Evidence map›Paper›PMID 34958116›Full record

ArticleOncology reports2022

Inhibition of triple‑negative breast cancer proliferation and motility by reactivating p53 and inhibiting overactivated Akt.

Wei Cao, Renhui Shen, Seth Richard, Yu Liu, Mohammad Jalalirad, Margot P Cleary, Antonio B D'Assoro, Sergio A Gradilone, Da-Qing Yang

Open access · bronzeAbstract read
PubMed Full text at PMC Publisher
In one paragraph

Article in Oncology reports, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 11 papers.

0numbers the graph read from it
0cells of the map it votes in
11citing papers in PubMed
2.1field-weighted citation impact, top 12% 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

11 citing papers in PubMed, 28 citations in OpenAlex.

  1. Article
  2. Review
  3. Article
  4. Review
  5. Review
  6. Omics-Based Investigations of Breast Cancer.Molecules (Basel, Switzerland) · 2023
    Review
  7. Article
  8. Review
  9. Adlay Seed (Molecules (Basel, Switzerland) · 2022
    Article
  10. Article
  11. 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

9 authors at 4 institutions in 2 countries.

Wei Cao *The Hormel Institute, University of Minnesota, Austin, MN 55912, USA.
Renhui Shen *The Hormel Institute, University of Minnesota, Austin, MN 55912, USA.
Seth RichardThe Hormel Institute, University of Minnesota, Austin, MN 55912, USA.
Yu LiuSir Run Run Shaw Hospital, Nanjing Medical University, Nanjing, Jiangsu 211166, P.R. China.
Mohammad JalaliradMayo Clinic, Rochester, MN 55905, USA.
Margot P ClearyThe Hormel Institute, University of Minnesota, Austin, MN 55912, USA.
Antonio B D'AssoroMayo Clinic, Rochester, MN 55905, USA.
Sergio A GradiloneThe Hormel Institute, University of Minnesota, Austin, MN 55912, USA.
Da-Qing YangThe Hormel Institute, University of Minnesota, Austin, MN 55912, USA.
Hormel (United States) · USUniversity of Minnesota · USMayo Clinic in Arizona · USSir Run Run Shaw Hospital · CN

Funding

Targeting Aurora-A Kinase to Overcome Endocrine Resistance in ER+ Breast CancerR01CA214893 · NCI · MAYO CLINIC ROCHESTER · PI D'ASSORO, ANTONIO BONAVENTURA, HADDAD, TUFIA C · 2017 to 2021
$1.6M
Prevention of mammary tumors by metformin in comparison to calorie restrictionR01CA157012 · NCI · UNIVERSITY OF MINNESOTA · PI CLEARY, MARGOT P · 2011 to 2015
$1.6M
NCI NIH HHS R01 CA157012NCI NIH HHS R01 CA214893
6 · The paper itself

Abstract

Mutations of p53 tumor suppressors occur more frequently in cancers at advanced stages or in more malignant cancer subtypes such as triple‑negative breast cancer. Thus, restoration of p53 tumor suppressor function constitutes a valuable cancer therapeutic strategy. In the present study, it was revealed that a specific inhibitor of histone deacetylase 6, ACY‑1215, caused increased acetylation of p53 in breast cancer cells with mutated p53, which was accompanied by increased expression of p21. These results suggested that ACY‑1215 may lead to enhanced transcriptional activity of p53. It was also determined that ACY‑1215 treatment resulted in G1 cell cycle arrest and apoptosis in these cancer cells. Furthermore, ACY‑1215 displayed a synergistic effect with specific inhibitors of ATM, an activator of Akt, in inducing cancer cell apoptosis and inhibiting their motility. More importantly, it was observed that combination of ACY‑1215 and ATM inhibitors exhibited markedly more potent antitumor activity than the individual compound in xenograft mouse models of breast cancer with mutant p53. Collectively, our results demonstrated that ACY‑1215 is a novel chemotherapeutic agent that could restore mutant p53 function in cancer cells with strong antitumor activity, either alone or in combination with inhibitors of the ATM protein kinase.

Indexed as

AnimalsAntineoplastic AgentsApoptosisAtaxia Telangiectasia Mutated ProteinsCell Line, TumorCell ProliferationDisease Models, AnimalDrug Therapy, CombinationG1 Phase Cell Cycle CheckpointsHistone Deacetylase InhibitorsHumansHydroxamic AcidsMammary Neoplasms, ExperimentalMiceProtein Kinase InhibitorsProto-Oncogene Proteins c-aktAntineoplastic AgentsAtaxia Telangiectasia Mutated ProteinsHistone Deacetylase InhibitorsHydroxamic AcidsProtein Kinase InhibitorsProto-Oncogene Proteins c-aktPyrimidinesricolinostatTumor Suppressor Protein p53ACY‑1215ATMKU-55933KU-60019p53triple-negative breast cancer

Identifiers

PMID34958116
PMCPMC8759100
OpenAlexW4200070140

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.