Javascript must be enabled to continue!
Abstract 3432: Role of M2 macrophages in chemoresistance about the tumor microenvironment of epithelial ovarian cancer
View through CrossRef
Abstract
OBJECTIVE:
One of the hallmark characteristics of ovarian cancer is the development of resistance to chemotherapeutics. The mutual interactions with tumor cells and stromal microenvironment contribute to phenotypically polarization of tumor associated macrophages. Macrophages consist of at least two subgroups, M1 and M2. M2 macrophages are endowed with a repertoire of tumor-promoting capabilities involving immuno-suppression, angiogenesis and neovascularization, as well as stromal activation and remodeling. Therefore, there is a need for more practical targets to inhibit chemotherapeutic drug resistance and cancer progression due to ovarian cancer-macrophage interactions. To better understand the mechanism of chemoresistance in ovarian cancer cells, we aimed to investigate the influence of macrophages on the tumor cell response to carboplatin and identify the genes associated with chemoresistance.
METHODS:
Macrophages were differentiated into M1 and M2 macrophages by cytokine treatment of monocytes. The tumor microenvironment (TME) was modified by transwell co-culture assay. We treated the carboplatin and tested chemoresistance. We also examined expression of key genes associated with EMT (Epithelial-Mesenchymal Transition), PD-L1 and chemoresistance. Nanostring analysis identified gene expression changes in tumor signaling pathways in ovarian cancer cells co-cultured with M2 macrophages compared to single-cultures. Functional study (proliferation, migration, invasion, wound healing) were performed to determine the role of the M2 macrophage in ovarian cancer.
RESULTS:
Compared to single-cultured ovarian cancer cells, iNOS was downregulated in co-cultured with M2 macrophages, while PD-L1,CD206,TGF-b,MDR1,CSF-1 and Arg1 were upregulated. PD-L1 was also upregulated in M2 macrophages. Ovarian cancer cells co-cultured with M2 macrophages showed higher carboplatin resistance compared to single-cultured ovarian cancer cells. EMT-promoting related genes CD2,VIM, ZEB1 and SNAIL1 were upregulated in ovarian cancer cells co-cultured with M2 macrophages. Nanostring analysis revealed changes in the expression levels of genes associated with tumor signaling pathway activation and EMT. Ovarian cancer cells co-cultured with M2 macrophages performed functional study, we found that the functional abilities of the cancer cells were all significantly increased.
CONCLUSION:
We identified changes in the expression of various genes in ovarian cancer cells which were co-cultured with M2 macrophages, and identified upregulation of PD-L1 as a key factor in chemoresistance. We have also conducted additional nanostrings to refine the impact of M2 macrophage and ovarian cancer cell interactions on tumour signalling pathways as well as chemoresistance in the tumour microenvironment, and will be analysing these data and conducting further experiments.
Citation Format:
Jaesung Ryu, Baek MooJun, HyoWook Gil, Eunjung Yang, Kwangseock Kim, Taewan Kim, Kong Hyejeong, Beamjun Park, Seob Jeon. Role of M2 macrophages in chemoresistance about the tumor microenvironment of epithelial ovarian cancer [abstract]. In: Proceedings of the American Association for Cancer Research Annual Meeting 2026; Part 1 (Regular Abstracts); 2026 Apr 17-22; San Diego, CA. Philadelphia (PA): AACR; Cancer Res 2026;86(7 Suppl):Abstract nr 3432.
American Association for Cancer Research (AACR)
Title: Abstract 3432: Role of M2 macrophages in chemoresistance about the tumor microenvironment of epithelial ovarian cancer
Description:
Abstract
OBJECTIVE:
One of the hallmark characteristics of ovarian cancer is the development of resistance to chemotherapeutics.
The mutual interactions with tumor cells and stromal microenvironment contribute to phenotypically polarization of tumor associated macrophages.
Macrophages consist of at least two subgroups, M1 and M2.
M2 macrophages are endowed with a repertoire of tumor-promoting capabilities involving immuno-suppression, angiogenesis and neovascularization, as well as stromal activation and remodeling.
Therefore, there is a need for more practical targets to inhibit chemotherapeutic drug resistance and cancer progression due to ovarian cancer-macrophage interactions.
To better understand the mechanism of chemoresistance in ovarian cancer cells, we aimed to investigate the influence of macrophages on the tumor cell response to carboplatin and identify the genes associated with chemoresistance.
METHODS:
Macrophages were differentiated into M1 and M2 macrophages by cytokine treatment of monocytes.
The tumor microenvironment (TME) was modified by transwell co-culture assay.
We treated the carboplatin and tested chemoresistance.
We also examined expression of key genes associated with EMT (Epithelial-Mesenchymal Transition), PD-L1 and chemoresistance.
Nanostring analysis identified gene expression changes in tumor signaling pathways in ovarian cancer cells co-cultured with M2 macrophages compared to single-cultures.
Functional study (proliferation, migration, invasion, wound healing) were performed to determine the role of the M2 macrophage in ovarian cancer.
RESULTS:
Compared to single-cultured ovarian cancer cells, iNOS was downregulated in co-cultured with M2 macrophages, while PD-L1,CD206,TGF-b,MDR1,CSF-1 and Arg1 were upregulated.
PD-L1 was also upregulated in M2 macrophages.
Ovarian cancer cells co-cultured with M2 macrophages showed higher carboplatin resistance compared to single-cultured ovarian cancer cells.
EMT-promoting related genes CD2,VIM, ZEB1 and SNAIL1 were upregulated in ovarian cancer cells co-cultured with M2 macrophages.
Nanostring analysis revealed changes in the expression levels of genes associated with tumor signaling pathway activation and EMT.
Ovarian cancer cells co-cultured with M2 macrophages performed functional study, we found that the functional abilities of the cancer cells were all significantly increased.
CONCLUSION:
We identified changes in the expression of various genes in ovarian cancer cells which were co-cultured with M2 macrophages, and identified upregulation of PD-L1 as a key factor in chemoresistance.
We have also conducted additional nanostrings to refine the impact of M2 macrophage and ovarian cancer cell interactions on tumour signalling pathways as well as chemoresistance in the tumour microenvironment, and will be analysing these data and conducting further experiments.
Citation Format:
Jaesung Ryu, Baek MooJun, HyoWook Gil, Eunjung Yang, Kwangseock Kim, Taewan Kim, Kong Hyejeong, Beamjun Park, Seob Jeon.
Role of M2 macrophages in chemoresistance about the tumor microenvironment of epithelial ovarian cancer [abstract].
In: Proceedings of the American Association for Cancer Research Annual Meeting 2026; Part 1 (Regular Abstracts); 2026 Apr 17-22; San Diego, CA.
Philadelphia (PA): AACR; Cancer Res 2026;86(7 Suppl):Abstract nr 3432.
Related Results
Complex Collision Tumors: A Systematic Review
Complex Collision Tumors: A Systematic Review
Abstract
Introduction: A collision tumor consists of two distinct neoplastic components located within the same organ, separated by stromal tissue, without histological intermixing...
Abstract LB-323: Comparative miRNA microarray profiling indicates miR-363 promotes chemoresistance in ovarian cancer cells by targeting the Hippo member, LATS2
Abstract LB-323: Comparative miRNA microarray profiling indicates miR-363 promotes chemoresistance in ovarian cancer cells by targeting the Hippo member, LATS2
Abstract
Ovarian cancer is the most aggressive female reproductive tract tumours. Taxane (TX) is widely used for ovarian cancer treatment. However, ovarian cancer of...
Abstract 1636: The role of the ROR receptors in ovarian cancer progression and chemoresistance
Abstract 1636: The role of the ROR receptors in ovarian cancer progression and chemoresistance
Abstract
BACKGROUND: Despite recent advances in our understanding of the underlying genetic profile of distinct subtypes of ovarian cancer, overall survival remains ...
Abstract B8: Molecular subtyping of epithelial ovarian cancer reveals connections to intrinsic breast cancer subtypes
Abstract B8: Molecular subtyping of epithelial ovarian cancer reveals connections to intrinsic breast cancer subtypes
Abstract
Aim: Epithelial ovarian cancer is one of the most lethal female cancers. It is a heterogeneous group of neoplasms and the different histologic subtypes are ...
ALKBH5 modulates macrophages polarization in tumor microenvironment of ovarian cancer
ALKBH5 modulates macrophages polarization in tumor microenvironment of ovarian cancer
Abstract
Background
Macrophages play an essential role in regulating ovarian cancer immune microenvironment. Studies have shown that m6A methylation...
Abstract IA31: Molecular epidemiology of ovarian cancer
Abstract IA31: Molecular epidemiology of ovarian cancer
Abstract
Epithelial ovarian cancer (EOC) accounts for 5% of all cancer deaths and is the fifth leading cause of cancer death in women in the United States. While the...
Loss Of MHC Class I Related Gene Expression Inhibited The M1 Macrophages Infiltration In Tumor Microenvironment Of Ovarian Serous Cystadenocarcinoma
Loss Of MHC Class I Related Gene Expression Inhibited The M1 Macrophages Infiltration In Tumor Microenvironment Of Ovarian Serous Cystadenocarcinoma
Abstract
Background: Previous studies have shown that tumor immune microenvironment was an important factor affecting the progression and prognosis of ovarian cancer. The p...
Abstract 2208: Clinicopathological and genetic study of ovarian cancer in Algerian women: First report
Abstract 2208: Clinicopathological and genetic study of ovarian cancer in Algerian women: First report
Abstract
Background: Ovarian cancer represents the fourth most common cause of mortality among Algerian women. Of all gynecological malignancies, ovarian cancer caus...

