ArticleOncology letters2017
Lentivirus-mediated RNA interference of tripartite motif 68 inhibits the proliferation of colorectal cancer cell lines SW1116 and HCT116
Article in Oncology letters, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 11 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.
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Who cites it
11 citing papers in PubMed, 12 citations in OpenAlex.
- UBB as an early-stage potential biomarker for breast cancer via modulation of the ubiquitination pathway.Scientific reports · 2026Article
- TRIM68 regulates ubiquitinated degradation of Rabex-5 and plays a role in progression of breast cancer through Rab5-Rac1.American journal of cancer research · 2026Article
- PPA1, TRIM68 and FBXO46: Potential Therapeutic Targets for Triple Negative Breast Cancer.Current protein & peptide science · 2025Article
- Exploring the Mechanisms, Biomarkers, and Therapeutic Targets of TRIM Family in Gastrointestinal Cancer.Drug design, development and therapy · 2024Review
- High-Intensity Aerobic Exercise Suppresses Cancer Growth by Regulating Skeletal Muscle-Derived Oncogenes and Tumor Suppressors.Frontiers in molecular biosciences · 2022Article
- Comprehensive Analysis of the Expression and Prognosis for Tripartite Motif-Containing Genes in Breast Cancer.Frontiers in genetics · 2022Article
- Multifaceted Roles of TRIM Proteins in Colorectal Carcinoma.International journal of molecular sciences · 2020Review
- Review
- High PLK4 expression promotes tumor progression and induces epithelial‑mesenchymal transition by regulating the Wnt/β‑catenin signaling pathway in colorectal cancer.International journal of oncology · 2019Article
- ARHGAP24 regulates cell ability and apoptosis of colorectal cancer cells via the regulation of P53.Oncology letters · 2018Article
- TRIM27 functions as an oncogene by activating epithelial-mesenchymal transition and p-AKT in colorectal cancer.International journal of oncology · 2018Article
Corrections and comments
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Authors and funding
7 authors at 3 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Colorectal cancer is one of the most common types of cancer worldwide. Previous studies have revealed that certain members of tripartite motif (TRIM) proteins are involved in carcin ogenesis regulation, but little is known about the function of TRIM68 in human colorectal cancer. To investigate the role of TRIM68 in colorectal cancer SW1116 and HCT116 cell lines, the present study conducted lentivirus-mediated knockdown against TRIM68 and demonstrated that depletion of TRIM68 notably inhibits colorectal cancer cell proliferation and colony formation ability. Cell cycle arrest in the G0/G1 phase and cycle accumulation in sub-G1 phase provided evidence that TRIM68 may participate in the regulation of colorectal cancer tumorigenesis. The results revealed the significant role of
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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.