Evidence map›Paper›PMID 32671070›Full record

ReviewFrontiers in cell and developmental biology2020

Apoptin as a Tumor-Specific Therapeutic Agent: Current Perspective on Mechanism of Action and Delivery Systems.

Waseem Akram Malla, Richa Arora, Raja Ishaq Nabi Khan, Sonalika Mahajan, Ashok Kumar Tiwari

Open access · goldAbstract readReview
In one paragraph

Review in Frontiers in cell and developmental biology, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 20 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
20citing papers in PubMed, 1 pooled it
4.1field-weighted citation impact, top 6% 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

20 citing papers in PubMed, 1 synthesis or guideline pooled it, 44 citations in OpenAlex.

  1. Pooled it
  2. Article
  3. Recombinant RGD-Apoptins Decrease Human Melanoma Cell Viability.International journal of molecular sciences · 2025
    Article
  4. Article
  5. Review
  6. Article
  7. A Super-Assembled Synergistically Nanoplatform AP@ZIF-8International journal of nanomedicine · 2025
    Article
  8. Review
  9. Article
  10. Review
  11. Cytotoxic Effect ofAdvances in pharmacological and pharmaceutical sciences · 2024
    Article
  12. Article
  13. Article
  14. Review
  15. Article
  16. Article
  17. Article
  18. Review
  19. Review
  20. 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

5 authors at 1 institution in 1 country.

Waseem Akram MallaDivision of Veterinary Biotechnology, ICAR-Indian Veterinary Research Institute, Izatnagar, India.
Richa AroraDivision of Veterinary Biotechnology, ICAR-Indian Veterinary Research Institute, Izatnagar, India.
Raja Ishaq Nabi KhanDivision of Veterinary Biotechnology, ICAR-Indian Veterinary Research Institute, Izatnagar, India.
Sonalika MahajanDivision of Veterinary Biotechnology, ICAR-Indian Veterinary Research Institute, Izatnagar, India.
Ashok Kumar TiwariDivision of Biological Standardisation, ICAR-Indian Veterinary Research Institute, Izatnagar, India.
Indian Veterinary Research Institute · IN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Cancer remains one of the leading causes of death worldwide in humans and animals. Conventional treatment regimens often fail to produce the desired outcome due to disturbances in cell physiology that arise during the process of transformation. Additionally, development of treatment regimens with no or minimum side-effects is one of the thrust areas of modern cancer research. Oncolytic viral gene therapy employs certain viral genes which on ectopic expression find and selectively destroy malignant cells, thereby achieving tumor cell death without harming the normal cells in the neighborhood. Apoptin, encoded by Chicken Infectious Anemia Virus' VP3 gene, is a proline-rich protein capable of inducing apoptosis in cancer cells in a selective manner. In normal cells, the filamentous Apoptin becomes aggregated toward the cell margins, but is eventually degraded by proteasomes without harming the cells. In malignant cells, after activation by phosphorylation by a cancer cell-specific kinase whose identity is disputed, Apoptin accumulates in the nucleus, undergoes aggregation to form multimers, and prevents the dividing cancer cells from repairing their DNA lesions, thereby forcing them to undergo apoptosis. In this review, we discuss the present knowledge about the structure of Apoptin protein, elaborate on its mechanism of action, and summarize various strategies that have been used to deliver it as an anticancer drug in various cancer models.

Indexed as

anticancer genesapoptincancer gene therapyCAVchicken infectious anemiaoncolytic viral genesoncotherapyVP3

Identifiers

PMID32671070
PMCPMC7330108
OpenAlexW3037070782

What OpenQuestion holds

Textmetadata
LicenceCC BY
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.