B7-H3 promotes multiple myeloma cell survival and proliferation by ROS-dependent activation of Src/STAT3 and c-Cbl-mediated degradation of SOCS3

Lin, Liang; Cao, Linfeng; Liu, Yang; Wang, Ke; Zhang, Xinwei; Qin, Xiaodan; Zhao, Dandan; Hao, Jie; Chang, Ying‐Jun; Huang, Xiao‐Jun; Liu, Bei; Zhang, Jun; Ge, Qing

doi:10.1038/s41375-018-0331-6

Cited by 51 publications

(48 citation statements)

References 49 publications

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“…20,21 Notably, B7-H3 can upregulate the expression of JAK/STAT3 to facilitate the distant metastasis of myeloma cells, suggesting that JAK/STAT3 signaling may have a role in B7-H7-induced tumor progression. 22 In our study, we observed that B7-H3 was highly expressed in malignant glioma tissues. Importantly, we found that enhanced B7-H3 expression could significantly promote glioma cell proliferation and invasion both in vitro and in vivo, resulting in poor clinical prognosis.…”

Section: Introductionmentioning

confidence: 57%

“…Previous reports indicated that IL-6 could activate JAK-STAT and inhibit SOCS-3 (suppressor of cytokine signaling 3) and SHP-1 (Src homology 2 [SH2]containing phosphatase-1). 16 We therefore examined the expression of SOCS-3, SHP-1, and Src in LN229-vector, LN229-B7-H3 OE, U87-vector, and U87-B7-H3 OE cells.…”

Section: B7-h3 Regulated Tumor Progression Through Activation Of Thementioning

confidence: 99%

“…Several studies have indicated that B7-H3 can activate prosurvival signaling pathways in tumor cells, resulting in sustained tumor growth and progression. 15,16 The JAK/ STAT3 signal, which is associated with somatic cell proliferation and differentiation, has been detected in various tumor cells and is known to promote tumor progression. [17][18][19] Activation of JAK/STAT3 signaling can directly regulate tumor growth and promote EMT processes, resulting in the invasion and metastasis of gastric and ovarian cancer cells.…”

Section: Introductionmentioning

confidence: 99%

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B7-H3 Regulates Glioma Growth and Cell Invasion Through a JAK2/STAT3/Slug-Dependent Signaling Pathway

Zhong¹,

Tao²,

Chen³

et al. 2020

OTT

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The aim of this study was to explore the potential role of B7-H3 in malignant glioma progression and identify an innovative approach in clinical glioma therapy. Methods: The protein expression of B7-H3 in high-and low-grade tumor tissues from glioma patients was assessed by immunohistochemistry. The proliferative and invasive ability of B7-H3-overexpressing or knockout glioma cells was analyzed in vitro and in vivo by CCK-8 assay and an orthotopic mouse glioma model, respectively. Activation of the JAK2/STAT3/Slug signaling pathway and epithelial-mesenchymal transition (EMT) was examined by Western blotting and immunofluorescence. The anticancer effects of napabucasin (NAP) and temozolomide (TMZ) were analyzed in an orthotopic mouse glioma model. Results: The expression of B7-H3 was higher in high-grade than in low-grade tumor tissues from glioma patients. In line with this, overexpression of B7-H3 enhanced glioma cell proliferation, induced sustained glioma growth, and promoted glioma cell invasion in vitro and in vivo. Moreover, these effects were mediated through the activation of the JAK2/ STAT3/Slug signaling pathway in B7-H3 overexpression glioma cells. We also found that B7-H3 induced EMT processes through downregulation of E-cadherin and upregulation of MMP-2/-9 expression, resulting in enhanced invasion of glioma cells. Finally, we show that the combination of NAP and TMZ significantly suppressed glioma growth and glioma cell invasion, both in vitro and in vivo. Conclusion: B7-H3 overexpression facilitated sustained glioma growth and promoted glioma cell invasion through a JAK2/STAT3/Slug-dependent signaling pathway. Application of the STAT3 inhibitor NAP significantly suppressed glioma growth and invasion, and has potential as a therapeutic strategy for the treatment of glioma.

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Section: Introductionmentioning

confidence: 57%

Section: B7-h3 Regulated Tumor Progression Through Activation Of Thementioning

confidence: 99%

Section: Introductionmentioning

confidence: 99%

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B7-H3 Regulates Glioma Growth and Cell Invasion Through a JAK2/STAT3/Slug-Dependent Signaling Pathway

Zhong¹,

Tao²,

Chen³

et al. 2020

OTT

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“…8 Also, Qing Ge and his colleagues have reported that B7-H3 could promote multiple myeloma cell survival and proliferation through a ROS-dependent signaling pathway. 9 Notably, B7-H3 is an attractive target for cancer immunotherapy due to its specific expression in various tumor tissues. B7-H3-specific monoclonal antibodies and CAR-T technologies reveal dramatic anticancer effects along with a good safety profiles, which provide new targets in cancer therapy.…”

Section: Introductionmentioning

confidence: 99%

B7-H3 Induces Ovarian Cancer Drugs Resistance Through An PI3K/AKT/BCL-2 Signaling Pathway

Zhou¹,

Zhao²

2019

CMAR

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Purpose: This study was aimed to investigate the underlying mechanism of B7-H3 induced ovarian cancer proliferation and drugs resistance. Materials and methods: We compared the expression of B7-H3 in ovarian tumor tissues from high-malignant or low-malignant patients by immunohistochemistry. We established B7-H3 overexpression and knockout ovarian cells by CRISPR-Cas9 technology and examined the expression of the PI3K/AKT/BCL-2 signals in tumor cells by Western blot or immunofluorescence. We detected the B7-H3 overexpression ovarian cancer cells drugs resistance by CCK8 cell proliferation analysis and Annexin V/PI staining. Tumor-bearing mice were used to investigate the anticancer effects of PI3K/AKT inhibitors in combination with B7-H3 neutralizing antibodies. Results: Enhanced expression of B7-H3 was observed in ovarian tumor tissues from highmalignant patients compared to those from low-malignant patients. Notably, B7-H3 overexpression caused enhanced cells proliferation and chemo-resistance in vitro and in vivo through the activation of PI3K/AKT signaling pathways and up-regulation of BCL-2 protein.Combination of chemotherapeutic agents and B7-H3 neutralizing antibodies efficiently reverses the drugs resistance induced by B7-H3, resulting in improved anticancer effects in ovarian cancer. Conclusion: B7-H3 expression induces the activation the PI3K/AKT signaling pathway and up-regulates BCL-2 in protein level, resulting in the sustained growth and chemo-resistance in ovarian cancer. Blockade of B7-H3 signals efficiently reverses the chemo-resistance, which provides an innovative target in ovarian cancer treatment.

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“…It plays an important role in the occurrence and development of in ammatory diseases, viral infections, obesity and tumors [21]. Studies have shown that SOCS3 can affect tumor proliferation and development through Src/STAT3 and c-cbl mediated oxidative stress [22]. NUPL2 is a member of the nuclear pore gene family, which may play an important role in DNA damage caused by oxidative stress and affect tumor progression [23].…”

Section: Identifcation Of Hub Genes In the Salmon Module And Darkoranmentioning

confidence: 99%

The Oxidative Stress Pathway May be an Important Pathway Leading to The Recurrence of Ewing Sarcoma —— Based On Weighted Gene Co-Expression Network Analysis

Song

et al. 2020

Preprint

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Background The role of gene and pathway in recurrence of Ewing sarcoma (ES) was not clear. Thus, we investigated the biological role and underlying mechanism of gene and pathway in recurrence of ES.Methods Data sets of patients with ES were collected from the GEO database. We used dataset GSE63155 and GSE63156 to construct co-expression networks by weighted gene co-expression network analysis (WGCNA). Gene Ontology (GO) and Kyoto Encyclopedia of Genes and Genomes (KEGG) enrichment analyses were performed by Database for Annotation, Visualization and Integrated Discovery (DAVID). ResultsWe can find that genes with significant interactions in the genes of the recurrence group include SRSF11, TRIM39, SOCS3,NUPL2,COPS5. They work primarily through the oxidative stress pathway.Conclusion Through our research, for the first time found that ES by SRSF11 TRIM39, SOCS3, NUPL2, COPS5 interaction, activation of phosphorylation of bone and oxidative stress is affecting tumor recurrence. 4.SelvanathanSP, Graham GT, Grego AR, Baker TM, Hogg JR, Simpson M, Batish M, Crompton B, Stegmaier K, Tomazou EM et al: EWS-FLI1 modulated alternative splicing of ARID1A reveals novel oncogenic function through the BAF complex. Nucleic acids research 2019, 47(18):9619-9636. 5. Zhang B, Horvath S: A general framework for weighted gene co-expression network analysis. Statistical applications in genetics and molecular biology 2005, 4:Article17. 6. The Gene Ontology (GO) project in 2006. Nucleic acids research 2006, 34(Database issue):D322-326. 7. Dwight SS, Eppig JT et al: Gene ontology: tool for the unification of biology. The Gene Ontology Consortium. Nature genetics 2000, 25(1):25-29.8.

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B7-H3 promotes multiple myeloma cell survival and proliferation by ROS-dependent activation of Src/STAT3 and c-Cbl-mediated degradation of SOCS3

Cited by 51 publications

References 49 publications

<p>B7-H3 Regulates Glioma Growth and Cell Invasion Through a JAK2/STAT3/Slug-Dependent Signaling Pathway</p>

<p>B7-H3 Regulates Glioma Growth and Cell Invasion Through a JAK2/STAT3/Slug-Dependent Signaling Pathway</p>

<p>B7-H3 Induces Ovarian Cancer Drugs Resistance Through An PI3K/AKT/BCL-2 Signaling Pathway</p>

The Oxidative Stress Pathway May be an Important Pathway Leading to The Recurrence of Ewing Sarcoma —— Based On Weighted Gene Co-Expression Network Analysis

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