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组织蛋白酶 S 通过肿瘤相关巨噬细胞和激活的中性粒细胞促进胃癌进展

Legumain Promotes Gastric Cancer Progression Through Tumor-associated Macrophages and .

机构信息

Division of Gastroenterology and Hepatology, Key Laboratory of Gastroenterology and Hepatology, Ministry of Health, Shanghai Institute of Digestive Disease, Renji Hospital Affiliated to Shanghai Jiao Tong University School of Medicine, Shanghai, China.

Department of Gastroenterology, Punan Hospital, Pudong New Area, Shanghai, China.

出版信息

Int J Biol Sci. 2020 Jan 1;16(1):172-180. doi: 10.7150/ijbs.36467. eCollection 2020.

DOI:10.7150/ijbs.36467
PMID:31892854
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC6930372/
Abstract

Tumor-associated macrophages (TAMs) play a crucial role in the tumor microenvironment. Legumain (LGMN) has been shown to be a tumor-promoting protein, but the effect of LGMN on TAMs in the progression of gastric cancer (GC) is under exploration. Our studies included the construction of LGMN-knockdown and LGMN-overexpressing TAMs induced from the human cell line THP-1 (PMA/IL-4/IL-13) and murine cell line Raw264.7 (IL-4/IL-13). A CCK-8 assay and transwell migration assay indicated that upregulation of LGMN expression in TAMs stimulated cell proliferation, migration and invasion while downregulation of LGMN expression reduced cell proliferation, migration and invasion. experiments revealed slower growth, less angiogenesis, and less Ki67 expression in LGMN-knockdown TAMs injected with gastric cancer cells compared to control TAMs injected with GC cells. Together, these study results suggested that LGMN TAMs which may serve as a potential target for GC treatment, promoted gastric cancer cell proliferation and angiogenesis and .

摘要

肿瘤相关巨噬细胞（TAMs）在肿瘤微环境中发挥着关键作用。组织蛋白酶 L（LGMN）已被证明是一种促进肿瘤的蛋白质，但 LGMN 对胃癌（GC）进展中 TAMs 的影响仍在探索中。我们的研究包括从人源细胞系 THP-1（PMA/IL-4/IL-13）和鼠源细胞系 Raw264.7（IL-4/IL-13）诱导构建 LGMN 敲低和 LGMN 过表达的 TAMs。CCK-8 检测和 Transwell 迁移实验表明，TAMs 中 LGMN 表达的上调刺激了细胞的增殖、迁移和侵袭，而 LGMN 表达的下调则降低了细胞的增殖、迁移和侵袭。体内实验显示，与注射 GC 细胞的对照 TAMs 相比，注射胃癌细胞的 LGMN 敲低 TAMs 生长更慢、血管生成更少、Ki67 表达更少。综上所述，这些研究结果表明，LGMN TAMs 可能成为 GC 治疗的潜在靶点，促进了胃癌细胞的增殖和血管生成。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/a639/6930372/c30e0a50547a/ijbsv16p0172g006.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/a639/6930372/bfc10f34d0c3/ijbsv16p0172g001.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/a639/6930372/44453edf146d/ijbsv16p0172g002.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/a639/6930372/5f688eae3b52/ijbsv16p0172g003.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/a639/6930372/582449726a7e/ijbsv16p0172g004.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/a639/6930372/89a251de5aaa/ijbsv16p0172g005.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/a639/6930372/c30e0a50547a/ijbsv16p0172g006.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/a639/6930372/bfc10f34d0c3/ijbsv16p0172g001.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/a639/6930372/44453edf146d/ijbsv16p0172g002.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/a639/6930372/5f688eae3b52/ijbsv16p0172g003.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/a639/6930372/582449726a7e/ijbsv16p0172g004.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/a639/6930372/89a251de5aaa/ijbsv16p0172g005.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/a639/6930372/c30e0a50547a/ijbsv16p0172g006.jpg

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[3]
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[5]
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[6]
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[7]
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[8]
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[9]
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[10]
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本文引用的文献

[1]
Role of Asparagine Endopeptidase in Mediating Wild-Type p53 Inactivation of Glioblastoma.

J Natl Cancer Inst. 2020-4-1

[2]
Tumors and Their Microenvironment Dual-Targeting Chemotherapy with Local Immune Adjuvant Therapy for Effective Antitumor Immunity against Breast Cancer.

Adv Sci (Weinh). 2019-1-30

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Macrophage-Derived Legumain Promotes Pulmonary Hypertension by Activating the MMP (Matrix Metalloproteinase)-2/TGF (Transforming Growth Factor)-β1 Signaling.

Arterioscler Thromb Vasc Biol. 2019-4

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Legumain, an asparaginyl endopeptidase, mediates the effect of M2 macrophages on attenuating renal interstitial fibrosis in obstructive nephropathy.

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Int J Mol Sci. 2017-9-20

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Tumor-Associated Macrophages Promote Epigenetic Silencing of Gelsolin through DNA Methyltransferase 1 in Gastric Cancer Cells.

Cancer Immunol Res. 2017-8-23

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