Inhibitor of Differentiation 1 (Id1) in Cancer and Cancer Therapy

Zhao, Zhengxiao; Bo, Zhiyuan; Gong, Wei; Guo, Yinglu

doi:10.7150/ijms.42805

Cited by 64 publications

(44 citation statements)

References 121 publications

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“…ID1 protein is a member of the helix-loop-helix family of transcriptional regulatory proteins. As a known target of USP1 10 , 13 , the dysregulation of ID1 has been widely reported in multiple types of human tumors, which is essential for processes such as proliferation, cell migration and stem cell renewal 19 - 21 . In B-ALL patients, high expression level of ID1 is associated with the poor outcome 22 .…”

Section: Discussionmentioning

confidence: 99%

Inhibition of USP1 induces apoptosis via ID1/AKT pathway in B-cell acute lymphoblastic leukemia cells

Kuang¹,

Xiong²,

Lü³

et al. 2021

Int. J. Med. Sci.

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Deubiquitylating enzyme ubiquitin-specific protease 1 (USP1) has been reported to be aberrantly overexpressed in cancers, and it plays a critical role in regulating various cellular processes, such as cell proliferation, apoptosis, and cell differentiation. However, the role of USP1 in B-cell acute lymphoblastic leukemia (B-ALL) remains largely undefined. USP1 expression in 30 newly diagnosed B-ALL patients was detected by real-time PCR and western blot. We found that USP1 was generally upregulated in the bone marrow cells derived from B-ALL patients. Knockdown of USP1 by siRNA decreased B-ALL cell growth and induced apoptosis. Similarly, pharmacological inhibition of USP1 by SJB3-019A significantly repressed cell proliferation and triggered B-ALL cell apoptosis. Finally, we found that inhibition of USP1 downregulated the expression of ID1 and p-AKT, and upregulated ID1 expression could reverse the suppressive effects of USP1 inhibitor in B-ALL cells. Taken together, these results demonstrate that USP1 promote B-ALL progression at least partially via the ID1/AKT signaling pathway, and USP1 inhibitors might be promising therapeutic application for B-ALL.

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Section: Discussionmentioning

confidence: 99%

Inhibition of USP1 induces apoptosis via ID1/AKT pathway in B-cell acute lymphoblastic leukemia cells

Kuang¹,

Xiong²,

Lü³

et al. 2021

Int. J. Med. Sci.

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“…Drugs such as tetramethylpyrazine, vinblastine, crizotinib, and fucoidan were found to inhibit tumor growth or metastasis by targeting ID1-associated signaling pathways. 22 We found that ID1 was a key target of regorafenib, and speculate that the combination therapy of regorafenib and the above-mentioned agents may benefit to improve the therapeutic effect of HCC.…”

Section: Regorafenib Suppresses Tumor Growth and Vm Formation In Pdmentioning

confidence: 77%

“…A variety of compounds have been found to exert antitumor effects via targeting ID1 or its related signaling pathways 15,21 . ID1 represents a promising target of antitumor therapeutics, on the strength of its cancer‐promoting properties 22 . Furtherly, numerous studies have revealed that ID1 plays an important role in tumor metastasis and angiogenesis in lung cancer, colon cancer, breast cancer and other tumors 15,21,23 .…”

Section: Introductionmentioning

confidence: 99%

“…15,21 ID1 represents a promising target of antitumor therapeutics, on the strength of its cancer-promoting properties. 22 Furtherly, numerous studies have revealed that ID1 plays an important role in tumor metastasis and angiogenesis in lung cancer, colon cancer, breast cancer and other tumors. 15,21,23 However, the function of ID1 in metastasis and VM of HCC remains unclear.…”

Section: Introductionmentioning

confidence: 99%

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Regorafenib inhibits migration, invasion, and vasculogenic mimicry of hepatocellular carcinoma via targeting ID1‐mediated EMT

Zhang

et al. 2021

Molecular Carcinogenesis

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Regorafenib is approved for patients with unresectable hepatocellular carcinoma (HCC) following sorafenib. However, the effect of regorafenib on HCC metastasis and its mechanism are poorly understood. Here, our data showed that regorafenib significantly restrained the migration, invasion and vasculogenic mimicry (VM) of HCC cells, and downregulated the expression of epithelial-to-mesenchymal transition (EMT)/VM-related molecules. Using RNAseq and cellular thermal shift assays, we found that inhibitor of differentiation 1 (ID1) was a key target of regorafenib. In HCC tissues, the protein expression of ID1 was positively correlated with EMT and VM formation (CD34 − /PAS +). Functionally, ID1 knockdown inhibited HCC cell migration, invasion, metastasis, and VM formation in vitro and in vivo, with upregulation of E-cadherin and downregulation of Snail and VE-cadherin. Moreover, Snail overexpression promoted the migration, invasion, and VM formation of ID1 knockdown cells. Snail knockdown reduced the migration, invasion, and VM formation of ID1 overexpression cells. Finally, regorafenib suppressed VM formation and decreased the expression of ID1, VE-cadherin and Snail in HCC PDX model. In conclusion, we manifested that regorafenib distinctly inhibited EMT in HCC cells via targeting ID1, leading to the suppression of cell migration, invasion and VM formation. These findings suggest that regorafenib may be developed as a suitable therapeutic agent for HCC metastasis.

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“…In our previous study, we have demonstrated that the over-expression of ID1 effectively promoted the carcinogenesis of OSCC [12,13]. ID1 is one of the inhibitors of DNA binding (Id) proteins [27]. During development, the Id proteins play a key role in the regulation of cell-cycle progression and cell differentiation by modulating different cellcycle regulators both by direct and indirect mechanisms [28].…”

Section: Discussionmentioning

confidence: 99%

C1QTNF6 promotes Oral squamous cell carcinoma tumorigenesis though enhancing proliferation and inhibiting apoptosis of OSCC cells

Song¹,

Li²,

Shi³

et al. 2021

Preprint

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BackgroundC1QTNF6 (CTRP6), a member of the CTRP family, has been recently implied to play a role in tumorigenesis. However, the expression status and the role of C1QTNF6 in oral squamous cell carcinoma (OSCC) remains unclear. MethodsImmunohistochemistry of OSCC tissue and data from TCGA both implied that C1QTNF6 was closely related to OSCC. We constructed lentivirus to knockdown C1QTNF6 in CAL27 cells and SCC-9 cells. Then the change of C1QTNF6 mRNA expression was detected with qRT-PCR, and the Western blot analysis was performed to detect changes in protein expression. Furthermore, Cell Cycle Analysis and Cell apoptosis analysis was measured. 4-week-old female BALB/c nude mice were purchased to observe the In vivo tumorigenicity. Finally, Pathway Analysis was performed.ResultsIn this study, we found that C1QTNF6 was overexpressed in OSCC tissues and cell lines, and the cellular proliferation was significantly decreased in C1QTNF6 knockdown OSCC cells. Knockdown of C1QTNF6 resulted in cell cycle arrest at the G2/M phase and enhanced apoptosis in OSCC cell lines. Further assays showed that C1QTNF6 silencing inhibits tumor growth of OSCC in vivo. Moreover, microarray analysis revealed that C1QTNF6 silencing results in significant alteration of many genes. Ingenuity Pathway Analysis (IPA) revealed that the Acute Phase Response signaling pathway was significantly activated following C1QTNF6 silencing. ConclusionsThese results suggested that C1QTNF6 play a promoting role in OSCC tumorigenesis, which may be a promising therapeutic target for OSCC treatment.

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Inhibitor of Differentiation 1 (Id1) in Cancer and Cancer Therapy

Cited by 64 publications

References 121 publications

Inhibition of USP1 induces apoptosis via ID1/AKT pathway in B-cell acute lymphoblastic leukemia cells

Inhibition of USP1 induces apoptosis via ID1/AKT pathway in B-cell acute lymphoblastic leukemia cells

Regorafenib inhibits migration, invasion, and vasculogenic mimicry of hepatocellular carcinoma via targeting ID1‐mediated EMT

C1QTNF6 promotes Oral squamous cell carcinoma tumorigenesis though enhancing proliferation and inhibiting apoptosis of OSCC cells

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