TGF-β1 promotes colorectal cancer immune escape by elevating B7-H3 and B7-H4<i>via</i>the miR-155/miR-143 axis

Zhou, Xinru; Mao, Yong; Zhu, Jianjie; Fang, Meng; Chen, Qi; Tao, Lihua; Li, Rui; Fu, Fengqing; Liu, Cuiping; Y, Hu; Wang, Weipeng; Zhang, Hongjian; Hua, Dong; Chen, Weichang; Zhang, Xueguang

doi:10.18632/oncotarget.11950

Cited by 72 publications

(63 citation statements)

References 50 publications

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“…The upregulated miR-155 attenuated miR-143 by inhibiting its direct target, the transcription factor CEBPB. The result reveals the mechanism by which TGF-β1 leads to T cell-mediated tumor evasion through an increase in B7-H3 and B7-H4 expression (67). …”

Section: B7-h4mentioning

confidence: 97%

“…B7-H4 expression is significantly associated with poor outcome in patients with RCC (65), lung cancer (66), CRC (67), cholangiocarcinoma (68), glioma (69), pancreatic cancer (70), oral squamous cell carcinoma (71), esophageal squamous cell carcinoma (72), gallbladder cancer (35), ovarian serous carcinoma (73) and gastric cancer (74). B7-H4 expression in RCC is associated with adverse clinical and pathologic features, including constitutional symptoms, tumor necrosis, and advanced tumor size, stage, and grade.…”

Section: B7-h4mentioning

confidence: 99%

“…In the context of CRC, over-expression of B7-H3 and B7-H4 in HCT-116 cells induces T cells to secrete TGF-β1, while B7-H3 and B7-H4 are the direct target genes of miR-143 (67). TGF-β1 elevated the expression of miR-155 in colorectal cancer cells through SMAD3 and SMAD4.…”

Section: B7-h4mentioning

confidence: 99%

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New B7 Family Checkpoints in Human Cancers

Dong

2017

Molecular Cancer Therapeutics

204

201

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T cells are the main effector cells in immune response against tumors. The activation of T cells is regulated by the innate immune system through positive and negative costimulatory molecules. Targeting immune checkpoint regulators such as programmed cell death 1 (PD-1)/PD-1 ligand 1 (PD-L1) and cytotoxic T lymphocyte antigen 4 (CTLA-4) has achieved notable benefit in a variety of cancers, which leads to multiple clinical trials with antibodies targeting the other related B7/CD28 family members. Recently five new B7 family ligands, B7-H3, B7-H4, B7-H5, B7-H6 and B7-H7, were identified. Here we review recent understanding of new B7 family checkpoint molecules since they have come to the front of cancer research with the concept that tumor cells exploit them to escape immune surveillance. The aim of this article is to address the structure and expression of the new B7 family molecules as well as their roles in controlling and suppressing immune responses of T cells as well as NK cells. We also discuss clinical significance and contribution of these checkpoint expressions in human cancers.

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Section: B7-h4mentioning

confidence: 97%

Section: B7-h4mentioning

confidence: 99%

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New B7 Family Checkpoints in Human Cancers

Dong

2017

Molecular Cancer Therapeutics

204

201

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“…Overexpressed B7-H3 and B7-H4 induce T cells to secret TGF-β 1 and immunosuppressive cytokines IL-2, IL-6 and IL-17. Despite B7-H3 and B7-H4, other coinhibitory factor B7-DC, CTLA4 and PD-1 are also inhibited by miR-143 [73]. In addition, KRAS-mediated KAP1/TRIM28 sumoylation is also involved in the KRAS-driven transformation in colorectal cancer [74].…”

Section: Conclusion and Perspectivementioning

confidence: 99%

Transcription Factor RREB1: from Target Genes towards Biological Functions

Deng¹,

Xia²,

Zhang³

et al. 2020

Int. J. Biol. Sci.

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The Ras-responsive element binding protein 1(RREB1) is a member of zinc finger transcription factors, which is widely involved in biological processes including cell proliferation, transcriptional regulation and DNA damage repair. New findings reveal RREB1 functions as both transcriptional repressors and transcriptional activators for transcriptional regulation of target genes. The activation of RREB1 is regulated by MAPK pathway. We have summarized the target genes of RREB1 and discussed RREB1 roles in the cancer development. In addition, increasing evidences suggest that RREB1 is a potential risk gene for type 2 diabetes and obesity. We also review the current clinical application of RREB1 as a biomarker for melanoma detection. In conclusion, RREB1 is a promising diagnostic biomarker or new drug target for cancers and metabolic diseases.

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“…miR-152 directly bind to B7-H1 3’ untranslated region and inhibits B7-H1 expression, which enhances T cell proliferation and effector cytokine production via inhibition of the B7-H1/ PD-1 pathway [19]. Furthermore, over-expression of B7-H4 promoted tumor growth through TGF-β1, which increased expression of miR-155 through SMAD3 and SMAD4 and attenuated miR-143 through CEBPB [20]. …”

Section: Introductionmentioning

confidence: 99%

MicroRNA Expression Profiling of Pancreatic Cancer Cell Line L3.6p1 Following B7-H4 Knockdown

Qian

Ling

et al. 2017

Cell Physiol Biochem

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Background/Aims: Co-stimulating molecule B7-H4 regulates T cell-mediated immune responses, participates in tumor immune escape, and promotes the proliferation and metastasis of pancreatic cancer cells. However, the specific mechanisms are unclear. MicroRNAs (miRNAs) participated in the pathogenesis and progression of cancer. Methods: In this study, a microarray technique was used to screen B7-H4-related differentially expressed miRNAs in a pancreatic cancer cell line find those associated with pancreatic cancer. Using a miRCURY^TM LNA Array approach, we compared the miRNA expression profiles of L3.6p1 pancreatic cancer cells transfected with B7-H4 siRNA for 72 h with those transfected with non-target siRNAs. Results: B7-H4 siRNA significantly up-regulated 57 miRNAs and down-regulated 14 miRNAs. Gene Ontology (GO) and Kyoto Encyclopedia of Genes and Genomes (KEGG) Pathway analysis of predicted miRNA targets showed that these genes were mainly involved in protein binding, pathways in cancer, mitogen-activated protein kinase (MAPK) signaling pathway, and phosphatidylinositol 3-kinase-Akt (PI3K-Akt) signaling pathway. Conclusions: This is the first description of target genes of B7-H4, showing that miRNAs participate in the B7-H4 mediated regulation of oncogenicity and pathogenesis of pancreatic cancer. These results may help us better understand the role of B7-H4 in the progression of pancreatic cancer and its possible mechanisms. We also provide novel biomarkers for potential treatments of pancreatic cancer.

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TGF-β1 promotes colorectal cancer immune escape by elevating B7-H3 and B7-H4viathe miR-155/miR-143 axis

Cited by 72 publications

References 50 publications

New B7 Family Checkpoints in Human Cancers

New B7 Family Checkpoints in Human Cancers

Transcription Factor RREB1: from Target Genes towards Biological Functions

MicroRNA Expression Profiling of Pancreatic Cancer Cell Line L3.6p1 Following B7-H4 Knockdown

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