Exosomal circ-PTPN22 and circ-ADAMTS6 mark T cell exhaustion and neutrophil extracellular traps in Asian intrahepatic cholangiocarcinoma

Wang, Xuezhu; Wang, Guanqun; Wu, Zilong; Dong, Yucheng; Shi, You; Yang, Fan; Chen, Xinyu; Wang, Jun; Du, Shunda; Xu, Haifeng; Zheng, Yongchang

doi:10.1016/j.omtn.2022.12.012

Cited by 16 publications

(12 citation statements)

References 58 publications

Supporting

Mentioning

Contrasting

Order By: Relevance

“…44 Furthermore, NETs induced by cholangiocarcinoma-derived exosomes can lead to T cell exhaustion, thereby mediating immunosuppression. 45…”

Section: Texs-induced Phenotypic Transformation Of Tan and Formation ...mentioning

confidence: 99%

“…In a mouse model of breast cancer, it was observed that 4T1‐derived exosomes induced NET formation in mice treated with granulocyte colony‐stimulating factor (G‐CSF), resulting in significantly accelerated venous thrombosis 44 . Furthermore, NETs induced by cholangiocarcinoma‐derived exosomes can lead to T cell exhaustion, thereby mediating immunosuppression 45 …”

Section: Texs‐induced Phenotypic Transformation Of Tan and Formation ...mentioning

confidence: 99%

See 1 more Smart Citation

Shaping the immune‐suppressive microenvironment on tumor‐associated myeloid cells through tumor‐derived exosomes

Wang,

Liu,

Zhan

et al. 2024

Intl Journal of Cancer

View full text Add to dashboard Cite

Tumor‐associated myeloid cells (TAMCs) play a crucial role in orchestrating the dynamics of the tumor immune microenvironment. This heterogeneous population encompasses myeloid‐derived suppressor cells, tumor‐associated macrophages and dendritic cells, all of which contribute to the establishment of an immunosuppressive milieu that fosters tumor progression. Tumor‐derived exosomes (TEXs), small extracellular vesicles secreted by tumor cells, have emerged as central mediators in intercellular communication within the tumor microenvironment. In this comprehensive review, we explore the intricate mechanisms through which TEXs modulate immune‐suppressive effects on TAMCs and their profound implications in cancer progression. We delve into the multifaceted ways in which TEXs influence TAMC functions, subsequently affecting tumor immune evasion. Furthermore, we elucidate various therapeutic strategies aimed at targeting TEX‐mediated immune suppression, with the ultimate goal of bolstering antitumor immunity.

show abstract

“…44 Furthermore, NETs induced by cholangiocarcinoma-derived exosomes can lead to T cell exhaustion, thereby mediating immunosuppression. 45…”

Section: Texs-induced Phenotypic Transformation Of Tan and Formation ...mentioning

confidence: 99%

Section: Texs‐induced Phenotypic Transformation Of Tan and Formation ...mentioning

confidence: 99%

Shaping the immune‐suppressive microenvironment on tumor‐associated myeloid cells through tumor‐derived exosomes

Wang,

Liu,

Zhan

et al. 2024

Intl Journal of Cancer

View full text Add to dashboard Cite

show abstract

“…sEVs are also involved in regulating tumor progression by participating in immune regulation (84)(85)(86). Luo et al found that exosomes derived from tumor cells carrying miR-183-5p increased the numbers of PD-L1-expressing macrophages, inducing both immune suppression and tumorigenesis in iCCA by activating the miR-183-5p/ PTEN/AKT/PD-L1 axis (87).…”

Section: Rnas Of Sevsmentioning

confidence: 99%

Clinical significance of small extracellular vesicles in cholangiocarcinoma

Wang,

Shi,

Yin

et al. 2024

Front. Oncol.

View full text Add to dashboard Cite

Cholangiocarcinoma is an aggressive and heterogeneous malignancy originating from the bile duct epithelium. It is associated with poor prognosis and high mortality. The global incidence of cholangiocarcinoma is rising, and there is an urgent need for effective early diagnosis and treatment strategies to reduce the burden of this devastating tumor. Small extracellular vesicles, including exosomes and microparticles, are nanoscale vesicles formed by membranes that are released both normally and pathologically from cells, mediating the intercellular transfer of substances and information. Recent studies have demonstrated the involvement of small extracellular vesicles in numerous biological processes, as well as the proliferation, invasion, and metastasis of tumor cells. The present review summarizes the tumorigenic roles of small extracellular vesicles in the cholangiocarcinoma microenvironment. Owing to their unique composition, accessibility, and stability in biological fluids, small extracellular vesicles have emerged as ideal biomarkers for use in liquid biopsies for diagnosing and outcome prediction of cholangiocarcinoma. Specific tissue tropism, theoretical biocompatibility, low clearance, and strong biological barrier penetration of small extracellular vesicles make them suitable drug carriers for cancer therapy. Furthermore, the potential value of small extracellular vesicle-based therapies for cholangiocarcinoma is also reviewed.

show abstract

“…By screening the circRNAs that take part in cell growth, scholars found that the most of circRNAs not only play generic housekeeping roles but rather function in a regulatory and cell/tissue‐type‐specific manner 8 . Therefore, following the development of biotechnology, finding and analysing circRNAs has important clinical application value for drug action targets, gene therapy drugs or diagnostic biomarkers 9–11 …”

Section: Introductionmentioning

confidence: 99%

“…8 Therefore, following the development of biotechnology, finding and analysing circRNAs has important clinical application value for drug action targets, gene therapy drugs or diagnostic biomarkers. [9][10][11] In our previous study, the dramatically dysfunctional cir-cRNAs were screened out from the plasma of IPF patients via circRNA microarray analysis. 12 Zhao group once has selected circANKRD42, circGRHPR, circCDC27, circZMYM2, circARH-GAP26 and circTADA2A to prove our data.…”

mentioning

confidence: 99%

circELP2 reverse‐splicing biogenesis and function as a pro‐fibrogenic factor by targeting mitochondrial quality control pathway

Zhang,

Tu,

Liu

et al. 2023

J Cellular Molecular Medi

View full text Add to dashboard Cite

Idiopathic pulmonary fibrosis (IPF) is considered as a chronic, fibrosing interstitial pneumonia with unknown mechanism. The present work aimed to explore the function, biogenesis and regulatory mechanism of circELP2 in pulmonary fibrosis and evaluate the value of blocking circELP2‐medicated signal pathway for IPF treatment. The results showed that heterogeneous nuclear ribonucleoprotein L initiated reverse splicing of circELP2 resulting in the increase of circELP2 generation. The biogenetic circELP2 activated the abnormal proliferation and migration of fibroblast and extracellular matrix deposition to promote pulmonary fibrogenesis. Mechanistic studies demonstrated that cytoplasmic circELP2 sponged miR‐630 to increase transcriptional co‐activators Yes‐associated protein 1 (YAP1) and transcriptional co‐activator with PDZ‐binding motif (TAZ). Then, YAP1/TAZ bound to the promoter regions of their target genes, such as mTOR, Raptor and mLST8, which in turn activated or inhibited the genes expression in mitochondrial quality control pathway. Finally, the overexpressed circELP2 and miR‐630 mimic were packaged into adenovirus vector for spraying into the mice lung to evaluate therapeutic effect of blocking circELP2‐miR‐630‐YAP1/TAZ‐mitochondrial quality control pathway in vivo. In conclusion, blocking circELP2‐medicated pathway can alleviate pulmonary fibrosis, and circELP2 may be a potential target to treat lung fibrosis.

show abstract

Exosomal circ-PTPN22 and circ-ADAMTS6 mark T cell exhaustion and neutrophil extracellular traps in Asian intrahepatic cholangiocarcinoma

Cited by 16 publications

References 58 publications

Shaping the immune‐suppressive microenvironment on tumor‐associated myeloid cells through tumor‐derived exosomes

Shaping the immune‐suppressive microenvironment on tumor‐associated myeloid cells through tumor‐derived exosomes

Clinical significance of small extracellular vesicles in cholangiocarcinoma

circELP2 reverse‐splicing biogenesis and function as a pro‐fibrogenic factor by targeting mitochondrial quality control pathway

Contact Info

Product

Resources

About