inhibited NCI-H358 cell growth. Moreover, based on gene set enrichment analysis (GSEA) with The Cancer Genome Atlas (TCGA) dataset, we found that TRIM65 was positive related to cell cycle, metastasis up and RHOA-REG pathways, which was further validated by RT-PCR and Western blot in TRIM65 knockdown lung cancer cells and indicated a possible mechanism underlying its effects on lung cancer. In summary, our study suggests that TRIM65 may work as an oncogene and a new effective therapeutic target for lung cancer treatment.
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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.