The Role of Shcbp1 in Signaling and Disease

Zhang, Gengyuan; Ma, Zhijian; Wang, Long; Jiao, Zuoyi; Jiang, Xiangyan; Yang, Xujuan; Long, Bo; Ye, Huili; Zhang, Shuze; Yu, Zeyuan; Shi, Wengui; Zhang, Jiao

doi:10.2174/1568009619666190620114928

Cited by 23 publications

(16 citation statements)

References 77 publications

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“…Recent studies have shown that SHCBP1 acts as a Shc SH2domain binding protein 1 and is involved in the regulation of various signaling pathways including MAPK, PI3K/AKT. NF-kB, MAPK/ERK, b-catenin, and TGF-b1/Smad pathways (7). SHCBP1 has been demonstrated to play important roles in different types of cancer, such as breast cancer, synovial sarcoma, gastric cancer, and lung cancer (12-14, 33, 34).…”

Section: Discussionmentioning

confidence: 99%

“…Therefore, unveiling molecular mechanism of the mechanism of progression and metastasis for PTC is critical for improving the clinical management for patients with advanced PTC. SHCBP1 (SHC SH2 Domain-Binding Protein 1) is first characterized as a protein binging to p52Shc, a subunit of SHC protein, which locates on chromosome 16q11.2 (7). SHCBP1 is evolutionarily conserved in eukaryotes, human SHCBP1 shares 78% identity with mouse's and 23% with the Drosophila melanogaster homolog (8).…”

Section: Introductionmentioning

confidence: 99%

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RETRACTED: SHCBP1 Promotes Papillary Thyroid Carcinoma Carcinogenesis and Progression Through Promoting Formation of Integrin and Collagen and Maintaining Cell Stemness

Geng

Guo

et al. 2021

Front. Endocrinol.

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Papillary thyroid carcinoma (PTC) is the most common thyroid cancer with a rapidly increasing incidence globally. Bioinformatics analyses suggested that SHCBP1 (SHC SH2 Domain-Binding Protein 1) was significantly up-regulated in PTC tumor tissues, which was further confirmed by immunohistochemical staining and qPCR analyses in Xuzhou cohort. Moreover, the results indicated that the mRNA level of SHCBP1 was negatively associated with patients’ disease-free survival rate, and further analysis reveals that patients with high SHCBP1 expression tend to have more lymph node metastasis. Afterward, MTT, colony formation, cell-cycle assay, FACS apoptosis assay, invasion, migration, as well as scratch assay were performed to study the phenotypes change of PTC cells after knocking down SHCBP1. The in vivo subcutaneous tumor model was developed to study the proliferation ability of PTC cells after SHCBP1 knockdown. We show that knock down of SHCBP1 significantly inhibits PTC cell proliferation, cell cycle, invasion and migration in vivo and in vitro. Western blot and qRT-PCR showed that knockdown of SHCBP1 could significantly reduce MYC, KLF4, CD44, ITGA6, ITGB1, ITGB5, and COL4A2 expression at both RNA and protein levels, which indicated that SHCBP1 might be involved in PTC carcinogenesis and progression through targeting formation of integrin and collagen and cell stemness pathways, and can be a potential diagnosis biomarker and therapeutic target for PTC.

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Section: Discussionmentioning

confidence: 99%

Section: Introductionmentioning

confidence: 99%

RETRACTED: SHCBP1 Promotes Papillary Thyroid Carcinoma Carcinogenesis and Progression Through Promoting Formation of Integrin and Collagen and Maintaining Cell Stemness

Geng

Guo

et al. 2021

Front. Endocrinol.

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“…SHC SH2 domain-binding protein 1 (SHCBP1), a member of the Src homolog and collagen homolog (SHC) family, plays an essential role in the regulation of multiple signal transduction pathways, such as EGF/EGFR, FGF, NF-κB, MAPK/ERK, PI3K/Akt, TGF-β1/Smad and Wnt/β-catenin [ 3 ]. Increasing evidence has shown that SHCBP1 is involved in the occurrence and development of various types of tumors, accelerating the progression of diseases and facilitating the growth and maintenance of a tumorigenic state.…”

Section: Introductionmentioning

confidence: 99%

EGF-induced nuclear translocation of SHCBP1 promotes bladder cancer progression through inhibiting RACGAP1-mediated RAC1 inactivation

et al. 2022

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Bladder cancer is a highly heterogeneous and aggressive malignancy with a poor prognosis. EGF/EGFR activation causes the detachment of SHC-binding protein 1 (SHCBP1) from SHC adapter protein 1 (SHC1), which subsequently translocates into the nucleus and promotes cancer development via multiple signaling pathways. However, the role of the EGF-SHCBP1 axis in bladder cancer progression remains unexplored. Herein, we report that SHCBP1 is upregulated in bladder cancer tissues and cells, with cytoplasmic or nuclear localization. Released SHCBP1 responds to EGF stimulation by translocating into the nucleus following Ser273 phosphorylation. Depletion of SHCBP1 reduces EGF-induced cell migration and invasiveness of bladder cancer cells. Mechanistically, SHCBP1 binds to RACGAP1 via its N-terminal domain of amino acids 1 ~ 428, and this interaction is enhanced following EGF treatment. Furthermore, SHCBP1 facilitates cell migration by inhibiting RACGAP-mediated GTP-RAC1 inactivation, whose activity is indispensable for cell movement. Collectively, we demonstrate that the EGF-SHCBP1-RACGAP1-RAC1 axis acts as a novel regulatory mechanism of bladder cancer progression, which offers a new clinical therapeutic strategy to combat bladder cancer.

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“…To characterize the downstream targets of miR-33b in RB, we conducted a bioinformatics prediction and characterized SHCBP1 as a possible target. SHCBP1 has been shown to positively regulate tumor progression and its expression remains high in malignant cells 40 . Additionally, high SHCBP1 levels can be observed during the β-selection checkpoint of T cell development, which is necessary for thymic proliferation 41 , 42 .…”

Section: Discussionmentioning

confidence: 99%

Long Non-Coding RNA TP53TG1 Upregulates SHCBP1 to Promote Retinoblastoma Progression by Sponging miR-33b

Wang

Zhang

et al. 2021

Cell Transplant

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Long non-coding RNA (lncRNA) TP53 target 1 (TP53TG1) is known to be strongly associated with tumor and cancer progression. However, its expression profile, unique role, and regulatory pathways in retinoblastoma (RB) are not known. Here, we revealed a large expression of TP53TG1 in RB tissues and cell lines. Conversely, we showed marked suppression of cell proliferation, migration, and invasion in TP53TG1 knocked down RB cells. Mechanistically, we established that TP53TG1 directly interacted with microRNA (miR)-33b in RB cells. Furthermore, TP53TG1 transcripts were found to be inversely correlated with miR-33b in RB tissues. We also showed that miR-33b suppression partly reversed the TP53TG1 knockdown mediated effects on tumor biology. Finally, TP53TG1 was shown to modulate the levels of SHC Binding and Spindle Associated 1 (SHCBP1), a direct target of miR-33b in RB cells. Based on the above data, we propose that TP53TG1 regulates RB progression via its modulation of the miR-33b/SHCBP1 pathway.

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The Role of Shcbp1 in Signaling and Disease

Cited by 23 publications

References 77 publications

RETRACTED: SHCBP1 Promotes Papillary Thyroid Carcinoma Carcinogenesis and Progression Through Promoting Formation of Integrin and Collagen and Maintaining Cell Stemness

RETRACTED: SHCBP1 Promotes Papillary Thyroid Carcinoma Carcinogenesis and Progression Through Promoting Formation of Integrin and Collagen and Maintaining Cell Stemness

EGF-induced nuclear translocation of SHCBP1 promotes bladder cancer progression through inhibiting RACGAP1-mediated RAC1 inactivation

Long Non-Coding RNA TP53TG1 Upregulates SHCBP1 to Promote Retinoblastoma Progression by Sponging miR-33b

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