Id1 enhances human ovarian cancer endothelial progenitor cell angiogenesis via PI3K/Akt and NF-κB/MMP-2 signaling pathways

Su, Yajuan; Gao, Liyuan; Teng, Lichen; Wang, Ying; Cui, Jialin; Peng, Siqi; Fu, Songbin

doi:10.1186/1479-5876-11-132

Cited by 48 publications

(37 citation statements)

References 24 publications

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“…We also found that ID1 knockdown suppressed the expression and activity of the matrix metalloproteinases, MMP2 and MMP9, in vitro, suggesting that ID1-KD may protect against angiogenic destruction of the extracellular matrix of regional blood vessels during adjacent and distal invasion and metastasis (29)(30)(31). ID1 knockdown induced suppression of angiogenesis may likely be explained in part by the ID1/NF-κB/MMP-2 or ID1/PI3K/Akt signaling pathways identified in ovarian cancer (32) and integrins (α3, α6 and β1)/laminin adhesion in pancreatic cancer (33).…”

Section: Discussionmentioning

confidence: 63%

Inhibitor of DNA-binding protein 1 knockdown arrests the growth of colorectal cancer cells and suppresses hepatic metastasis in vivo

et al. 2014

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Abstract. Inhibitor of DNA-binding protein 1 (ID1) is commonly abnormally overexpressed in colorectal cancer (CRC); yet, the functional significance of ID1 in the growth and invasive properties of CRC cells remains largely unclear. The present study investigated the effects of ID1 downregulation on the cell growth and metastatic features of CRC. Using lentiviral shRNA infection, stable ID1-knockdown (KD) HCT116 and SW620 cells, human metastatic CRC cell lines, were created. In vitro, the migration/invasion capacity of the ID1-KD CRC cells was assessed by a wound healing assay. The activities of MMP2 and MMP-9 were measured by gelatin zymography. The expression of CXC chemokine receptor 4 (CXCR4), PCNA and survivin were determined by immunoblot analysis and qRT-PCR. The effects of ID1 knockdown on tumor growth and hepatic metastasis were demonstrated by a xenograft study in mice. The results showed evident decreases in proliferation, migration and invasion and an increased apoptosis rate in the ID1-KD CRC cells. Similarly, ID1 knockdown significantly decreased mRNA and protein levels of PCNA, survivin, CXCR4, MMP2 and MMP9. Overexpression of CXCR4 antagonized the negative effect on the migration and invasion abilities of the ID1-KD cells. As compared with the control, ID1 knockdown prevented tumor growth and profoundly suppressed hepatic metastasis in vivo. The present study demonstrated the significance of ID1 in colon cancer progression, and its effect on tumor invasiveness and metastatic properties may be partly dependent on CXCR4.

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Section: Discussionmentioning

confidence: 63%

Inhibitor of DNA-binding protein 1 knockdown arrests the growth of colorectal cancer cells and suppresses hepatic metastasis in vivo

et al. 2014

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“…ID1 belongs to the basic helix-loop helix family of genes, which have been detected in multiple malignant tumors. In addition, the expression levels of these genes have been associated with invasive features of cancer (52,53). Increasing evidence has indicated that ID1 is upregulated in HCC samples and induces cellular proliferation.…”

Section: Ar and Inhibitor Of Differentiation 1 (Id1)mentioning

confidence: 99%

“…p38 kinases are a class of mitogen-activated protein kinases, which convert extracellular stimuli into a number of cellular responses, including survival, proliferation, migration and differentiation (52). Deregulation of p38 has been identified to be involved in hepatocarcinogenesis (59,60).…”

Section: Ar Suppresses Hcc Metastasismentioning

confidence: 99%

Androgen receptor in hepatocarcinogenesis: Recent developments and perspectives

et al. 2015

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Abstract. Previous studies have indicated that males are at a higher risk of developing hepatocellular carcinoma (HCC) compared with females. Identifying the factors that cause this gender-specific difference in the incidence of HCC has long been considered important for revealing the molecular mechanisms involved in hepatocarcinogenesis. Given the unprecedented tools that are now available for molecular research, genetic studies have established that the androgen receptor (AR) may be partly responsible for gender disparity in HCC. AR has a dual role, promoting HCC initiation and development, as well as suppressing HCC metastasis. The present review provides an overview of the involvement of AR signaling in HCC. The review highlighted important studies, examples of the direct AR transcriptional target genes involved in HCC and novel theories concerning the conventional concept, suggesting that targeting the AR, rather than the androgen, may provide an improved therapeutic approach for the treatment of HCC.

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“…Inhibition of GSK3-β by PI3K/AKT upregulates the expression of hypoxia-inducible factor-1α, inducing VEGF transcriptional activation to promote angiogenesis (17). In early 2013, Su et al (18) reported that PI3K/AKT is mediated by inhibitor of DNA binding/differentiation 1 to enhance endothelial progenitor cell angiogenesis in ovarian cancer. In a study by You et al (19), extracellular signal-regulated kinases and PI3K signaling pathways showed strong involvement in the forkhead box protein C2-mediated angiogenesis process.…”

Section: Evidence and Discussionmentioning

confidence: 99%

SGK3 (CISK) may induce tumor angiogenesis (Hypothesis)

Hou

Lai

et al. 2015

Oncology Letters

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Abstract. Serum-and glucocorticoid-inducible protein kinase 3 (SGK3), also known as cytokine-independent survival kinase (CISK), encoded by chromosome 8q12.2, is a downstream mediator of phosphatidylinositol 3-kinase (PI3K) oncogenic signaling. As a downstream target of PI3K, SGK3 has been reported to mediate pivotal roles in oncogenic progress in various cancers, including breast cancer, ovarian cancer and hepatocellular carcinoma. Functionally parallel to v-akt murine thymoma viral oncogene homolog (AKT)/protein kinase B, SGK3 serves as a hallmark mediating glycogen synthase kinase-β (GSK3-β), B-cell lymphoma (Bcl)-2-associated death promoter, forkead family of transcription factors, Bcl-extra large, Bcl-2, mammalian target of rapamycin, C-X-C chemokine receptor type 4 (CXCR4) and numerous other molecules in cell proliferation, growth, survival, migration and even tumor angiogenesis. Tumor angiogenesis is recognized as an essential step for tumor growth, invasion and metastasis, and it has become an intriguing target for anticancer drug development for tumor investigators worldwide. An abundance of experiments have been performed to investigate the role of the phosphoinositide 3-kinase (PI3K)/AKT pathway in regulating tumor angiogenesis. The mechanism of angiogenesis regulated by the PI3K/AKT pathway is, to a certain extent, clear. Although a number of SGK3 target molecules, including CXCR4 and GSK3β, have demonstrated potential roles in promoting angiogenesis, the exact association between angiogenesis and SGK3 remains unclear. Thus, we hypothesize that SGK3, parallel to AKT, may also be important in mediating angiogenesis. Identifying the role of SGK3 in tumor angiogenesis will certainly present a novel perspective on the malignant transformation of tumors, as well as a target for tumor therapy.

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Id1 enhances human ovarian cancer endothelial progenitor cell angiogenesis via PI3K/Akt and NF-κB/MMP-2 signaling pathways

Cited by 48 publications

References 24 publications

Inhibitor of DNA-binding protein 1 knockdown arrests the growth of colorectal cancer cells and suppresses hepatic metastasis in vivo

Inhibitor of DNA-binding protein 1 knockdown arrests the growth of colorectal cancer cells and suppresses hepatic metastasis in vivo

Androgen receptor in hepatocarcinogenesis: Recent developments and perspectives

SGK3 (CISK) may induce tumor angiogenesis (Hypothesis)

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