Evidence map›Paper›PMID 33732356›Full record

ArticleOncology letters2021

Triptolide inhibits human telomerase reverse transcriptase by downregulating translation factors SP1 and c-Myc in Epstein-Barr virus-positive B lymphocytes.

Cong Long, Qiu-Bo Xu, Li Ding, Liu Yang, Wei Ji, Feng Gao, Yong Ji

Open access · diamondAbstract read
In one paragraph

Article in Oncology letters, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 5 papers.

0numbers the graph read from it
0cells of the map it votes in
5citing papers in PubMed
1.0field-weighted citation impact, top 27% of its field
1 · What the graph read from it

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.

2 · The registry

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.

3 · Its place in the literature

Who cites it

5 citing papers in PubMed, 10 citations in OpenAlex.

  1. Major bioactive metabolites derived fromFrontiers in pharmacology · 2026
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4 · The record

Corrections and comments

PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.

5 · Who and what money

Authors and funding

7 authors at 1 institution in 1 country.

Cong LongClinical Laboratory, Jingjiang People's Hospital, Jingjiang, Jiangsu 214500, P.R. China.
Qiu-Bo XuClinical Laboratory, Jingjiang People's Hospital, Jingjiang, Jiangsu 214500, P.R. China.
Li DingClinical Laboratory, Jingjiang People's Hospital, Jingjiang, Jiangsu 214500, P.R. China.
Liu YangClinical Laboratory, Jingjiang People's Hospital, Jingjiang, Jiangsu 214500, P.R. China.
Wei JiClinical Laboratory, Jingjiang People's Hospital, Jingjiang, Jiangsu 214500, P.R. China.
Feng GaoDepartment of General Surgery, Jingjiang People's Hospital, Jingjiang, Jiangsu 214500, P.R. China.
Yong JiDepartment of General Surgery, Jingjiang People's Hospital, Jingjiang, Jiangsu 214500, P.R. China.
First People's Hospital of Jingzhou · CN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Epstein-Barr virus (EBV) mainly causes infectious mononucleosis and is associated with several neoplasms, including Burkitt's lymphoma, nasopharyngeal carcinoma and lymphoproliferative disease. Human telomerase reverse transcriptase (hTERT) regulates enzymatic activity of telomerase and is closely associated with tumorigenesis and senescence evasion. Triptolide (TP) is a diterpenoid triepoxide, with a broad-spectrum anticancer and immunosuppressive bioactivity profile. The present study investigated whether TP inhibited hTERT expression and suppressed its activity. The mRNA and protein levels of hTERT were examined by reverse transcription-quantitative PCR and western blotting. The activity of hTERT promoter was determined by dual-luciferase reporter assay. Cell Counting Kit-8 assays were performed to analyze cell proliferation. The present study used EBV-positive B lymphoma cells as a model system, and the results demonstrated that TP significantly decreased hTERT transcription and protein expression. Mechanistically, TP attenuated the hTERT promoter activity by downregulating the expression levels of specificityprotein 1 and c-Myc transcription factors. Consistently, inhibition of hTERT via shRNA transfection efficiently enhanced the suppression of cell proliferation by TP. Furthermore, TP increased virus latent replication and promoted the lytic cycle of EBV in EBV-positive B lymphoma cells, increasing the number of lytic cells and inhibiting the viability of tumor cells. Taken together, the results of the present study revealed a molecular mechanism of the pharmacological inhibition of tumor cell proliferation by TP, encouraging the translation of TP-based therapeutics in EBV-positive B lymphoma treatment.

Indexed as

c-MycEpstein-Barr virushuman telomerase reverse transcriptasespecificity protein 1triptolide

Identifiers

PMID33732356
PMCPMC7905526
OpenAlexW3127759038

What OpenQuestion holds

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LicenceCC BY-NC-ND
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Registered trials

None linked

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.