---
title: "Dual inhibition of SLC6A14 and autophagy/macropinocytosis improves therapy in PDAC"
id: "pubmed-41952621"
canonical_url: "https://medichelpline.com/clinical-feed/pubmed-41952621"
content_type: "clinical_feed_article"
specialty: "Oncology"
source_name: "PubMed / NCBI"
source_url: "https://pubmed.ncbi.nlm.nih.gov/41952621/"
doi: "10.1042/BCJ20250155"
published_at: "2026-08-05T00:00:00.000Z"
evidence_level: "Journal Article"
license: "CC-BY-NC-4.0 / Informational Use"
---
# Dual inhibition of SLC6A14 and autophagy/macropinocytosis improves therapy in PDAC
## Provenance & Clinical Metadata
- **Canonical URL:** https://medichelpline.com/clinical-feed/pubmed-41952621
- **Specialty:** [Oncology](https://medichelpline.com/clinical-feed/oncology.md)
- **Primary Source:** PubMed / NCBI
- **Source URL:** [Original Journal Publication](https://pubmed.ncbi.nlm.nih.gov/41952621/)
- **DOI:** [10.1042/BCJ20250155](https://doi.org/10.1042%2FBCJ20250155)
- **Published At:** 2026-08-05T00:00:00.000Z
- **Evidence Rating:** Journal Article
## Executive GIST (TL;DR)
- Pancreatic ductal adenocarcinoma (**PDAC**) shows high desmoplasia and metabolic reprogramming that sustains tumor growth. - The amino acid transporter **SLC6A14** was identified by the authors as a novel therapeutic target in PDAC; higher expression correlates with poorer patient survival. - Genetic deletion or pharmacological blockade of SLC6A14 with **α‑MLT** reduces PDAC growth by causing amino acid deprivation. - Amino acid or nutrient stress triggers compensatory nutrient-scavenging pathways, notably **autophagy** and **macropinocytosis**, which can blunt the efficacy of SLC6A14 blockade. - The study tested whether SLC6A14 inhibition induces autophagy/macropinocytosis and whether combining SLC6A14 blockade with an autophagy/macropinocytosis inhibitor (hydroxychloroquine, **HCQ**) enhances antitumor effects. - In vitro assays (MTT viability and colony-formation) showed that the combination of **α‑MLT + HCQ** significantly reduced PDAC cell viability and clonogenic potential versus either agent alone. - In a subcutaneous xenograft model in athymic nude mice, the combination therapy produced a superior therapeutic outcome compared with monotherapy. - Mechanistically, the combination creates a metabolic trap: **α‑MLT** induces nutrient stress while **HCQ** blocks autophagic and macropinocytic compensation, leading to enhanced tumor attenuation. - Experimental readouts included western blots for LC3B and mTORC1 pathway effectors, confocal imaging of mCherry‑EGFP‑LC3B reporters, and use of controls such as rapamycin, BafA1 to assess autophagy. - The dual-blockade approach is presented as a novel, previously unexplored therapeutic strategy for PDAC. - The source reports qualitative and experimental outcomes but does not provide full numeric values for all assays within the abstract; detailed quantitative results are reported in the full text figures and supplement.
## Clinical Analysis & Structured Key Points
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more resources ](https://pubmed.ncbi.nlm.nih.gov/41952621/#linkout) Title & authors Abstract Conflict of interest statement Figures Similar articles References MeSH terms Substances Related information Grants and funding LinkOut - more resources Biochem J Actions * [ Search in PubMed ](https://pubmed.ncbi.nlm.nih.gov/?term=%22Biochem+J%22%5Bjour%5D&sort=date&sort_order=desc) * [ Search in NLM Catalog ](https://www.ncbi.nlm.nih.gov/nlmcatalog?term=%22Biochem+J%22%5BTitle+Abbreviation%5D) * [ Add to Search ](https://pubmed.ncbi.nlm.nih.gov/41952621/) . 2026 Aug 5;483(8):1369-1390. doi: 10.1042/BCJ20250155. # Dual targeting of SLC6A14 and autophagy/macropinocytosis enhances therapeutic efficacy in pancreatic ductal adenocarcinoma [Mosharaf Mahmud Syed](https://pubmed.ncbi.nlm.nih.gov/?term=Mahmud+Syed+M&cauthor_id=41952621)[ 1 ](https://pubmed.ncbi.nlm.nih.gov/41952621/#full-view-affiliation-1 "Department of Cell Biology and Biochemistry, Texas Tech University Health Sciences Center, Lubbock, TX 79430, U.S.A."), [Devaraja Rajasekaran](https://pubmed.ncbi.nlm.nih.gov/?term=Rajasekaran+D&cauthor_id=41952621)[ 1 ](https://pubmed.ncbi.nlm.nih.gov/41952621/#full-view-affiliation-1 "Department of Cell Biology and Biochemistry, Texas Tech University Health Sciences Center, Lubbock, TX 79430, U.S.A."), [Souad R Sennoune](https://pubmed.ncbi.nlm.nih.gov/?term=Sennoune+SR&cauthor_id=41952621)[ 1 ](https://pubmed.ncbi.nlm.nih.gov/41952621/#full-view-affiliation-1 "Department of Cell Biology and Biochemistry, Texas Tech University Health Sciences Center, Lubbock, TX 79430, U.S.A."), [Tanima Sharker](https://pubmed.ncbi.nlm.nih.gov/?term=Sharker+T&cauthor_id=41952621)[ 1 ](https://pubmed.ncbi.nlm.nih.gov/41952621/#full-view-affiliation-1 "Department of Cell Biology and Biochemistry, Texas Tech University Health Sciences Center, Lubbock, TX 79430, U.S.A."), [Oscar Sanchez](https://pubmed.ncbi.nlm.nih.gov/?term=Sanchez+O&cauthor_id=41952621)[ 1 ](https://pubmed.ncbi.nlm.nih.gov/41952621/#full-view-affiliation-1 "Department of Cell Biology and Biochemistry, Texas Tech University Health Sciences Center, Lubbock, TX 79430, U.S.A."), [Mary Katherine Jurek](https://pubmed.ncbi.nlm.nih.gov/?term=Jurek+MK&cauthor_id=41952621)[ 2 ](https://pubmed.ncbi.nlm.nih.gov/41952621/#full-view-affiliation-2 "Department of Psychiatry, Tufts Medical Center, 800 Washington St., Boston, MA 02111, U.S.A."), [Longfa Kou](https://pubmed.ncbi.nlm.nih.gov/?term=Kou+L&cauthor_id=41952621)[ 3 ](https://pubmed.ncbi.nlm.nih.gov/41952621/#full-view-affiliation-3 "Department of Pharmacy, Wenzhou Municipal Key Laboratory of Pediatric Pharmacy, The Second Affiliated Hospital and Yuying Children's Hospital of Wenzhou Medical University, Wenzhou 325027, China."), [Ruijie Chen](https://pubmed.ncbi.nlm.nih.gov/?term=Chen+R&cauthor_id=41952621)[ 3 ](https://pubmed.ncbi.nlm.nih.gov/41952621/#full-view-affiliation-3 "Department of Pharmacy, Wenzhou Municipal Key Laboratory of Pediatric Pharmacy, The Second Affiliated Hospital and Yuying Children's Hospital of Wenzhou Medical University, Wenzhou 325027, China."), [Vadivel Ganapathy](https://pubmed.ncbi.nlm.nih.gov/?term=Ganapathy+V&cauthor_id=41952621)[ 1 ](https://pubmed.ncbi.nlm.nih.gov/41952621/#full-view-affiliation-1 "Department of Cell Biology and Biochemistry, Texas Tech University Health Sciences Center, Lubbock, TX 79430, U.S.A."), [Yangzom D Bhutia](https://pubmed.ncbi.nlm.nih.gov/?term=Bhutia+YD&cauthor_id=41952621)[ 1 ](https://pubmed.ncbi.nlm.nih.gov/41952621/#full-view-affiliation-1 "Department of Cell Biology and Biochemistry, Texas Tech University Health Sciences Center, Lubbock, TX 79430, U.S.A.") Affiliations Expand ### Affiliations * 1 Department of Cell Biology and Biochemistry, Texas Tech University Health Sciences Center, Lubbock, TX 79430, U.S.A. * 2 Department of Psychiatry, Tufts Medical Center, 800 Washington St., Boston, MA 02111, U.S.A. * 3 Department of Pharmacy, Wenzhou Municipal Key Laboratory of Pediatric Pharmacy, The Second Affiliated Hospital and Yuying Children's Hospital of Wenzhou Medical University, Wenzhou 325027, China. * PMID: **41952621** * PMCID: [ PMC13329288 ](https://pmc.ncbi.nlm.nih.gov/articles/PMC13329288/) * DOI: [ 10.1042/BCJ20250155 ](https://doi.org/10.1042/bcj20250155) Item in Clipboard # Dual targeting of SLC6A14 and autophagy/macropinocytosis enhances therapeutic efficacy in pancreatic ductal adenocarcinoma Mosharaf Mahmud Syed et al. Biochem J. 2026. Show details Display options Display options Format Abstract PubMed PMID Biochem J Actions * [ Search in PubMed ](https://pubmed.ncbi.nlm.nih.gov/?term=%22Biochem+J%22%5Bjour%5D&sort=date&sort_order=desc) * [ Search in NLM Catalog ](https://www.ncbi.nlm.nih.gov/nlmcatalog?term=%22Biochem+J%22%5BTitle+Abbreviation%5D) * [ Add to Search ](https://pubmed.ncbi.nlm.nih.gov/41952621/) . 2026 Aug 5;483(8):1369-1390. doi: 10.1042/BCJ20250155. ### Authors [Mosharaf Mahmud Syed](https://pubmed.ncbi.nlm.nih.gov/?term=Mahmud+Syed+M&cauthor_id=41952621)[ 1 ](https://pubmed.ncbi.nlm.nih.gov/41952621/#short-view-affiliation-1 "Department of Cell Biology and Biochemistry, Texas Tech University Health Sciences Center, Lubbock, TX 79430, U.S.A."), [Devaraja Rajasekaran](https://pubmed.ncbi.nlm.nih.gov/?term=Rajasekaran+D&cauthor_id=41952621)[ 1 ](https://pubmed.ncbi.nlm.nih.gov/41952621/#short-view-affiliation-1 "Department of Cell Biology and Biochemistry, Texas Tech University Health Sciences Center, Lubbock, TX 79430, U.S.A."), [Souad R Sennoune](https://pubmed.ncbi.nlm.nih.gov/?term=Sennoune+SR&cauthor_id=41952621)[ 1 ](https://pubmed.ncbi.nlm.nih.gov/41952621/#short-view-affiliation-1 "Department of Cell Biology and Biochemistry, Texas Tech University Health Sciences Center, Lubbock, TX 79430, U.S.A."), [Tanima Sharker](https://pubmed.ncbi.nlm.nih.gov/?term=Sharker+T&cauthor_id=41952621)[ 1 ](https://pubmed.ncbi.nlm.nih.gov/41952621/#short-view-affiliation-1 "Department of Cell Biology and Biochemistry, Texas Tech University Health Sciences Center, Lubbock, TX 79430, U.S.A."), [Oscar Sanchez](https://pubmed.ncbi.nlm.nih.gov/?term=Sanchez+O&cauthor_id=41952621)[ 1 ](https://pubmed.ncbi.nlm.nih.gov/41952621/#short-view-affiliation-1 "Department of Cell Biology and Biochemistry, Texas Tech University Health Sciences Center, Lubbock, TX 79430, U.S.A."), [Mary Katherine Jurek](https://pubmed.ncbi.nlm.nih.gov/?term=Jurek+MK&cauthor_id=41952621)[ 2 ](https://pubmed.ncbi.nlm.nih.gov/41952621/#short-view-affiliation-2 "Department of Psychiatry, Tufts Medical Center, 800 Washington St., Boston, MA 02111, U.S.A."), [Longfa Kou](https://pubmed.ncbi.nlm.nih.gov/?term=Kou+L&cauthor_id=41952621)[ 3 ](https://pubmed.ncbi.nlm.nih.gov/41952621/#short-view-affiliation-3 "Department of Pharmacy, Wenzhou Municipal Key Laboratory of Pediatric Pharmacy, The Second Affiliated Hospital and Yuying Children's Hospital of Wenzhou Medical University, Wenzhou 325027, China."), [Ruijie Chen](https://pubmed.ncbi.nlm.nih.gov/?term=Chen+R&cauthor_id=41952621)[ 3 ](https://pubmed.ncbi.nlm.nih.gov/41952621/#short-view-affiliation-3 "Department of Pharmacy, Wenzhou Municipal Key Laboratory of Pediatric Pharmacy, The Second Affiliated Hospital and Yuying Children's Hospital of Wenzhou Medical University, Wenzhou 325027, China."), [Vadivel Ganapathy](https://pubmed.ncbi.nlm.nih.gov/?term=Ganapathy+V&cauthor_id=41952621)[ 1 ](https://pubmed.ncbi.nlm.nih.gov/41952621/#short-view-affiliation-1 "Department of Cell Biology and Biochemistry, Texas Tech University Health Sciences Center, Lubbock, TX 79430, U.S.A."), [Yangzom D Bhutia](https://pubmed.ncbi.nlm.nih.gov/?term=Bhutia+YD&cauthor_id=41952621)[ 1 ](https://pubmed.ncbi.nlm.nih.gov/41952621/#short-view-affiliation-1 "Department of Cell Biology and Biochemistry, Texas Tech University Health Sciences Center, Lubbock, TX 79430, U.S.A.") ### Affiliations * 1 Department of Cell Biology and Biochemistry, Texas Tech University Health Sciences Center, Lubbock, TX 79430, U.S.A. * 2 Department of Psychiatry, Tufts Medical Center, 800 Washington St., Boston, MA 02111, U.S.A. * 3 Department of Pharmacy, Wenzhou Municipal Key Laboratory of Pediatric Pharmacy, The Second Affiliated Hospital and Yuying Children's Hospital of Wenzhou Medical University, Wenzhou 325027, China. * PMID: **41952621** * PMCID: [ PMC13329288 ](https://pmc.ncbi.nlm.nih.gov/articles/PMC13329288/) * DOI: [ 10.1042/BCJ20250155 ](https://doi.org/10.1042/bcj20250155) Item in Clipboard Full text links Cite Display options Display options Format Abstract PubMed PMID ## Abstract Pancreatic ductal adenocarcinoma (PDAC) is highly desmoplastic and undergoes metabolic reprogramming to sustain its growth and proliferation. Our laboratory has identified SLC6A14, an amino acid transporter, as a novel drug target for PDAC. Genetic deletion of SLC6A14 or its pharmacological blockade with α-MLT attenuates PDAC growth by inducing amino acid deprivation. However, nutrient stress, particularly amino acid deprivation, can induce nutrient scavenging mechanisms like autophagy and macropinocytosis, thereby undermining the full anticancer potential of SLC6A14 blockade. To address this, the current work was conducted to test whether SLC6A14 blockade induces autophagy and/or macropinocytosis and to further investigate whether dual inhibition of SLC6A14 (α-MLT) and autophagy/macropinocytosis (HCQ) would yield a better therapeutic outcome in PDAC as opposed to targeting SLC6A14 alone. In vitro assays (MTT and colony formation) revealed that the combination treatment significantly reduced PDAC cell viability and clonogenic potential as opposed to monotherapy. The treatment model subcutaneous xenograft in athymic nude mice demonstrated a superior therapeutic outcome with the combination regimen. Collectively, our study demonstrates that the afore-described combination therapy creates a metabolic trap wherein α-MLT induces nutrient stress, while HCQ prevents autophagic and macropinocytosis compensation, thus culminating in a more potent tumor attenuation. This dual blockade represents a hitherto unexplored treatment strategy for PDAC. **Keywords:** Alpha-methyl-l-tryptophan; Macropinocytosis; Pancreatic ductal adenocarcinoma; SLC6A14; autophagy; hydroxychloroqine. © 2026 The Author(s). [PubMed Disclaimer](https://pubmed.ncbi.nlm.nih.gov/disclaimer/) ## Conflict of interest statement The authors declare that there are no competing interests associated with the manuscript. ## Figures [ ![Figure 1](https://cdn.ncbi.nlm.nih.gov/pmc/blobs/6b92/13329288/794f3b5b8bb2/bcj-483-bcj20250155-g1.gif) ](https://cdn.ncbi.nlm.nih.gov/pmc/blobs/6b92/13329288/862cf33a34b8/bcj-483-bcj20250155-g1.jpg) ** Figure 1. SLC6A14 is highly up-regulated in… ** ** Figure 1. SLC6A14 is highly up-regulated in PDAC and the higher expression is associated with… ** **Figure 1. SLC6A14 is highly up-regulated in PDAC and the higher expression is associated with decreased overall patient survival** (**A**) Interactive body map showing median SLC6A14 expression in PDAC tumor versus normal pancreas (Scale: Log2(TPM +1); (**B**) Box plot map showing SLC6A14 expression in PDAC tumor [tumor (T), _n_ = 179; normal (N), _n_ = 171] versus normal pancreas; (**C**) Kaplan–Meier curve showing survival probability between high and low SLC6A14 expression. Data are given as mean ± SEM. *_P <_0.05. [ ![Figure 2](https://cdn.ncbi.nlm.nih.gov/pmc/blobs/6b92/13329288/289ab53e27ef/bcj-483-bcj20250155-g2.gif) ](https://cdn.ncbi.nlm.nih.gov/pmc/blobs/6b92/13329288/8e9ecd5915b8/bcj-483-bcj20250155-g2.jpg) ** Figure 2. SLC6A14 blockade induces autophagy in… ** ** Figure 2. SLC6A14 blockade induces autophagy in PDAC cells ** ( **A** ) Western blot showing… **Figure 2. SLC6A14 blockade induces autophagy in PDAC cells** (**A**) Western blot showing levels of LC3B, its upstream target proteins, and mTORC1 downstream effector proteins in CFPAC-1 cells. Rapamycin, an mTORC1 inhibitor, was used as a positive control; BafA1, an autophagy inhibitor, was used to assess flux, and α-MLT was used as a blocker of SLC6A14. Protein bands were quantified by densitometric analysis using ImageJ software. Normalized protein expression was calculated for each target, and the data are presented as the ratio of phosphorylated to the total protein. (**B**) Confocal microscopy in CFPAC-1/mCherry-EGFP-LC3B cells showing EGFP or mCherry signal following treatment with α-MLT, either singly or in combination with BafA1 and HCQ. Image magnification: 60×. [ ![Figure 3](https://cdn.ncbi.nlm.nih.gov/pmc/blobs/6b92/13329288/cf33aee07ad7/bcj-483-bcj20250155-g3.gif) ](https://cdn.ncbi.nlm.nih.gov/pmc/blobs/6b92/13329288/5b94d453d789/bcj-483-bcj20250155-g3.jpg) ** Figure 3. SLC6A14 blockade induces autophagy in… ** ** Figure 3. SLC6A14 blockade induces autophagy in PDAC cells and KPC mouse pancreas ** ( **A,B** … **Figure 3. SLC6A14 blockade induces autophagy in PDAC cells and KPC mouse pancreas** (**A,B**) Confocal microscopy in CFPAC-1/mCherry-EGFP-LC3B and HPAF-II/mCherry-EGFP-LC3B cells showing EGFP or mCherry signal following treatment with α-MLT, either singly or in combination with HCQ. Image magnification: 100×. (**C**) Western blots showing levels of LC3B, its upstream target proteins, and mTORC1 downstream effector proteins in KPC and KPCS mouse pancreas. GAPDH was used as a loading control. (**D**) Protein bands were quantified by densitometric analysis using ImageJ software. Normalized protein expression was calculated for each target, and the data are presente
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