---
title: "Gum acacia–gelatin nanohydrogel co-delivering metformin and doxorubicin inhibits TNT-driven breast"
id: "pubmed-42605874"
canonical_url: "https://medichelpline.com/clinical-feed/pubmed-42605874"
content_type: "clinical_feed_article"
specialty: "Oncology"
source_name: "PubMed / NCBI"
source_url: "https://pubmed.ncbi.nlm.nih.gov/42605874/"
doi: "10.1039/d6bm00697c"
published_at: "2026-09-29T00:00:00.000Z"
evidence_level: "Journal Article"
license: "CC-BY-NC-4.0 / Informational Use"
---
# Gum acacia–gelatin nanohydrogel co-delivering metformin and doxorubicin inhibits TNT-driven breast
## Provenance & Clinical Metadata
- **Canonical URL:** https://medichelpline.com/clinical-feed/pubmed-42605874
- **Specialty:** [Oncology](https://medichelpline.com/clinical-feed/oncology.md)
- **Primary Source:** PubMed / NCBI
- **Source URL:** [Original Journal Publication](https://pubmed.ncbi.nlm.nih.gov/42605874/)
- **DOI:** [10.1039/d6bm00697c](https://doi.org/10.1039%2Fd6bm00697c)
- **Published At:** 2026-09-29T00:00:00.000Z
- **Evidence Rating:** Journal Article
## Executive GIST (TL;DR)
- Tunneling nanotubes (TNTs) are nanoscale intercellular conduits that enable transfer of cellular content and promote cancer cell invasion and metastasis. - Macrophages and TNT-mediated intercellular communication contribute to breast cancer progression and drug resistance; the role of macrophage-induced TNTs in co-delivery strategies was explored. - Researchers formulated a **gum acacia–gelatin nanohydrogel** to co-load the antidiabetic drug **metformin (MET)** and the chemotherapeutic **doxorubicin (DOX)** for combined delivery. - The DOX/MET co-loaded nanohydrogel produced the largest reduction in viability of **MCF-7** breast cancer cells compared with single agents or other formulations. - Co-delivery activated apoptosis strongly, evidenced by robust activation of **caspase-3**, indicating enhanced execution-phase cell death. - Cellular internalization followed by lysosomal release allowed MET to activate **AMPK** signaling. AMPK activation led to suppression of the **PI3K/AKT/mTOR** pathway and inhibition of TNT formation, disrupting intercellular networks. - DOX localized to the nucleus where it disrupted DNA replication and produced direct cytotoxic effects on proliferative cells. - The combined mechanism targets both proliferative capacity and cellular networking, suggesting a dual therapeutic benefit: enhanced cytotoxicity and dismantling of TNT-mediated communication that may underlie metastasis and resistance. - The study supports the concept that combined MET and DOX delivery via a biopolymer nanohydrogel may limit breast cancer progression and metastasis by inhibiting TNTs; further details and broader validation were not reported in the abstract.
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Affiliations Expand ### Affiliations * 1 Redox Biology & Proteomics Laboratory, Department of Zoology, Ravenshaw University, Cuttack 753003, Odisha, India. lsamanta@ravenshawuniversity.ac.in. * 2 Department of Chemistry, Odisha University of Technology and Research, Bhubaneswar 751029, Odisha, India. subhraseema@gmail.com. * 3 Department of Chemistry, Ravenshaw University, Cuttack 753003, Odisha, India. * PMID: **42605874** * DOI: [ 10.1039/d6bm00697c ](https://doi.org/10.1039/d6bm00697c) Item in Clipboard # Dual delivery of metformin and doxorubicin _via_ the gum acacia-gelatin nanohydrogel disrupts tunnelling nanotube-mediated breast cancer progression Soumya Ranjan Jena et al. Biomater Sci. 2026. Show details Display options Display options Format Abstract PubMed PMID Biomater Sci Actions * [ Search in PubMed ](https://pubmed.ncbi.nlm.nih.gov/?term=%22Biomater+Sci%22%5Bjour%5D&sort=date&sort_order=desc) * [ Search in NLM Catalog ](https://www.ncbi.nlm.nih.gov/nlmcatalog?term=%22Biomater+Sci%22%5BTitle+Abbreviation%5D) * [ Add to Search ](https://pubmed.ncbi.nlm.nih.gov/42605874/) . 2026 Sep 29;14(19):5170-5185. doi: 10.1039/d6bm00697c. ### Authors [Soumya Ranjan Jena](https://pubmed.ncbi.nlm.nih.gov/?term=Jena+SR&cauthor_id=42605874)[ 1 ](https://pubmed.ncbi.nlm.nih.gov/42605874/#short-view-affiliation-1 "Redox Biology & Proteomics Laboratory, Department of Zoology, Ravenshaw University, Cuttack 753003, Odisha, India. lsamanta@ravenshawuniversity.ac.in."), [Anwesha Pradhan](https://pubmed.ncbi.nlm.nih.gov/?term=Pradhan+A&cauthor_id=42605874)[ 1 ](https://pubmed.ncbi.nlm.nih.gov/42605874/#short-view-affiliation-1 "Redox Biology & Proteomics Laboratory, Department of Zoology, Ravenshaw University, Cuttack 753003, Odisha, India. lsamanta@ravenshawuniversity.ac.in."), [Ganeswar Dalei](https://pubmed.ncbi.nlm.nih.gov/?term=Dalei+G&cauthor_id=42605874)[ 2 ](https://pubmed.ncbi.nlm.nih.gov/42605874/#short-view-affiliation-2 "Department of Chemistry, Odisha University of Technology and Research, Bhubaneswar 751029, Odisha, India. subhraseema@gmail.com."), [Subhraseema Das](https://pubmed.ncbi.nlm.nih.gov/?term=Das+S&cauthor_id=42605874)[ 2 ](https://pubmed.ncbi.nlm.nih.gov/42605874/#short-view-affiliation-2 "Department of Chemistry, Odisha University of Technology and Research, Bhubaneswar 751029, Odisha, India. subhraseema@gmail.com.")[ 3 ](https://pubmed.ncbi.nlm.nih.gov/42605874/#short-view-affiliation-3 "Department of Chemistry, Ravenshaw University, Cuttack 753003, Odisha, India."), [Luna Samanta](https://pubmed.ncbi.nlm.nih.gov/?term=Samanta+L&cauthor_id=42605874)[ 1 ](https://pubmed.ncbi.nlm.nih.gov/42605874/#short-view-affiliation-1 "Redox Biology & Proteomics Laboratory, Department of Zoology, Ravenshaw University, Cuttack 753003, Odisha, India. lsamanta@ravenshawuniversity.ac.in.") ### Affiliations * 1 Redox Biology & Proteomics Laboratory, Department of Zoology, Ravenshaw University, Cuttack 753003, Odisha, India. lsamanta@ravenshawuniversity.ac.in. * 2 Department of Chemistry, Odisha University of Technology and Research, Bhubaneswar 751029, Odisha, India. subhraseema@gmail.com. * 3 Department of Chemistry, Ravenshaw University, Cuttack 753003, Odisha, India. * PMID: **42605874** * DOI: [ 10.1039/d6bm00697c ](https://doi.org/10.1039/d6bm00697c) Item in Clipboard Full text links Cite Display options Display options Format Abstract PubMed PMID Linked Discoveries ## Abstract Tunneling nanotubes (TNTs) are nano-scale intracellular conduits facilitating the transfer of cellular content. Intercellular communication between cancer cells _via_ TNTs promotes invasion and metastasis. Given the important role of TNTs and macrophages in cancer, the role of macrophage-induced TNTs in the co-delivery of metformin (MET) and the chemotherapeutic drug doxorubicin (DOX) in mediating drug resistance is not fully understood. In this study, the inhibition of TNT-mediated breast cancer progression was mechanistically explored through DOX/MET co-delivery. For cargo delivery, the co-drugs were loaded onto gelatin and gum acacia. The DOX/MET co-loaded nanohydrogel induced the most substantial reduction in cell viability in MCF-7 breast cancer cells. The combination of DOX-MET resulted in the robust activation of caspase-3, indicating the enhanced execution of apoptosis. Upon internalization and lysosomal release, MET activates AMPK signaling, which in turn suppresses the PI3K/AKT/mTOR axis and inhibits TNT formation, thereby blocking intercellular communication. Concurrently, DOX localizes to the nucleus, where it disrupts DNA replication and directly induces cytotoxicity. This combined approach not only targets proliferative capacity but also dismantles cellular networking mechanisms. Overall, the results of this study endorse that this combined therapeutic strategy might offer enhanced efficacy in limiting breast cancer progression and metastasis through the inhibition of TNTs. [PubMed Disclaimer](https://pubmed.ncbi.nlm.nih.gov/disclaimer/) ## MeSH terms * Antineoplastic Agents* / administration & dosage Actions * [ Search in PubMed ](https://pubmed.ncbi.nlm.nih.gov/?term=%22Antineoplastic+Agents%2Fadministration+and+dosage%22%5BMAJR%5D&sort=date&sort_order=desc) * [ Search in MeSH ](https://www.ncbi.nlm.nih.gov/mesh?term=Antineoplastic+Agents) * [ Add to Search ](https://pubmed.ncbi.nlm.nih.gov/42605874/) * Antineoplastic Agents* / chemistry Actions * [ Search in PubMed ](https://pubmed.ncbi.nlm.nih.gov/?term=%22Antineoplastic+Agents%2Fchemistry%22%5BMAJR%5D&sort=date&sort_order=desc) * [ Search in MeSH ](https://www.ncbi.nlm.nih.gov/mesh?term=Antineoplastic+Agents) * [ Add to Search ](https://pubmed.ncbi.nlm.nih.gov/42605874/) * Antineoplastic Agents* / pharmacology Actions * [ Search in PubMed ](https://pubmed.ncbi.nlm.nih.gov/?term=%22Antineoplastic+Agents%2Fpharmacology%22%5BMAJR%5D&sort=date&sort_order=desc) * [ Search in MeSH 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