Cancer-FOXP3 directly activated CCL5 to recruit FOXP3+Treg cells in pancreatic ductal adenocarcinoma

Wang, Xiuchao; Lang, Mingxiao; Zhao, Tiansuo; Feng, Xiaoming; Chen, Zheng; Huang, Chongbiao; Hao, Jihui; Dong, Jie; Luo, Ling; Li, X; Lan, Chungen; Yu, Wenwen; Yu, Man; Yang, Shengyu; Ren, He

doi:10.1038/onc.2016.458

Cited by 179 publications

(158 citation statements)

References 49 publications

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“…23 However, the functions of Foxp3 on different cancer are controversial. [24][25][26] Our previous research found that ectopic tumoral Foxp3 can promote gastric cancer proliferation, migration and invasion. 27 Therefore, it is necessary to verify whether Foxp3 is involved in miR-664a-3p/MOB1A axis.…”

Section: Introductionmentioning

confidence: 99%

RETRACTED: miR‐664a‐3p functions as an oncogene by targeting Hippo pathway in the development of gastric cancer

Wang

Zhang

et al. 2019

Cell Proliferation

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Objectives: It has been accounted that miR-664a-3p has different functions in several malignancies; however, the precise role and underlying mechanism in gastric cancer have not been elucidated. Our study aims to explore the function of miR-664a-3p on the progression of gastric cancer (GC).Methods: qRT-PCR was applied to detect the expression of miR-664a-3p in GC tissues and cells. The functions of miR-664a-3p on GC in vitro were examined by cell proliferation assay, and transwell assay. Related proteins of epithelial-mesenchymal transition (EMT) and signal pathway were evaluated by Western blot and immunofluorescence analysis. The bioinformatic, dual-luciferase assay or ChIP assay were employed to identify the interaction between miR-664a-3p and its target gene or Foxp3. The effects in vivo were investigated through a mouse tumorigenicity model. Results: miR-664a-3p was frequently upregulated in GC tissues and cells. Elevated expression of miR-664a-3p significantly promoted proliferation and invasion in vitro and in vivo. MOB1A was confirmed to be a target of miR-664a-3p and restoration of MOB1A attenuated the effects of miR-664a-3p. A series of investigations indicated that miR-664a-3p contributed to EMT process and inactivated the Hippo pathway by downregulating MOB1A. Conclusion:Taken together, we revealed that miR-664a-3p functions as an oncogene by targeting Hippo pathway in the development of gastric cancer.

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Section: Introductionmentioning

confidence: 99%

RETRACTED: miR‐664a‐3p functions as an oncogene by targeting Hippo pathway in the development of gastric cancer

Wang

Zhang

et al. 2019

Cell Proliferation

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“…The latter is additionally supported by the fact that in the whole NPC group there was worse survival if macrophage markers and FOXP3 were low. Blockade of Tregs as a therapeutic option in NPC50 should therefore be cautiously studied as FOXP3 has also been shown to be a tumour suppressor 51…”

Section: Discussionmentioning

confidence: 99%

Prognostic role of tumour-associated macrophages and regulatory T cells in EBV-positive and EBV-negative nasopharyngeal carcinoma

et al. 2017

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AimsTumour-associated macrophages (TAMs) and regulatory T cells (Tregs) form a special niche supporting tumour progression, and both correlate with worse survival in head and neck cancers. However, the prognostic role of TAM and Tregs in nasopharyngeal carcinoma (NPC) is still unknown. Therefore, we determined differences in TAMs and Tregs in different NPC subtypes, and their prognostic significance.MethodsTissue of 91 NPCs was assessed for TAMs and Tregs by determination of CD68, CD163, CD206 and FOXP3 expression in the tumour microenvironment. Clinicopathological correlations were assessed using Pearson X2 test, Fisher’s exact test, analysis of variance and Mann-Whitney U test. Survival was analysed using Kaplan-Meier curves and Cox regression.ResultsCD68 and FOXP3 counts were higher in Epstein-Barr virus (EBV)-positive NPC, while CD68−/FOXP3−, CD163+/FOXP3− and CD206+/FOXP3− infiltrates were more common in EBV-negative NPC. In the whole NPC group, CD68−/FOXP3− correlated with worse overall survival (OS), and after multivariate analysis high FOXP3 count showed better OS (HR 0.352, 95% CI 0.128 to 0.968). No difference in M2 counts existed between EBV-positive and negative NPC.ConclusionsFOXP3, a Treg marker, seems to be an independent prognostic factor for better OS in the whole NPC group. Therefore, immune-based therapies targeting Tregs should be carefully evaluated. M2 spectrum macrophages are probably more prominent in EBV-negative NPC with also functional differences compared with EBV-positive NPC.

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“…PDAC cells recruit immunosuppressive tumourassociated macrophages (TAMs) and myeloid-derived suppressor cells (MDSCs) from the peripheral circulation via the CCL2/CCR2 axis [14]. PDAC cells express high levels of CCL5 to recruit regulatory T cells (Treg cells) through CCR5 [15], and this process may partially explain the recruitment of Treg cells to PDAC lesions [16]. Approximately 12.5% of PDAC patients are reported to positively express programmed cell death protein ligand-1 (PD-L1) [17], which induces T cell anergy and apoptosis through programmed cell death protein-1 (PD-1) expressed on T Fig.…”

Section: Pdac Epithelial Cellsmentioning

confidence: 99%

Current advances and outlooks in immunotherapy for pancreatic ductal adenocarcinoma

et al. 2020

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Pancreatic ductal adenocarcinoma (PDAC) is an incurable cancer resistant to traditional treatments, although a limited number of early-stage patients can undergo radical resection. Immunotherapies for the treatment of haematological malignancies as well as solid tumours have been substantially improved over the past decades, and impressive results have been obtained in recent preclinical and clinical trials. However, PDAC is likely the exception because of its unique tumour microenvironment (TME). In this review, we summarize the characteristics of the PDAC TME and focus on the network of various tumour-infiltrating immune cells, outlining the current advances in PDAC immunotherapy and addressing the effect of the PDAC TME on immunotherapy. This review further explores the combinations of different therapies used to enhance antitumour efficacy or reverse immunodeficiencies and describes optimizable immunotherapeutic strategies for PDAC. The concordant combination of various treatments, such as targeting cancer cells and the stroma, reversing suppressive immune reactions and enhancing antitumour reactivity, may be the most promising approach for the treatment of PDAC. Traditional treatments, especially chemotherapy, may also be optimized for individual patients to remodel the immunosuppressive microenvironment for enhanced therapy.

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Cancer-FOXP3 directly activated CCL5 to recruit FOXP3+Treg cells in pancreatic ductal adenocarcinoma

Cited by 179 publications

References 49 publications

RETRACTED: miR‐664a‐3p functions as an oncogene by targeting Hippo pathway in the development of gastric cancer

RETRACTED: miR‐664a‐3p functions as an oncogene by targeting Hippo pathway in the development of gastric cancer

Prognostic role of tumour-associated macrophages and regulatory T cells in EBV-positive and EBV-negative nasopharyngeal carcinoma

Current advances and outlooks in immunotherapy for pancreatic ductal adenocarcinoma

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