---
title: "SEC31A drives gastric cancer growth via PI3K/AKT/mTOR and CCL5-mediated M2 macrophage recruitment"
id: "pubmed-42885291"
canonical_url: "https://medichelpline.com/clinical-feed/pubmed-42885291"
content_type: "clinical_feed_article"
specialty: "Oncology"
source_name: "PubMed / NCBI"
source_url: "https://pubmed.ncbi.nlm.nih.gov/42885291/"
doi: "10.3892/or.2026.9211"
published_at: "2026-10-16T12:00:00.000Z"
evidence_level: "Journal Article"
license: "CC-BY-NC-4.0 / Informational Use"
---
# SEC31A drives gastric cancer growth via PI3K/AKT/mTOR and CCL5-mediated M2 macrophage recruitment
## Provenance & Clinical Metadata
- **Canonical URL:** https://medichelpline.com/clinical-feed/pubmed-42885291
- **Specialty:** [Oncology](https://medichelpline.com/clinical-feed/oncology.md)
- **Primary Source:** PubMed / NCBI
- **Source URL:** [Original Journal Publication](https://pubmed.ncbi.nlm.nih.gov/42885291/)
- **DOI:** [10.3892/or.2026.9211](https://doi.org/10.3892%2For.2026.9211)
- **Published At:** 2026-10-16T12:00:00.000Z
- **Evidence Rating:** Journal Article
## Executive GIST (TL;DR)
- Investigators reported that **SEC31A** expression was elevated in gastric cancer tissue samples and in gastric cancer cell lines, based on western blotting and immunohistochemistry. - The study team observed that suppression of **SEC31A** reduced epithelial–mesenchymal transition (EMT) features, cellular proliferation, migration and invasion in in vitro gastric cancer models, indicating a pro‑tumor role. - Data indicated overexpression of **SEC31A** activated the **PI3K/AKT/mTOR** signaling cascade; this pathway was implicated mechanistically in the observed increases in malignant phenotypes. - The PI3K inhibitor LY294002 was applied and investigators reported it counteracted SEC31A-driven increases in proliferation, migration, invasion and EMT, linking SEC31A activity to PI3K pathway mediation. - Co‑culture experiments using THP‑1 monocyte‑derived macrophages and gastric cancer cells showed that SEC31A enhanced macrophage recruitment and drove M2 polarization via **CCL5** within the tumor microenvironment. - The authors used M2 macrophage‑conditioned medium (M2‑CM) to test paracrine effects; M2‑CM partially reversed the inhibitory effects of SEC31A knockdown on malignant behaviors, implying M2 macrophages sustain tumor phenotypes. - In preclinical anti‑PD‑1 experiments reported by the authors, diminished SEC31A expression improved the efficacy of anti‑PD‑1 therapy in gastric cancer models; the study did not report clinical validation in human patients. - Methods summarized by the authors included western blotting, immunohistochemistry, functional cellular assays (proliferation, migration, invasion, EMT markers), pharmacologic inhibition with LY294002, THP‑1 co‑culture and M2‑CM experiments; the source did not provide specific experimental parameters in the abstract.
## Clinical Analysis & Structured Key Points
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Epub 2026 Oct 16. # SEC31A promotes gastric cancer progression by inducing the PI3K/AKT/mTOR pathway and enhancing the CCL5‑mediated M2 polarization and recruitment of tumor‑associated macrophages [Xixian Zhao](https://pubmed.ncbi.nlm.nih.gov/?term=Zhao+X&cauthor_id=42885291)[ 1 ](https://pubmed.ncbi.nlm.nih.gov/42885291/#full-view-affiliation-1 "Department of Gastroenterology, Yantai Yuhuangding Hospital of Qingdao University, Yantai, Shandong 264000, P.R. China."), [Liuye Huang](https://pubmed.ncbi.nlm.nih.gov/?term=Huang+L&cauthor_id=42885291)[ 1 ](https://pubmed.ncbi.nlm.nih.gov/42885291/#full-view-affiliation-1 "Department of Gastroenterology, Yantai Yuhuangding Hospital of Qingdao University, Yantai, Shandong 264000, P.R. China.") Affiliations Expand ### Affiliation * 1 Department of Gastroenterology, Yantai Yuhuangding Hospital of Qingdao University, Yantai, Shandong 264000, P.R. China. * PMID: **42885291** * DOI: [ 10.3892/or.2026.9211 ](https://doi.org/10.3892/or.2026.9211) Item in Clipboard # SEC31A promotes gastric cancer progression by inducing the PI3K/AKT/mTOR pathway and enhancing the CCL5‑mediated M2 polarization and recruitment of tumor‑associated macrophages Xixian Zhao et al. Oncol Rep. 2026 Dec. Show details Display options Display options Format Abstract PubMed PMID Oncol Rep Actions * [ Search in PubMed ](https://pubmed.ncbi.nlm.nih.gov/?term=%22Oncol+Rep%22%5Bjour%5D&sort=date&sort_order=desc) * [ Search in NLM Catalog ](https://www.ncbi.nlm.nih.gov/nlmcatalog?term=%22Oncol+Rep%22%5BTitle+Abbreviation%5D) * [ Add to Search ](https://pubmed.ncbi.nlm.nih.gov/42885291/) . 2026 Dec;56(6):205. doi: 10.3892/or.2026.9211. Epub 2026 Oct 16. ### Authors [Xixian Zhao](https://pubmed.ncbi.nlm.nih.gov/?term=Zhao+X&cauthor_id=42885291)[ 1 ](https://pubmed.ncbi.nlm.nih.gov/42885291/#short-view-affiliation-1 "Department of Gastroenterology, Yantai Yuhuangding Hospital of Qingdao University, Yantai, Shandong 264000, P.R. China."), [Liuye Huang](https://pubmed.ncbi.nlm.nih.gov/?term=Huang+L&cauthor_id=42885291)[ 1 ](https://pubmed.ncbi.nlm.nih.gov/42885291/#short-view-affiliation-1 "Department of Gastroenterology, Yantai Yuhuangding Hospital of Qingdao University, Yantai, Shandong 264000, P.R. China.") ### Affiliation * 1 Department of Gastroenterology, Yantai Yuhuangding Hospital of Qingdao University, Yantai, Shandong 264000, P.R. China. * PMID: **42885291** * DOI: [ 10.3892/or.2026.9211 ](https://doi.org/10.3892/or.2026.9211) Item in Clipboard Cite Display options Display options Format Abstract PubMed PMID Linked Discoveries ## Abstract SEC31 homolog A (SEC31A) is associated with a variety of cancers. This study elucidated the role of SEC31A in gastric cancer (GC). The expression of SEC31A in GC was analyzed using western blotting and immunohistochemistry. Functional experiments were performed to detect the impact of SEC31A on GC proliferation, migration and invasion. The PI3K inhibitor LY294002 was used to explore the regulation of the biological functions by SEC31A through the PI3K/AKT/mTOR pathway in GC cells. Co‑culture of THP‑1 (human leukemia cell line of monocytic origin) and GC cells was conducted to investigate the impact of SEC31A on the M2 macrophage polarization in tumor immune microenvironment. Our investigation observed elevated expression of SEC31A in both GC tissue and cell lines. Through functional studies, suppression of SEC31A was found to decrease epithelial‑mesenchymal transition (EMT), proliferation, migration and invasion in GC cells. Overexpression of SEC31A led to activation of the PI3K/AKT/mTOR signaling cascade. The PI3K inhibitor LY294002 counteracted the increases in proliferation, migration, invasion and EMT triggered by SEC31A. Co‑culture experiments involving THP‑1 and GC cells indicated that SEC31A enhanced the recruitment and M2 polarization of macrophages via CCL5 within the GC tumor microenvironment (ME). To assess the influence of M2 macrophages on malignant behavior of GC cells, M2 macrophage‑conditioned medium (M2‑CM) was applied. M2‑CM mitigated the inhibitory effects on malignant phenotypes in GC cells following SEC31A knockdown. Moreover, diminished SEC31A expression enhanced the efficacy of anti‑PD‑1 therapy in GC models. Collectively, SEC31A promoted GC progression via activating the PI3K/AKT/mTOR pathway and facilitating CCL5‑mediated M2 polarization and recruitment of tumor‑associated macrophages. SEC31A knockdown may augment the anti‑tumor response to anti‑PD‑1 treatment in GC. These findings highlight SEC31A as a valuable prognostic indicator and potential target for immunotherapy in GC, offering novel strategies to enhance the effectiveness of anti‑PD‑1 therapy. **Keywords:** M2 macrophage; PI3K/AKT/mTOR; SEC31 homolog A; anti‑PD‑1; gastric cancer. 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