Correction: Macrophage-derived CCL5 facilitates immune escape of colorectal cancer cells via the p65/STAT3-CSN5-PD-L1 pathway

Liu, Chao; Yao, Zhaoying; Wang, Jianbo; Zhang, Wen; Yang, Yan; Zhang, Yan; Qu, Xinliang; Zhu, Yubing; Zou, Jianjun; Peng, Sishi; Zhao, Yan; Zhao, Shuli; He, Bangshun; Mi, Qiong‐Yu; Liu, Xiuting; Zhang, Xu; Du, Qianming

doi:10.1038/s41418-020-0506-3

Cited by 51 publications

(6 citation statements)

References 44 publications

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“…CC[ 99 ], colon cancer[ 100 ], melanoma[ 101 , 102 , 106 ], lung cancer[ 101 ], esophageal squamous cell carcinoma[ 105 ]…”

Section: Micrornasmentioning

confidence: 99%

“…Additionally, berberine binds to CSN5 and diminishes its deubiquitination activity, leading to PD-L1 ubiquitination and degradation and promoting anti-tumor immunity [ 98 ]. LPS or high-cholesterol diet (HCD)-induced macrophage infiltration significantly activates the C-C motif chemokine ligand 5 (CCL5)-P65/STAT3-CSN5-PD-L1 signaling pathway in azoxymethane-induced CC mouse models and is correlated with poor prognosis [ 99 ]. In contrast to CSN5, the deubiquitinase USP8 removes TNF receptor associated factor 6 (TRAF6)-mediated K63-linked ubiquitination, thereby promoting PD-L1 degradation in mouse models of lung and colon cancer [ 100 ].…”

Section: Ubiquitinationmentioning

confidence: 99%

“…MLL1 ↑PC [134] NRF2 ↑HCC [22] ATF3 ↑melanoma and NSCLC [55] Epigenetic regulation of PD-L1 DNA methylation ↓melanoma [62,64], leukemia [39] Histone modification ↓BC and B cell lymphomas [53,185], lung cancer [66] MicroRNAs shown in Table 1 N6-methyladenosine ↑OSCC [90], ↑BC [91] LncRNA and circRNA HOTTIP, SNHG12, EMX2OS-↑OC[76, 77, 81] SNHG20-↑esophagus cancer [78] CASC11-↑HCC [80] SNHG14-↑DLBCL [79] NUTM2A-AS1-↑GC [82] Hoxa-AS2-↑nasopharyngeal carcinoma [83] IFITM4P-↑OSCC [84] LncMX1-215-↓HNSCC [85] Hsa_circ_0000190-↑NSCLC [186] HasCircRNA-002178-↑ LUAD [87] CDR1-AS-↑CC [88] PD-L1 regulation at the protein level Ubiquitination ↓ BC [97], NSCLC [98], CC [99], colon cancer [100], melanoma [101,102,106], lung cancer [101], esophageal squamous cell carcinoma [105] Glycosylation ↑AML [108], TNBC [109,111], colon cancer [110], prostate cancer [111], glioma [112] Phosphorylation ↓ BC [114,116], HCC [115] Acetylation ↓ multiple cancers [117] Palmitoylation ↑ BC and colon cancer [118,…”

Section: Regulators Of Pd-l1 Cancer Typementioning

confidence: 99%

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Current insight into the regulation of PD-L1 in cancer

Liu

et al. 2022

Exp Hematol Oncol

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The molecular mechanisms underlying cancer immune escape are a core topic in cancer immunology research. Cancer cells can escape T cell-mediated cellular cytotoxicity by exploiting the inhibitory programmed cell-death protein 1 (PD-1)/programmed cell death ligand 1 (PD-L1, CD274) immune checkpoint. Studying the PD-L1 regulatory pattern of tumor cells will help elucidate the molecular mechanisms of tumor immune evasion and improve cancer treatment. Recent studies have found that tumor cells regulate PD-L1 at the transcriptional, post-transcriptional, and post-translational levels and influence the anti-tumor immune response by regulating PD-L1. In this review, we focus on the regulation of PD-L1 in cancer cells and summarize the underlying mechanisms.

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“…CC[ 99 ], colon cancer[ 100 ], melanoma[ 101 , 102 , 106 ], lung cancer[ 101 ], esophageal squamous cell carcinoma[ 105 ]…”

Section: Micrornasmentioning

confidence: 99%

Section: Ubiquitinationmentioning

confidence: 99%

Section: Regulators Of Pd-l1 Cancer Typementioning

confidence: 99%

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Current insight into the regulation of PD-L1 in cancer

Liu

et al. 2022

Exp Hematol Oncol

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“…Tumor-associated macrophages (TAMs) also contribute to tumor invasion and metastasis, while they are sub-classified into two types: (i) anti-tumorigenic M1 and (ii) pro-tumorigenic M2 [ 136 ]. Myeloid-derived suppressor cells (MDSCs) are also present in TME in high amounts, contributing to tumor invasion and growth [ 137 ], while they are regulated by many tumor-derived substances, such as CCL5, as well as CCL2 [ 138 ].…”

Section: Immunotherapy In Colorectal Cancermentioning

confidence: 99%

“…In this vaccine, a genetically modified viral vector, the oncolytic Herpes virus type 1 (HSV-1), infects the malignant tumor cells and targets the GM-CSF gene, while the use of oncolytic viruses is considered significantly potent as an anti-cancer therapy for solid malignant neoplasms [ 143 ]. A combinational treatment, including immune checkpoint blockade and cancer vaccine, is also under evaluation, such as the above vaccine with a PD-L1 inhibitor, atezolizumab, for end-stage CRC cases characterized by MSS [ 138 ]. There was a recent clinical trial (MASTERKEY-318) that evaluatedtalimogene laherparepvec vaccination as a monotherapy for solid metastatic tumors, such as in the case of secondary hepatic lesions, where intrahepatic administration is performed, while the combination of with talimogene laherparepvec vaccination treatment is also studied for HCC or metastatic hepatic disease [ 144 ].…”

Section: Immunotherapy In Colorectal Cancermentioning

confidence: 99%

Immunotherapy as a Therapeutic Strategy for Gastrointestinal Cancer—Current Treatment Options and Future Perspectives

Koustas

Trifylli

Sarantis

et al. 2022

IJMS

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Gastrointestinal (GI) cancer constitutes a highly lethal entity among malignancies in the last decades and is still a major challenge for cancer therapeutic options. Despite the current combinational treatment strategies, including chemotherapy, surgery, radiotherapy, and targeted therapies, the survival rates remain notably low for patients with advanced disease. A better knowledge of the molecular mechanisms that influence tumor progression and the development of optimal therapeutic strategies for GI malignancies are urgently needed. Currently, the development and the assessment of the efficacy of immunotherapeutic agents in GI cancer are in the spotlight of several clinical trials. Thus, several new modalities and combinational treatments with other anti-neoplastic agents have been identified and evaluated for their efficiency in cancer management, including immune checkpoint inhibitors, adoptive cell transfer, chimeric antigen receptor (CAR)-T cell therapy, cancer vaccines, and/or combinations thereof. Understanding the interrelation among the tumor microenvironment, cancer progression, and immune resistance is pivotal for the optimal therapeutic management of all gastrointestinal solid tumors. This review will shed light on the recent advances and future directions of immunotherapy for malignant tumors of the GI system.

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Colorectal Cancer‐Derived Small Extracellular Vesicles Promote Tumor Immune Evasion by Upregulating PD‐L1 Expression in Tumor‐Associated Macrophages

et al. 2022

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Tumor‐associated macrophages (TAMs) are one of the most abundant cell types in colorectal cancer (CRC) tumor microenvironment (TME). Recent studies observed complicated “cross‐talks” between cancer cells and macrophages in TME. However, the underlying mechanisms are still poorly elucidated. Here, PD‐L1 levels are very low in CRC cells but highly abundant in TAMs, and a specific PD‐L1+CD206+ macrophage subpopulation are identified, which is induced by tumor cells and associated with a poor prognosis. Mechanistic investigations reveal that CRC cells can secrete small extracellular vesicles (sEVs) taken up by macrophages that induce M2 like polarization and PD‐L1 expression, resulting in increased PD‐L1+CD206+ macrophage abundance and decreased T cell activity in CRC TME. sEV‐derived miR‐21‐5p and miR‐200a are identified as key signaling molecules mediating the regulatory effects of CRC on macrophages. Further studies reveal that CRC‐derived miR‐21‐5p and miR‐200a synergistically induces macrophage M2 like polarization and PD‐L1 expression by regulating the PTEN/AKT and SCOS1/STAT1 pathways, resulting in decreased CD8+ T cell activity and increased tumor growth. This study suggests that inhibiting the secretion of specific sEV‐miRNAs from CRC and targeting PD‐L1 in TAMs may serve as novel methods for CRC treatment as well as a sensitization method for anti‐PD‐L1 therapy in CRC.

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Correction: Macrophage-derived CCL5 facilitates immune escape of colorectal cancer cells via the p65/STAT3-CSN5-PD-L1 pathway

Cited by 51 publications

References 44 publications

Current insight into the regulation of PD-L1 in cancer

Current insight into the regulation of PD-L1 in cancer

Immunotherapy as a Therapeutic Strategy for Gastrointestinal Cancer—Current Treatment Options and Future Perspectives

Colorectal Cancer‐Derived Small Extracellular Vesicles Promote Tumor Immune Evasion by Upregulating PD‐L1 Expression in Tumor‐Associated Macrophages

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