Evidence map›Paper›PMID 33042412›Full record

ReviewAmerican journal of translational research2020

Cyclin E: a potential treatment target to reverse cancer chemoresistance by regulating the cell cycle.

Wei Pang, Yashan Li, Weihua Guo, Hong Shen

Abstract readReview
In one paragraph

Review in American journal of translational research, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 24 papers.

0numbers the graph read from it
0cells of the map it votes in
24citing papers in PubMed
–field-weighted citation impact
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

24 citing papers in PubMed.

  1. Article
  2. Article
  3. Review
  4. Article
  5. Review
  6. Targeting CDK2 to combat drug resistance in cancer therapy.Future oncology (London, England) · 2024
    Review
  7. Article
  8. Article
  9. Article
  10. Characterization, modes of interactions with DNA/BSA biomolecules and anti-tumor activity of newly synthesized dinuclear platinum(II) complexes with pyridazine bridging ligand.Journal of biological inorganic chemistry : JBIC : a publication of the Society of Biological Inorganic Chemistry · 2024
    Article
  11. Frontiers in pharmacology · 2024
    Article
  12. Article
  13. Review
  14. Article
  15. Frontiers in oncology · 2023
    Article
  16. Article
  17. Knockdown ofAnnals of translational medicine · 2022
    Article
  18. Review
  19. The botanical drug PBI-05204, a supercritical COFrontiers in pharmacology · 2022
    Article
  20. Cell Cycle-Related Clinical Applications.Methods in molecular biology (Clifton, N.J.) · 2022
    Review
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

4 authors.

Wei PangKey Laboratory for Molecular Radiation Oncology of Hunan Province, Xiangya Hospital, Central South University Changsha 410008, Hunan, China.
Yashan LiKey Laboratory for Molecular Radiation Oncology of Hunan Province, Xiangya Hospital, Central South University Changsha 410008, Hunan, China.
Weihua GuoKey Laboratory for Molecular Radiation Oncology of Hunan Province, Xiangya Hospital, Central South University Changsha 410008, Hunan, China.
Hong ShenKey Laboratory for Molecular Radiation Oncology of Hunan Province, Xiangya Hospital, Central South University Changsha 410008, Hunan, China.

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

The cyclin family plays important roles in regulating the proliferative cycle of mammalian cells. Among the members of this family, cyclin E regulates multiple downstream molecules, such as the retinoblastoma susceptibility gene (RB1) and the transcription factor E2F, by interacting with cyclin-dependent kinases (CDKs) and plays an important role in the cell cycle transition from G1 to S phase. Over the years, studies have shown that cyclin E is closely related to the chemotherapy resistance of tumor cells and that its expression in tumor cells is closely related to prognosis. The dysregulated expression of cyclin E has a definite effect not only on the cell cycle regulation of tumor cells but also on the presence of low-molecular-weight cyclin E (LMW-E) and other cyclins that render tumor cells resistant. In addition, many studies in recent years have confirmed that chemotherapy resistance mediated by cyclin E can be reversed. For example, the combination of a cyclin-dependent kinase inhibitor (CKI) with anticancer drugs or the therapeutic targeting of related genes improves chemotherapy resistance by reducing the level or activity of cyclin E in tumor cells. This review summarizes the specific processes by which cyclin E regulates the cell cycle, its relationship to chemotherapy resistance in cancer, and its potential as a clinical therapeutic target to reverse chemotherapy resistance.

Indexed as

cell cycle. cancerchemotherapy resistanceCyclin E

Identifiers

PMID33042412
PMCPMC7540110

What OpenQuestion holds

Textmetadata
Read underepoch 390

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.