Редактирование: DIP2A

Disco-interacting protein 2 homolog A (EC 6.2.1.1) (DIP2 homolog A) [C21orf106] [DIP2] [KIAA0184]

==Publications==

{{medline-entry
|title=Blocking the [[FSTL1]]-[[DIP2A]] Axis Improves Anti-tumor Immunity.
|pubmed-url=https://pubmed.ncbi.nlm.nih.gov/30110636
|abstract=Immune dysfunction is a strong factor in the resistance of cancer to treatment. Blocking immune checkpoint pathways is a promising approach to improve anti-tumor immunity, but the clinical efficacies are still limited. We previously identified follistatin-like 1 ([[FSTL1]]) as a determinant of immune dysfunction mediated by mesenchymal stromal/stem cells (MSCs) and immunoregulatory cells. Here, we demonstrate that blocking [[FSTL1]] but not immune checkpoint pathways significantly suppresses cancer progression and metastasis in several mouse tumor models with increased MSCs. Expression of [[DIP2A]] (the receptor of [[FSTL1]]) in tumor cells is critical for [[FSTL1]]-induced immunoresistance. [[FSTL1]]/[[DIP2A]] co-positivity in tumor tissues correlates with poor prognosis in NSCLC patients. Thus, breaking the [[FSTL1]]-[[DIP2A]] axis may be a useful strategy for successfully inducing anti-tumor immunity.
|mesh-terms=* Animals
* Carcinoma, Non-Small-Cell Lung
* Carrier Proteins
* Case-Control Studies
* Cell Line, Tumor
* Cell Movement
* Cell Proliferation
* Disease Progression
* Female
* Follistatin-Related Proteins
* Gene Expression Regulation, Neoplastic
* Humans
* Immunity, Innate
* Lung Neoplasms
* Male
* Mesenchymal Stem Cells
* Mice
* Mice, Inbred BALB C
* Mice, Inbred C57BL
* Nuclear Proteins
* Prognosis
* RNA, Small Interfering
* Signal Transduction
* Survival Analysis
* Tumor Burden
* Xenograft Model Antitumor Assays
|keywords=* FSTL1
* aging
* antibody
* cancer metastasis
* immune checkpoint
* immune exhaustion
* immunosuppression
* lung cancer
* mesenchymal stromal/stem cells
|full-text-url=https://sci-hub.do/10.1016/j.celrep.2018.07.043
}}