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Title[redir]:
LincRNA-p21 knockdown reversed tumor-associated macrophages function by promoting MDM2 to antagonize* p53 activation and alleviate breast cancer development | Cancer Immunology, Immunotherapy
Description:
Tumor-associated macrophages (TAMs) are important regulators of the complex interplay between immune system and breast cancer. TAMs fuel the cancer progression and metastasis by reprogramming their specific functional phenotype in cancer settings. Therefore, it is important to clarify the mechanisms of shaping specific functional phenotype of macrophages in tumor milieu. LncRNA profiles of TAMs were identified by LncRNA microarray. Flow cytometry was used to detect the surface markers of TAMs. The co-localization among lincRNA-p21, p53 and Mouse Double Minute 2 (MDM2) was identified by FISH probe and immunofluorescence. PyVT-MMTV and BALB/c mice were used for in vivo analysis. In the present work, we found that lincRNA-p21 significantly up-regulated in 4T1 educated macrophages. LincRNA-p21 knockdown facilitated macrophage polarization into pro-inflammatory M1 in tumor microenvironment, which might be caused by MDM2 eliciting proteasome-dependent degradation to p53 and activated NF-κB and STAT3 pathway. TAMs with lincRNA-p21 knockdown induced cancer cell apoptosis, inhibited tumor cell migration and invasion. In vivo, lincRNA-p21 knockdown macrophage adoptive transfer could alleviate breast cancer progression. Our results indicated that lincRNA-p21 was a key regulator of TAMs function in tumor milieu. Our data also shed a light on novel therapeutic targets of tumors characterized by monocytes/macrophages infiltration.
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Keywords {🔍}
pubmed, article, cancer, google, scholar, cas, central, breast, cell, macrophage, lincrnap, macrophages, tumor, tumorassociated, polarization, tams, rev, zhou, microenvironment, noncoding, immunol, jiangsu, knockdown, mdm, metastasis, access, long, rna, yang, privacy, cookies, function, content, research, tian, guo, pathway, nat, role, chen, wang, data, information, publish, search, activation, lining, zhaoliang, immune, progression,
Topics {✒️}
hif-1/akt/mtor/p70s6k pathway activating rage/nf-kappab pathway month download article/chapter macrophages-induced lncrna rp11-627g18 nf-kappab/stat3 pathway activation huaxi xu & zhaoliang su lincrna-p21 impacts prognosis breast cancer biology macrophage-directed cancer immunotherapy article cancer immunology full article pdf revealing protein-lncrna interaction lincrna-p21 significantly advanced breast tumors hypoxic tumor cells related subjects breast cancer statistics invasive breast cancer tam receptor signaling privacy choices/manage cookies rna-p21 induction 4t1 educated macrophages ovarian cancer metastasis reactive oxygen species central laboratory social development foundation specific functional phenotype article zhou activated nf-κb lincrna-p21 enhancing p53 activity stat3 pathway anti-cancer strategies article log antagonize p53 activation european economic area population-based study de vries ege van der vegt p300 act synergistically coupled histone modifications nanjing medical university zhaoliang su fang guo long noncoding rnas breast cancer additional information publisher' conditions privacy policy nf90-binding long macrophage cross-talk
Questions {❓}
- Luo Z, Wang Q, Lau WB, Lau B, Xu L, Zhao L, Yang H, Feng M, Xuan Y, Yang Y, Lei L, Wang C, Yi T, Zhao X, Wei Y, Zhou S (2016) Tumor microenvironment: the culprit for ovarian cancer metastasis?
- Qiu SQ, Waaijer SJH, Zwager MC, de Vries EGE, van der Vegt B, Schroder CP (2018) Tumor-associated macrophages in breast cancer: innocent bystander or important player?
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headline:LincRNA-p21 knockdown reversed tumor-associated macrophages function by promoting MDM2 to antagonize* p53 activation and alleviate breast cancer development
description:Tumor-associated macrophages (TAMs) are important regulators of the complex interplay between immune system and breast cancer. TAMs fuel the cancer progression and metastasis by reprogramming their specific functional phenotype in cancer settings. Therefore, it is important to clarify the mechanisms of shaping specific functional phenotype of macrophages in tumor milieu. LncRNA profiles of TAMs were identified by LncRNA microarray. Flow cytometry was used to detect the surface markers of TAMs. The co-localization among lincRNA-p21, p53 and Mouse Double Minute 2 (MDM2) was identified by FISH probe and immunofluorescence. PyVT-MMTV and BALB/c mice were used for in vivo analysis. In the present work, we found that lincRNA-p21 significantly up-regulated in 4T1 educated macrophages. LincRNA-p21 knockdown facilitated macrophage polarization into pro-inflammatory M1 in tumor microenvironment, which might be caused by MDM2 eliciting proteasome-dependent degradation to p53 and activated NF-κB and STAT3 pathway. TAMs with lincRNA-p21 knockdown induced cancer cell apoptosis, inhibited tumor cell migration and invasion. In vivo, lincRNA-p21 knockdown macrophage adoptive transfer could alleviate breast cancer progression. Our results indicated that lincRNA-p21 was a key regulator of TAMs function in tumor milieu. Our data also shed a light on novel therapeutic targets of tumors characterized by monocytes/macrophages infiltration.
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