Evidence map›Paper›PMID 41510721›Full record

ReviewCurrent drug targets2026

Targeting STAT3 in Breast Cancer Using Innovative Natural and Synthetic Scaffolds to Trigger Apoptosis, Autophagy, and Halt Tumor Progression.

Bhavana Jayadevappa, Dhanya Dinesh, Allaka Nagalakshmi, Thungeshwari C Paramesh, Vidyashree K Shivaprakash, Prema Venkatesh, Ambika H Devarajanayaka, Anusha H Krishna, Archana A Shivanna, Chaithra A Chandru and 14 more

Abstract readReview
PubMed Publisher
In one paragraph

Review in Current drug targets, 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Not yet cited in PubMed.

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

0 citing papers in PubMed.

No citing paper in PubMed yet.

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

24 authors.

Bhavana JayadevappaDepartment of Studies in Molecular Biology, University of Mysore, Manasagangotri, Mysuru, Karnataka, 570006, India.
Dhanya DineshDepartment of Studies in Molecular Biology, University of Mysore, Manasagangotri, Mysuru, Karnataka, 570006, India.
Allaka NagalakshmiDepartment of Computer Science, St Philomena's College (Autonomous), Bangalore - Mysore Rd, Bannimantap, Mysuru, Karnataka, 570015, India.
Thungeshwari C ParameshDepartment of Studies in Molecular Biology, University of Mysore, Manasagangotri, Mysuru, Karnataka, 570006, India.
Vidyashree K ShivaprakashDepartment of Studies in Molecular Biology, University of Mysore, Manasagangotri, Mysuru, Karnataka, 570006, India.
Prema VenkateshDepartment of Studies in Molecular Biology, University of Mysore, Manasagangotri, Mysuru, Karnataka, 570006, India.
Ambika H DevarajanayakaDepartment of Studies in Molecular Biology, University of Mysore, Manasagangotri, Mysuru, Karnataka, 570006, India.
Anusha H KrishnaDepartment of Studies in Molecular Biology, University of Mysore, Manasagangotri, Mysuru, Karnataka, 570006, India.
Archana A ShivannaDepartment of Studies in Molecular Biology, University of Mysore, Manasagangotri, Mysuru, Karnataka, 570006, India.
Chaithra A ChandruDepartment of Studies in Molecular Biology, University of Mysore, Manasagangotri, Mysuru, Karnataka, 570006, India.
Harsha AgasimaneDepartment of Studies in Molecular Biology, University of Mysore, Manasagangotri, Mysuru, Karnataka, 570006, India.
Jennifer AnthonyDepartment of Studies in Molecular Biology, University of Mysore, Manasagangotri, Mysuru, Karnataka, 570006, India.
Noortaj J SubhanDepartment of Studies in Molecular Biology, University of Mysore, Manasagangotri, Mysuru, Karnataka, 570006, India.
Noureen Usman SabDepartment of Studies in Molecular Biology, University of Mysore, Manasagangotri, Mysuru, Karnataka, 570006, India.
Yashwanth RangaswamyDepartment of Studies in Molecular Biology, University of Mysore, Manasagangotri, Mysuru, Karnataka, 570006, India.
Yashaswi PuttarajuDepartment of Studies in Molecular Biology, University of Mysore, Manasagangotri, Mysuru, Karnataka, 570006, India.
Hemanth Vikram P RAmity Institute of Pharmacy, Amity University Kolkata, Major Arterial Road, AA II, Newtown, Kadampukur, Kolkata, West Bengal, 700135, India.
Dilipkumar Reddy KandulaDepartment of Pharmacy, Shri JJT University, Jhunjhunu, Rajasthan, India.
Klavdiya Turkandze AmiranovaDepartment of Infectious Diseases of the Institute of Public Health Named after F.F. Erisman I.M. Sechenov First Moscow State Medical University of the Russian Federation (Sechenov University), Moscow, Russia.
Padmanabha Reddy YDepartment of Pharmacy, Raghavendra Institute of Pharmaceutical Education and Research (RIPER), Anantapuramu, Chiyyedu, Andhra Pradesh, 515721, India.
Syed HidayathullaDepartment of Studies in Molecular Biology, University of Mysore, Manasagangotri, Mysuru, Karnataka, 570006, India.
Vladimir N NikolenkoAmity Institute of Pharmacy, Amity University Kolkata, Major Arterial Road, AA II, Newtown, Kadampukur, Kolkata, West Bengal, 700135, India.
Basappa BasappaDepartment of Studies in Molecular Biology, University of Mysore, Manasagangotri, Mysuru, Karnataka, 570006, India.
Narasimha M BeerakaDepartment of Studies in Molecular Biology, University of Mysore, Manasagangotri, Mysuru, Karnataka, 570006, India.

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

introductionSignal Transducer and Activator of Transcription 3 (STAT3) is a key mediator in Breast Cancer (BC) progression, contributing to tumor proliferation, metastasis, survival, and resistance to chemotherapy. Phosphorylation of STAT3 at tyrosine 705 promotes its dimerization and nuclear translocation, where it activates oncogenic transcriptional programs. Due to its central role in BC pathogenesis, STAT3 has emerged as a promising molecular target for therapeutic intervention.

objectiveTo synthesize, characterize, and evaluate the anticancer efficacy of synthetic and natural compounds with a focus on their ability to inhibit STAT3 phosphorylation, suppress breast cancer cell proliferation, and induce apoptosis and autophagy.

methodsA comprehensive literature review was conducted using databases such as PubMed, Scopus, Relemed, and ResearchGate. Relevant studies were identified that examined the synthesis, molecular mechanisms, and therapeutic potential of STAT3 inhibitors. Synthetic derivatives and phytochemicals were considered for their inhibitory effects on STAT3 activation and associated cellular outcomes in breast cancers.

resultsSeveral synthetic and natural compounds demonstrated significant inhibitory effects on STAT3 phosphorylation, leading to reduced breast cancer cell proliferation, migration, and survival. These agents effectively induced apoptosis and, in some cases, autophagy, highlighting their multifaceted anti-tumor mechanisms and elucidating the potential of these compounds as lead candidates for further preclinical and clinical development.

conclusionTargeting STAT3 can be a significant therapeutic strategy, as both synthetic and natural compounds capable of inhibiting STAT3 signaling have been shown in preclinical studies. These findings provide valuable insights for cancer biologists, molecular researchers, and clinicians to explore STAT3 inhibitors as potential breast cancer therapeutics.

Indexed as

Antineoplastic AgentsBiological ProductsBreast NeoplasmsSTAT3 Transcription FactorAnimalsApoptosisAutophagyCell ProliferationDisease ProgressionFemaleHumansPhosphorylationSignal TransductionAntineoplastic AgentsBiological ProductsSTAT3 protein, humanSTAT3 Transcription Factorapoptosisbreast cancermolecular oncologynatural productsphosphorylationSTAT3synthetic compoundstargeted therapy

Identifiers

PMID41510721

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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 OpenQuestion graph.