Evidence map›Paper›PMID 36615262›Full record

ReviewMolecules (Basel, Switzerland)2022

Multifunctional Roles of Betulinic Acid in Cancer Chemoprevention: Spotlight on JAK/STAT, VEGF, EGF/EGFR, TRAIL/TRAIL-R, AKT/mTOR and Non-Coding RNAs in the Inhibition of Carcinogenesis and Metastasis.

Ammad Ahmad Farooqi, Assiya Turgambayeva, Gulnara Tashenova, Aigul Tulebayeva, Aigul Bazarbayeva, Gulnara Kapanova, Symbat Abzaliyeva

Open access · goldAbstract readReview
In one paragraph

Review in Molecules (Basel, Switzerland), 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 9 papers.

0numbers the graph read from it
0cells of the map it votes in
9citing papers in PubMed
1.8field-weighted citation impact, top 14% 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

9 citing papers in PubMed, 21 citations in OpenAlex.

  1. Review
  2. Article
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  4. Review
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  6. Article
  7. Article
  8. STAT1 as a potential therapeutic target to treat bladder cancer.International journal of clinical and experimental pathology · 2024
    Article
  9. 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

7 authors at 5 institutions in 2 countries.

Ammad Ahmad FarooqiDepartment of Molecular Oncology, Institute of Biomedical and Genetic Engineering (IBGE), Islamabad 54000, Pakistan.ORCID 0000-0003-2209-7483
Assiya TurgambayevaDepartment of Public Health and Management, NJSC "Astana Medical University", Astana 010000, Kazakhstan.
Gulnara TashenovaAsfendiyarov Kazakh National Medical University, Almaty 050040, Kazakhstan.
Aigul TulebayevaAsfendiyarov Kazakh National Medical University, Almaty 050040, Kazakhstan.
Aigul BazarbayevaScientific Center of Pediatrics and Pediatric Surgery, Almaty 050060, Kazakhstan.
Gulnara KapanovaScientific Center of Anti-Infectious Drugs, 75 al-Faraby Ave, Almaty 050040, Kazakhstan.
Symbat AbzaliyevaAl-Farabi Kazakh National University, 71 al-Farabi Ave, Almaty 050040, Kazakhstan.
Al-Farabi Kazakh National University · KZKazakh National Medical University · KZAstana Medical University · KZInstitute of Biomedical and Genetic Engineering · PKKazakhstan Medical University · KZ

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

The pursual of novel anticancer molecules from natural sources has gained worthwhile appreciation, and a significant fraction of conceptual knowledge has revolutionized our understanding about heterogeneous nature of cancer. Betulinic acid has fascinated interdisciplinary researchers due to its tremendous pharmacological properties. Ground-breaking discoveries have unraveled previously unprecedented empirical proof-of-concept about momentous chemopreventive role of betulinic acid against carcinogenesis and metastasis. Deregulation of cell signaling pathways has been reported to play a linchpin role in cancer progression and colonization of metastatically competent cancer cells to the distant organs for the development of secondary tumors. Importantly, betulinic acid has demonstrated unique properties to mechanistically modulate oncogenic transduction cascades. In this mini-review, we have attempted to provide a sophisticated compendium of regulatory role of betulinic acid in cancer chemoprevention. We have partitioned this multi-component review into different sections in which we summarized landmark research-works which highlighted betulinic acid mediated regulation of JAK/STAT, VEGF, EGF/EGFR, TRAIL/TRAIL-R, AKT/mTOR and ubiquitination pathways in the inhibition of cancer. In parallel, betulinic acid mediated regulation of signaling cascades and non-coding RNAs will be critically analyzed in cell culture and animal model studies. Better comprehension of the pharmaceutical features of betulinic acid and mapping of the existing knowledge gaps will be valuable in the translatability of preclinical studies into rationally designed clinical trials.

Indexed as

Antineoplastic AgentsBetulinic AcidCarcinogenesisNeoplasmsAnimalsEpidermal Growth FactorErbB ReceptorsProto-Oncogene Proteins c-aktTOR Serine-Threonine KinasesVascular Endothelial Growth Factor AAntineoplastic AgentsBetulinic AcidEpidermal Growth FactorErbB ReceptorsProto-Oncogene Proteins c-aktTOR Serine-Threonine KinasesVascular Endothelial Growth Factor AAKT/mTORapoptosisbetulinic acidcancerEGF/EGFRJAK/STATVEGF/VEGFR

Identifiers

PMID36615262
PMCPMC9822120
OpenAlexW4312187323

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.