---
title: "WK-13-3D inhibits triple-negative breast cancer by blocking autophagic flux via AKT/mTOR inhibitio"
id: "pubmed-42177862"
canonical_url: "https://medichelpline.com/clinical-feed/pubmed-42177862"
content_type: "clinical_feed_article"
specialty: "Oncology"
source_name: "PubMed / NCBI"
source_url: "https://pubmed.ncbi.nlm.nih.gov/42177862/"
doi: "10.1016/j.bioorg.2026.110015"
published_at: "2026-09-05T00:00:00.000Z"
evidence_level: "Journal Article"
license: "CC-BY-NC-4.0 / Informational Use"
---
# WK-13-3D inhibits triple-negative breast cancer by blocking autophagic flux via AKT/mTOR inhibitio
## Provenance & Clinical Metadata
- **Canonical URL:** https://medichelpline.com/clinical-feed/pubmed-42177862
- **Specialty:** [Oncology](https://medichelpline.com/clinical-feed/oncology.md)
- **Primary Source:** PubMed / NCBI
- **Source URL:** [Original Journal Publication](https://pubmed.ncbi.nlm.nih.gov/42177862/)
- **DOI:** [10.1016/j.bioorg.2026.110015](https://doi.org/10.1016%2Fj.bioorg.2026.110015)
- **Published At:** 2026-09-05T00:00:00.000Z
- **Evidence Rating:** Journal Article
## Executive GIST (TL;DR)
- The study evaluated the antitumor activity of the antimicrobial peptide **WK-13-3D** against triple-negative breast cancer (TNBC) using MDA-MB-231 and MDA-MB-468 cell lines and a nude mouse xenograft model. - WK-13-3D reduced TNBC cell viability and clonogenic potential in vitro and produced antitumor effects in vivo. - Mechanistically, WK-13-3D inhibited the **AKT/mTOR** signaling pathway and bound directly to **BiP** (binding immunoglobulin protein), inducing endoplasmic reticulum (ER) stress. - Treatment caused blockade of **autophagic flux**, shown by increased autophagosome accumulation (higher LC3-II/I ratio) and impaired degradation of the autophagy substrate p62. - Lysosomal acidification and hydrolytic function were reported as preserved despite autophagic flux blockade, based on LysoTracker Red and acridine orange staining. - Activation of AKT with the activator SC79 partially reversed the autophagy dysregulation induced by WK-13-3D, indicating a role for AKT/mTOR inhibition in the observed autophagy blockade. - Overexpression of **BiP** restored autophagic flux and enhanced lysosomal activity, supporting BiP as a direct target mediating ER stress and lysosome-related effects. - The authors conclude that concurrent inhibition of **AKT/mTOR** signaling and targeting of **BiP** disrupts autophagy-lysosome crosstalk to produce an enhanced antitumor response in TNBC and propose WK-13-3D as a promising lead for further preclinical investigation.
## Clinical Analysis & Structured Key Points
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Epub 2026 May 22. # Antimicrobial peptide WK-13-3D inhibits triple-negative breast cancer by blocking autophagic flux through inhibiting the AKT/mTOR pathway and targeting binding immunoglobulin protein (BiP) [Xuhong Su](https://pubmed.ncbi.nlm.nih.gov/?term=Su+X&cauthor_id=42177862)[ 1 ](https://pubmed.ncbi.nlm.nih.gov/42177862/#full-view-affiliation-1 "College of Laboratory Medicine, Ningxia Medical University, Yinchuan 750004, China."), [Wenjing Zhang](https://pubmed.ncbi.nlm.nih.gov/?term=Zhang+W&cauthor_id=42177862)[ 1 ](https://pubmed.ncbi.nlm.nih.gov/42177862/#full-view-affiliation-1 "College of Laboratory Medicine, Ningxia Medical University, Yinchuan 750004, China."), [Juan Ma](https://pubmed.ncbi.nlm.nih.gov/?term=Ma+J&cauthor_id=42177862)[ 1 ](https://pubmed.ncbi.nlm.nih.gov/42177862/#full-view-affiliation-1 "College of Laboratory Medicine, Ningxia Medical University, Yinchuan 750004, China."), [Yuyang Bai](https://pubmed.ncbi.nlm.nih.gov/?term=Bai+Y&cauthor_id=42177862)[ 2 ](https://pubmed.ncbi.nlm.nih.gov/42177862/#full-view-affiliation-2 "Third Clinical Medical College, Ningxia Medical University, Yinchuan, Ningxia Hui Autonomous Region, 750001, China."), [Guangsong Xu](https://pubmed.ncbi.nlm.nih.gov/?term=Xu+G&cauthor_id=42177862)[ 1 ](https://pubmed.ncbi.nlm.nih.gov/42177862/#full-view-affiliation-1 "College of Laboratory Medicine, Ningxia Medical University, Yinchuan 750004, China."), [Mingxing Zhu](https://pubmed.ncbi.nlm.nih.gov/?term=Zhu+M&cauthor_id=42177862)[ 3 ](https://pubmed.ncbi.nlm.nih.gov/42177862/#full-view-affiliation-3 "College of Basic Medical Sciences, Ningxia Medical University, Yinchuan 750004, China. Electronic address: zmxnxmu@126.com."), [Xiuqing Wang](https://pubmed.ncbi.nlm.nih.gov/?term=Wang+X&cauthor_id=42177862)[ 4 ](https://pubmed.ncbi.nlm.nih.gov/42177862/#full-view-affiliation-4 "College of Laboratory Medicine, Ningxia Medical University, Yinchuan 750004, China; Ningxia Key Laboratory of Clinical Pathogenic Microorganisms, Ningxia Medical University, Yinchuan 750004, China. Electronic address: xiuqingwang1979@163.com.") Affiliations Expand ### Affiliations * 1 College of Laboratory Medicine, Ningxia Medical University, Yinchuan 750004, China. * 2 Third Clinical Medical College, Ningxia Medical University, Yinchuan, Ningxia Hui Autonomous Region, 750001, China. * 3 College of Basic Medical Sciences, Ningxia Medical University, Yinchuan 750004, China. Electronic address: zmxnxmu@126.com. * 4 College of Laboratory Medicine, Ningxia Medical University, Yinchuan 750004, China; Ningxia Key Laboratory of Clinical Pathogenic Microorganisms, Ningxia Medical University, Yinchuan 750004, China. Electronic address: xiuqingwang1979@163.com. * PMID: **42177862** * DOI: [ 10.1016/j.bioorg.2026.110015 ](https://doi.org/10.1016/j.bioorg.2026.110015) Free article Item in Clipboard # Antimicrobial peptide WK-13-3D inhibits triple-negative breast cancer by blocking autophagic flux through inhibiting the AKT/mTOR pathway and targeting binding immunoglobulin protein (BiP) Xuhong Su et al. Bioorg Chem. 2026. Free article Show details Display options Display options Format Abstract PubMed PMID Bioorg Chem Actions * [ Search in PubMed ](https://pubmed.ncbi.nlm.nih.gov/?term=%22Bioorg+Chem%22%5Bjour%5D&sort=date&sort_order=desc) * [ Search in NLM Catalog ](https://www.ncbi.nlm.nih.gov/nlmcatalog?term=%22Bioorg+Chem%22%5BTitle+Abbreviation%5D) * [ Add to Search ](https://pubmed.ncbi.nlm.nih.gov/42177862/) . 2026 Sep 5:179:110015. doi: 10.1016/j.bioorg.2026.110015. Epub 2026 May 22. ### Authors [Xuhong Su](https://pubmed.ncbi.nlm.nih.gov/?term=Su+X&cauthor_id=42177862)[ 1 ](https://pubmed.ncbi.nlm.nih.gov/42177862/#short-view-affiliation-1 "College of Laboratory Medicine, Ningxia Medical University, Yinchuan 750004, China."), [Wenjing Zhang](https://pubmed.ncbi.nlm.nih.gov/?term=Zhang+W&cauthor_id=42177862)[ 1 ](https://pubmed.ncbi.nlm.nih.gov/42177862/#short-view-affiliation-1 "College of Laboratory Medicine, Ningxia Medical University, Yinchuan 750004, China."), [Juan Ma](https://pubmed.ncbi.nlm.nih.gov/?term=Ma+J&cauthor_id=42177862)[ 1 ](https://pubmed.ncbi.nlm.nih.gov/42177862/#short-view-affiliation-1 "College of Laboratory Medicine, Ningxia Medical University, Yinchuan 750004, China."), [Yuyang Bai](https://pubmed.ncbi.nlm.nih.gov/?term=Bai+Y&cauthor_id=42177862)[ 2 ](https://pubmed.ncbi.nlm.nih.gov/42177862/#short-view-affiliation-2 "Third Clinical Medical College, Ningxia Medical University, Yinchuan, Ningxia Hui Autonomous Region, 750001, China."), [Guangsong Xu](https://pubmed.ncbi.nlm.nih.gov/?term=Xu+G&cauthor_id=42177862)[ 1 ](https://pubmed.ncbi.nlm.nih.gov/42177862/#short-view-affiliation-1 "College of Laboratory Medicine, Ningxia Medical University, Yinchuan 750004, China."), [Mingxing Zhu](https://pubmed.ncbi.nlm.nih.gov/?term=Zhu+M&cauthor_id=42177862)[ 3 ](https://pubmed.ncbi.nlm.nih.gov/42177862/#short-view-affiliation-3 "College of Basic Medical Sciences, Ningxia Medical University, Yinchuan 750004, China. Electronic address: zmxnxmu@126.com."), [Xiuqing Wang](https://pubmed.ncbi.nlm.nih.gov/?term=Wang+X&cauthor_id=42177862)[ 4 ](https://pubmed.ncbi.nlm.nih.gov/42177862/#short-view-affiliation-4 "College of Laboratory Medicine, Ningxia Medical University, Yinchuan 750004, China; Ningxia Key Laboratory of Clinical Pathogenic Microorganisms, Ningxia Medical University, Yinchuan 750004, China. Electronic address: xiuqingwang1979@163.com.") ### Affiliations * 1 College of Laboratory Medicine, Ningxia Medical University, Yinchuan 750004, China. * 2 Third Clinical Medical College, Ningxia Medical University, Yinchuan, Ningxia Hui Autonomous Region, 750001, China. * 3 College of Basic Medical Sciences, Ningxia Medical University, Yinchuan 750004, China. Electronic address: zmxnxmu@126.com. * 4 College of Laboratory Medicine, Ningxia Medical University, Yinchuan 750004, China; Ningxia Key Laboratory of Clinical Pathogenic Microorganisms, Ningxia Medical University, Yinchuan 750004, China. Electronic address: xiuqingwang1979@163.com. * PMID: **42177862** * DOI: [ 10.1016/j.bioorg.2026.110015 ](https://doi.org/10.1016/j.bioorg.2026.110015) Item in Clipboard Full text links Cite Display options Display options Format Abstract PubMed PMID ## Abstract **Purpose:** To investigate the antitumor efficacy of a novel antimicrobial peptide WK-13-3D, against triple-negative breast cancer (TNBC) and elucidate its mechanism of action via targeting binding immunoglobulin protein BiP and modulating the AKT/mTOR pathway to disrupt autophagy-lysosome homeostasis. **Methods:** TNBC cell lines MDA-MB-231 and MDA-MB-468 were employed as in vitro models. Cell viability and clonogenic potential were assessed using CCK-8 and colony formation assays. Autophagy-related proteins (LC3-II/I, p62) and phosphorylation levels of key AKT/mTOR pathway components were analyzed by Western blotting. Autophagosome formation was visualized via transmission electron microscopy and immunofluorescence. Autophagic flux was monitored using mCherry-GFP-LC3 tandem fluorescent adenovirus. Lysosomal acidification was evaluated by LysoTracker Red and acridine orange (AO) staining. Functional rescue experiments were conducted using the AKT activator SC79. The in vivo antitumor activity of WK-13-3D was validated in a nude mouse xenograft model. **Results:** WK-13-3D significantly suppressed TNBC cell viability and clonogenicity. Mechanistically, WK-13-3D concurrently inhibited AKT/mTOR signaling and directly bound to BiP, triggering endoplasmic reticulum (ER) stress. Notably, WK-13-3D treatment led to autophagic flux blockade, evidenced by autophagosome accumulation (increased LC3-II/I ratio) and impaired degradation of the autophagic substrate p62, without compromising lysosomal acidification or hydrolytic function. Activation of the AKT/mTOR pathway partially reversed WK-13-3D-induced autophagy dysregulation, whereas BiP overexpression restored autophagic flux and enhanced lysosomal activity. These dual-targeting effects converged to exert a potent and enhanced antitumor response. **Conclusions:** WK-13-3D disrupts autophagy-lysosome crosstalk in TNBC via coordinated inhibition of AKT/mTOR signaling and BiP-mediated ER stress, representing a promising lead candidate that provides mechanistic insights for TNBC treatment and warrants further preclinical investigation. **Keywords:** AKT/mTOR pathway; Autophagic flux; BiP; Lysosome; Triple-negative breast cancer; WK-13-3D. Copyright © 2026 The Authors. Published by Elsevier Inc. All rights reserved. [PubMed Disclaimer](https://pubmed.ncbi.nlm.nih.gov/disclaimer/) ## Conflict of interest statement Declaration of competing interest The authors declare that they have no known competing financial interests or personal relationships that could have appeared to influence the work reported in this paper. ## Similar articles * [ Antimicrobial peptide WK-13-3D promotes apoptosis, autophagy, and ubiquitination in triple-negative breast cancer via binding immunoglobulin protein (BiP). ](https://pubmed.ncbi.nlm.nih.gov/40294882/) Zhang W, Ma F, Su X, Zhu M, Wang X.Zhang W, et al.Chem Biol Interact. 2025 Jul 1;415:111530. doi: 10.1016/j.cbi.2025.111530. Epub 2025 Apr 26.Chem Biol Interact. 2025.PMID: 40294882 * [ A novel orally available seleno-purine molecule suppresses triple-negative breast cancer cell proliferation and progression to metastasis by inducing cytostatic autophagy. ](https://pubmed.ncbi.nlm.nih.gov/30773992/) Chang CH, Bijian K, Wernic D, Su J, da Silva SD, Yu H, Qiu D, Asslan M, Alaoui-Jamali MA.Chang CH, et al.Autophagy. 2019 Aug;15(8):1376-1390. doi: 10.1080/15548627.2019.1582951. Epub 2019 Mar 1.Autophagy. 2019.PMID: 30773992Free PMC article. * [ Thymoquinone Inhibits Proliferation and Migration of MDA-MB-231 Triple Negative Breast Cancer Cells by Suppressing Autophagy, Beclin-1 and LC3. ](https://pubmed.ncbi.nlm.nih.gov/32767958/) Ünal TD, Hamurcu Z, Delibaşı N, Çınar V, Güler A, Gökçe S, Nurdinov N, Ozpolat B.Ünal TD, et al.Anticancer Agents Med Chem. 2021;21(3):355-364. doi: 10.2174/1871520620666200807221047.Anticancer Agents Med Chem. 2021.PMID: 32767958 * [ Indole-2-Carboxamide Derivative LG25 Inhibits Triple-Negative Breast Cancer Growth By Suppressing Akt/mTOR/NF-κB Signalling Pathway. ](https://pubmed.ncbi.nlm.nih.gov/31631978/) Xu X, Rajamanickam V, Shu S, Liu Z, Yan T, He J, Liu Z, Guo G, Liang G, Wang Y.Xu X, et al.Drug Des Devel Ther. 2019 Oct 11;13:3539-3550. doi: 10.2147/DDDT.S216542. eCollection 2019.Drug Des Devel Ther. 2019.PMID: 31631978Free PMC article. * [ Endoplasmic reticulum stress sensitizes human esophageal cancer cell to radiation. ](https://pubmed.ncbi.nlm.nih.gov/23555162/) Pang XL, He G, Liu YB, Wang Y, Zhang B.Pang XL, et al.World J Gastroenterol. 2013 Mar 21;19(11):1736-48. doi: 10.3748/wjg.v19.i11.1736.World J Gastroenterol. 2013.PMID: 23555162Free PMC article. 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