Evidence map›Paper›PMID 39219410›Full record

ReviewAnimal models and experimental medicine2024

Targeting STAT3 signaling pathway by curcumin and its analogues for breast cancer: A narrative review.

Maryam Golmohammadi, Mohammad Yassin Zamanian, Ahmed Muzahem Al-Ani, Thaer L Jabbar, Ali Kamil Kareem, Zeinab Hashem Aghaei, Hossein Tahernia, Ahmed Hjazi, Saad Abdul-Ridh Jissir, Elham Hakimizadeh

Abstract readReview
PubMed Full text at PMC Publisher
In one paragraph

Review in Animal models and experimental medicine, 2024. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 21 papers.

0numbers the graph read from it
0cells of the map it votes in
21citing 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

21 citing papers in PubMed.

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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

10 authors.

Maryam GolmohammadiSchool of Medicine, Shahid Beheshti University of Medical Sciences, Tehran, Iran.
Mohammad Yassin ZamanianDepartment of Physiology, School of Medicine, Hamadan University of Medical Sciences, Hamadan, Iran.ORCID 0000-0003-0944-0320
Ahmed Muzahem Al-AniDepartment of Medical Laboratories Technology, AL-Nisour University College, Baghdad, Iraq.
Thaer L JabbarCollege of pharmacy, Al- Ayen University, Nasiriyah, Iraq.
Ali Kamil KareemBiomedical Engineering Department, Al-Mustaqbal University College, Hillah, Iraq.
Zeinab Hashem AghaeiPreventative Gynecology Research Center, Shahid Beheshti University of Medical Sciences, Tehran, Iran.
Hossein TaherniaMolecular Medicine Research Center, Research Institute of Basic Medical Sciences, Rafsanjan University of Medical Sciences, Rafsanjan, Iran.
Ahmed HjaziDepartment of Medical Laboratory Sciences, College of Applied Medical Sciences, Prince Sattam bin Abdulaziz University, Al-Kharj, Saudi Arabia.
Saad Abdul-Ridh JissirCollege of Nursing, Al-Bayan University, Baghdad, Iraq.
Elham HakimizadehPhysiology-Pharmacology Research Center, Research Institute of Basic Medical Sciences, Rafsanjan University of Medical Sciences, Rafsanjan, Iran.

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

backgroundBreast cancer (BC) continues to be a significant global health issue, with a rising number of cases requiring ongoing research and innovation in treatment strategies. Curcumin (CUR), a natural compound derived from Curcuma longa, and similar compounds have shown potential in targeting the STAT3 signaling pathway, which plays a crucial role in BC progression.

aimsThe aim of this study was to investigate the effects of curcumin and its analogues on BC based on cellular and molecular mechanisms. MATERIALS &

methodsThe literature search conducted for this study involved utilizing the Scopus, ScienceDirect, PubMed, and Google Scholar databases in order to identify pertinent articles.

resultsThis narrative review explores the potential of CUR and similar compounds in inhibiting STAT3 activation, thereby suppressing the proliferation of cancer cells, inducing apoptosis, and inhibiting metastasis. The review demonstrates that CUR directly inhibits the phosphorylation of STAT3, preventing its movement into the nucleus and its ability to bind to DNA, thereby hindering the survival and proliferation of cancer cells. CUR also enhances the effectiveness of other therapeutic agents and modulates the tumor microenvironment by affecting tumor-associated macrophages (TAMs). CUR analogues, such as hydrazinocurcumin (HC), FLLL11, FLLL12, and GO-Y030, show improved bioavailability and potency in inhibiting STAT3, resulting in reduced cell proliferation and increased apoptosis.

conclusionCUR and its analogues hold promise as effective adjuvant treatments for BC by targeting the STAT3 signaling pathway. These compounds provide new insights into the mechanisms of action of CUR and its potential to enhance the effectiveness of BC therapies.

Indexed as

Breast NeoplasmsCurcuminSignal TransductionSTAT3 Transcription FactorAnimalsAntineoplastic AgentsApoptosisCell ProliferationFemaleHumansAntineoplastic AgentsCurcuminSTAT3 protein, humanSTAT3 Transcription Factorapoptosiscell proliferationcurcumincurcumin analoguesSTAT3

Identifiers

PMID39219410
PMCPMC11680487

What Socratic holds

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Registered trials

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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 Socratic graph.