A deficient MIF-CD74 signaling pathway may play an important role in immunotherapy-induced hyper-progressive disease

Wang, Jiahui; Hong, Jinsheng; Fei-yu, Yang; Liu, Fangming; Wang, Xiangdong; Shen, Zan; Wu, Duojiao

doi:10.1007/s10565-021-09672-3

Cited by 8 publications

(6 citation statements)

References 35 publications

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“…These pieces of evidence are also consistent with a study that has reported that developed-exhausted CD4+ T cells and Tregs increasingly enriched, whereas some effector T cells decreased in HPD observed by scRNA-seq analysis (51). Such imbalance of immune cells may potentially account for the occurrence of HPD.…”

Section: Activation Of Protumoral Effect By Tregs and Tamsupporting

confidence: 91%

Hyperprogressive Disease in Malignant Carcinoma With Immune Checkpoint Inhibitor Use: A Review

Liu

Qiao

2022

Front. Nutr.

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Immune checkpoint inhibitors (ICIs) have shown durable remissions and improved long-term survival across a variety of cancer types. However, there is growing evidence that a significant subset of nonresponsive patients may exhibit hyperprogressive disease (HPD) during the initiation of immune checkpoint inhibitors (ICIs). Moreover, patients with HPD triggered by ICIs are always correlated with a deteriorating quality of life and poor prognosis. The ability to predict such rapid disease progression phenotypes is of great importance. More precision parameters to evaluate the response pattern to ICIs are urgently needed. To date, the mechanisms of HPD are still unclear. Aberrant alterations of driven genes, tumor microenvironment, or T cell immunophenotype may involve in HPD. In this article, we aim to provide an updated overview of available studies on HPD and summarize the potential predictors associated with HPD and the underlying mechanisms of HPD.

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Section: Activation Of Protumoral Effect By Tregs and Tamsupporting

confidence: 91%

Hyperprogressive Disease in Malignant Carcinoma With Immune Checkpoint Inhibitor Use: A Review

Liu

Qiao

2022

Front. Nutr.

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“…Furthermore, the ligand–receptor interaction CD74‐MIF, which plays a significant role in immunotherapy‐induced hyper‐progressive disease, was also observed between Treg and Epi C(4). 41 Additionally, the CD52‐SIGLEC10 interaction was noted to suppress T cell activity. 42 Changes in the interaction between CD4 + T cells and apCAFs could be relevant to brain metastasis in NSCLC.…”

Section: Resultsmentioning

confidence: 99%

Distinct fibroblast subpopulations associated with bone, brain or intrapulmonary metastasis in advanced non‐small‐cell lung cancer

Xu,

Wang,

Zou

et al. 2024

Clinical & Translational Med

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BackgroundBone or brain metastases may develop in 20–40% of individuals with late‐stage non‐small‐cell lung cancer (NSCLC), resulting in a median overall survival of only 4–6 months. However, the primary lung cancer tissue's distinctions between bone, brain and intrapulmonary metastases of NSCLC at the single‐cell level have not been underexplored.MethodsWe conducted a comprehensive analysis of 14 tissue biopsy samples obtained from treatment‐naïve advanced NSCLC patients with bone (n = 4), brain (n = 6) or intrapulmonary (n = 4) metastasis using single‐cell sequencing originating from the lungs. Following quality control and the removal of doublets, a total of 80 084 cells were successfully captured.ResultsThe most significant inter‐group differences were observed in the fraction and function of fibroblasts. We identified three distinct cancer‐associated fibroblast (CAF) subpopulations: myofibroblastic CAF (myCAF), inflammatory CAF (iCAF) and antigen‐presenting CAF (apCAF). Notably, apCAF was prevalent in NSCLC with bone metastasis, while iCAF dominated in NSCLC with brain metastasis. Intercellular signalling network analysis revealed that apCAF may play a role in bone metastasis by activating signalling pathways associated with cancer stemness, such as SPP1‐CD44 and SPP1‐PTGER4. Conversely, iCAF was found to promote brain metastasis by activating invasion and metastasis‐related molecules, such as MET hepatocyte growth factor. Furthermore, the interaction between CAFs and tumour cells influenced T‐cell exhaustion and signalling pathways within the tumour microenvironment.ConclusionsThis study unveils the direct interplay between tumour cells and CAFs in NSCLC with bone or brain metastasis and identifies potential therapeutic targets for inhibiting metastasis by disrupting these critical cell–cell interactions.

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“…The MIF signalling pathway in the tumour immune microenvironment plays an important role in the interaction between Treg cells and other cell types (31). It has also been reported that the lack of the MIF signalling pathway leads to inhibition of effector T-cell proliferation, which in turn leads to the possible transformation of tumour patients receiving immunotherapy into hyperprogressive disease (32). This also re ects the clinical translational value of the MIF signalling pathway of T cells in tumour tissue.…”

Section: Discussionmentioning

confidence: 97%

Nucleolar protein interacting with the FHA domain of MKI67 may be an important factor in promoting the development of colorectal cancer: a comprehensive study integrating bulk RNA-seq, scRNA-seq, protein immunohistochemistry and CRISPR

Li,

Tang,

Chen

et al. 2024

Preprint

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Background Limited evidence suggests that nucleolar protein interacting with the FHA domain of MKI67 (NIFK) plays a significant role in tumour occurrence and development. The mechanism and clinical value of NIFK in colorectal cancer (CRC) still lack a comprehensive evaluation. Materials and Methods Cancerous tissue and paracancerous tissue of 266 CRC patients were collected for immunohistochemistry, and the mRNA expression profiles of 2262 CRC tissue and 1297 non-CRC tissue worldwide were collected and analysed at the NIFK protein and mRNA levels. Analyse the effect of knocking out NIFK by CRISPR on the growth status of CRC cells in 43 CRC cell lines. Enrichment analysis was used to explore the potential biological behaviour of NIFK in the CRC. The impact of NIFK on the immune microenvironment and single-cell landscape of CRC tissue was also analysed. In addition, the clinical value of NIFK in CRC was also evaluated in terms of clinical pathology, targeted therapy, and immunotherapy. Results The expression levels of NIFK protein (p < 0.05) and mRNA (SMD = 2.13, p < 0.05) in CRC were significantly higher than those in non-CRC. CRC cells exhibit a strong requirement for NIFK for growth. Abnormal expression of NIFK may affect the progression of CRC by affecting the GALECTIN, ANGPTL, and GDF signalling pathways of malignant epithelial cells, the MIF signalling pathway of T cells, and the TGFb signalling pathway of NK cells. The high expression of NIFK protein and mRNA has a strong ability to identify CRC. Conclusion NIFK plays an important role in the occurrence and development of CRC. NIFK may promote the occurrence and development of CRC through the cell cycle, ribosome, and mitochondrial pathways. The T-cell MIF pathway may have certain clinical value in anti-tumour therapy.

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A deficient MIF-CD74 signaling pathway may play an important role in immunotherapy-induced hyper-progressive disease

Cited by 8 publications

References 35 publications

Hyperprogressive Disease in Malignant Carcinoma With Immune Checkpoint Inhibitor Use: A Review

Hyperprogressive Disease in Malignant Carcinoma With Immune Checkpoint Inhibitor Use: A Review

Distinct fibroblast subpopulations associated with bone, brain or intrapulmonary metastasis in advanced non‐small‐cell lung cancer

Nucleolar protein interacting with the FHA domain of MKI67 may be an important factor in promoting the development of colorectal cancer: a comprehensive study integrating bulk RNA-seq, scRNA-seq, protein immunohistochemistry and CRISPR

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