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LncRNA-HOXC-AS2 regulates tumor-associated macrophage polarization through the STAT1/SOCS1 and STAT1/CIITA pathways to promote the progression of non-small cell lung cancer

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收录情况： ◇ SCIE

作者：
Yin Cunli[1] ; Li Jing[2] ; Li Siru[1] ; Yang Xi[3] ; Lu Yingchun[1] ; Wang Chunyu[3] ; Liu Bin[4] ;
机构： [1]School of Medicine, University of Electronic Science and Technology of China, China. [2]Department of General Internal Medicine, Sichuan Clinical Research Center for Cancer, Sichuan Cancer Hospital & Institute, Sichuan Cancer Center, Affiliated Cancer Hospital of University of Electronic Science and Technology of China Chengdu, China. [3]School of Medicine and Life Sciences, Chengdu University of Traditional Chinese Medicine, China. [4]Department of Medical Oncology, Sichuan Clinical Research Center for Cancer, Sichuan Cancer Hospital & Institute, Sichuan Cancer Center, Affiliated Cancer Hospital of University of Electronic Science and Technology of China Chengdu, China
出处：
DOI： 10.1016/j.cellsig.2023.111031
ISSN：

关键词： Non-small cell lung cancer lncRNA-HOXC-AS2 Tumor-associated macrophage Polarization STAT1/SOCS1 and STAT1/CIITA pathways

摘要：
Tumor-associated macrophages (TAMs) mainly exhibit the characteristics of M2-type macrophages, and the regulation of TAM polarization is a new target for cancer therapy, among which lncRNAs are key regulatory molecules. This study aimed to explore the effects of lncRNA-HOXC-AS2 on non-small cell lung cancer (NSCLC) by regulating TAM polarization. THP-1 cells were used to differentiate into macrophages, and TAMs were obtained by coculture with A549 cells. The M1/M2 cell phenotype and HOXC-AS2 expression were detected, and A549-derived exosomes (A549-exo) were used to elucidate the effects of A549 on macrophage polarization and HOXC-AS2 expression. Then, by interfering with HOXC-AS2 or STAT1, the effects of HOXC-AS2 regulation of STAT1 on the TAM phenotype and STAT1/SOCS1 and STAT1/CIITA pathways were analyzed, and the proliferation and metastasis of NSCLC cells in the coculture system were also detected. Results showed that HOXC-AS2 expression in M2 macrophages and TAMs was significantly higher than that in M1 macrophages, and A549-exo promoted HOXC-AS2 expression and M2 polarization. Intervention HOXC-AS2 resulted in increased M1 marker expression, decreased M2 marker expression, and activation of STAT1/SOCS1 and STAT1/CIITA pathways in TAMs. In addition, HOXC-AS2 was mainly expressed in the cytoplasm of TAMs and could bind to STAT1. Further experiments confirmed that intervention HOXC-AS2 promoted the M1 polarization of TAMs by targeting STAT1 and weakened the promoting effects of TAMs on the proliferation and metastasis of NSCLC. In conclusion, HOXC-AS2 inhibited the activation of STAT1/SOCS1 and STAT1/CIITA pathways and promoted M2 polarization of TAMs by binding with STAT1, thus promoting NSCLC.Copyright © 2024 Elsevier Inc. All rights reserved.

基金：
This work was supported by the WU JIEPING Medical Foundation (No. 320.6750.2021-22-18).
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外文
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中科院(CAS)分区：
出版当年[2023]版：
大类 | 2 区 生物学
小类 | 3 区 细胞生物学
最新[2023]版：
大类 | 2 区 生物学
小类 | 3 区 细胞生物学
JCR分区：
出版当年[2023]版：
Q2 CELL BIOLOGY
最新[2023]版：
Q2 CELL BIOLOGY

影响因子： 最新[2023版] 最新五年平均 出版当年[2023版] 出版当年五年平均 出版前一年[2023版]

第一作者：
第一作者机构： [1]School of Medicine, University of Electronic Science and Technology of China, China.
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推荐引用方式(GB/T 7714)：
Yin Cunli,Li Jing,Li Siru,et al.LncRNA-HOXC-AS2 regulates tumor-associated macrophage polarization through the STAT1/SOCS1 and STAT1/CIITA pathways to promote the progression of non-small cell lung cancer[J].CELLULAR SIGNALLING.2024,115:doi:10.1016/j.cellsig.2023.111031.
APA：
Yin Cunli,Li Jing,Li Siru,Yang Xi,Lu Yingchun...&Liu Bin.(2024).LncRNA-HOXC-AS2 regulates tumor-associated macrophage polarization through the STAT1/SOCS1 and STAT1/CIITA pathways to promote the progression of non-small cell lung cancer.CELLULAR SIGNALLING,115,
MLA：
Yin Cunli,et al."LncRNA-HOXC-AS2 regulates tumor-associated macrophage polarization through the STAT1/SOCS1 and STAT1/CIITA pathways to promote the progression of non-small cell lung cancer".CELLULAR SIGNALLING 115.(2024)

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