ArticleOncotarget2017
Loss of thyroid hormone receptor interactor 13 inhibits cell proliferation and survival in human chronic lymphocytic leukemia.
Article in Oncotarget, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 17 papers.
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Who cites it
17 citing papers in PubMed, 25 citations in OpenAlex.
- Discovery of novel antimyeloma agents targeting TRIP13 by molecular modeling and bioassay.RSC medicinal chemistry · 2025Article
- Advancing the development of TRIP13 inhibitors: A high-throughput screening approach.SLAS discovery : advancing life sciences R & D · 2025Article
- Thyroid hormone receptor interacting protein 13 is associated with prognosis and immunotherapy efficacy in human cancers: a pan-cancer analysis.Discover oncology · 2025Article
- TRIP13 Plays an Important Role in the Sensitivity of Leukemia Cell Response to Sulforaphane Therapy.ACS omega · 2024Article
- Targeting TRIP13 for overcoming anticancer drug resistance (Review).Oncology reports · 2023Article
- TRIP13, identified as a hub gene of tumor progression, is the target of microRNA-4693-5p and a potential therapeutic target for colorectal cancer.Cell death discovery · 2022Article
- TRIP13 Induces Nedaplatin Resistance in Esophageal Squamous Cell Carcinoma by Enhancing Repair of DNA Damage and Inhibiting Apoptosis.BioMed research international · 2022Article
- TRIP13 modulates protein deubiquitination and accelerates tumor development and progression of B cell malignancies.The Journal of clinical investigation · 2021Article
- Investigation of the expression levels of CPEB4, APC, TRIP13, EIF2S3, EIF4A1, IFNg, PIK3CA and CTNNB1 genes in different stage colorectal tumorsTurkish journal of medical sciences · 2021Article
- KIAA0101 knockdown inhibits cell proliferation and induces cell cycle arrest and cell apoptosis in chronic lymphocytic leukemia cells.Annals of translational medicine · 2021Article
- TRIP13 predicts poor prognosis in clear cell renal cell carcinoma.American journal of cancer research · 2020Article
- Using chemical inhibitors to probe AAA protein conformational dynamics and cellular functions.Current opinion in chemical biology · 2019Review
- Insights into a Crucial Role of TRIP13 in Human Cancer.Computational and structural biotechnology journal · 2019Review
- Elevated TRIP13 drives cell proliferation and drug resistance in bladder cancer.American journal of translational research · 2019Article
- TRIP13 promotes tumor growth and is associated with poor prognosis in colorectal cancer.Cell death & disease · 2018Article
- Article
- LncRNA TINCR is associated with clinical progression and serves as tumor suppressive role in prostate cancer.Cancer management and research · 2018Article
Corrections and comments
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Authors and funding
9 authors at 2 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
backgroundThe genetic regulation of apoptosis and cell proliferation plays a role in the growth of chronic lymphocytic leukemia (CLL), the most common form of leukemia in the Western hemisphere. Although thyroid hormone receptor interactors (TRIPs) are known to play roles in cell cycle, the potential involvement of the novel family member TRIP13 in CLL has not yet been investigated.
methodsQuantitative PCR (qPCR) was used to detect expression of TRIP13 in 36 CLL patients and 33 healthy donors CD19+ B cells. Loss-of-function (siRNA) assays were used to alter TRIP13 expression levels. The effect of TRIP13 on cell proliferation and apoptosis was measured by MTT, Annexin V-based flow cytometry and Caspase 3/7 activity assay. Affymetrix GeneChip and Ingenuity Pathway Analysis (IPA) were used to describe an overview of TRIP13 potential biological function and downstream pathways. Dual-luciferase reporter assay was performed to assess the promoting effect of c-MYC on TRIP13 transcription.
resultsThe qPCR data showed that TRIP13 is significantly over-expressed in CLL patients. Microarray analyses indicated that the biological function of TRIP13 in CLL is majorly cell apoptosis and cell proliferation associated. TRIP13 siRNA expressing cells exhibited a slower cell proliferation rate and underwent apoptosis compared with control cells. TRIP13 knockdown induced CLL cells apoptosis through PUMA independent of p53. TRIP13 up-regulation is induced by c-MYC dependent transcriptional activation.
conclusionOverall, our data suggest the bio-function of TRIP13 in CLL cell for the first time, and that this gene might be a therapeutic target for CLL.
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