Prostate cancer cells modulate osteoblast mineralisation and osteoclast differentiation through Id-1

Hf, Yuen; Yt, Chiu; Chan, KK; Yp, Chan; Chua, Chee Wai; Cm, McCrudden; Tang, Kwan Ho; El‐Tanani, Mohamed; Wong, Y-C; Wang, X

doi:10.1038/sj.bjc.6605480

Cited by 20 publications

(17 citation statements)

References 56 publications

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“…Osteoblasts are the cells responsible for the formation and mineralization of new bone. We and others have previously shown that osteoblasts are stimulated by PC tumor cells . In addition, we demonstrated that osteoblasts induce a more aggressive phenotype along with osteomimicry in osteoblastic CRPC cells .…”

Section: Introductionsupporting

confidence: 73%

Tasquinimod inhibits prostate cancer growth in bone through alterations in the bone microenvironment

et al. 2015

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The present study shows that tasquinimod reduces establishment and progression of tumor growth in bone likely through a combination of effects on the pre-metastatic niche, homing, immunological status, and osteogenesis. It was concluded that tasquinimod interferes with the metastatic process, presumably by inhibition of tumor establishment. Hence, our data suggest that tasquinimod might be most effective in inhibiting the occurrence of new metastatic lesions.

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Section: Introductionsupporting

confidence: 73%

Tasquinimod inhibits prostate cancer growth in bone through alterations in the bone microenvironment

et al. 2015

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“…Immunohistochemical staining was performed as previously described using the Dako Envision system (Dako, Glostrup, Denmark) 32. Pea3 antibody (Santa Cruz Biotechnology, Santa Cruz, CA, USA) was used at a dilution of 1 : 50 and Snail antibody (Cell Signaling, Danvers, MA, USA) was used at a dilution of 1 : 100.…”

Section: Methodsmentioning

confidence: 99%

Polyomavirus enhancer activator 3 protein promotes breast cancer metastatic progression through Snail‐induced epithelial–mesenchymal transition

Yuen

Chan

Grills

et al. 2011

The Journal of Pathology

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Polyomavirus enhancer activator 3 protein (Pea3), also known as ETV4, is a member of the Ets-transcription factor family, which promotes metastatic progression in various types of solid cancer. Pea3-driven epithelial-mesenchymal transition (EMT) has been described in lung and ovarian cancers. The mechanisms of Pea3-induced EMT, however, are largely unknown. Here we show that Pea3 overexpression promotes EMT in human breast epithelial cells through transactivation of Snail (SNAI1), an activator of EMT. Pea3 binds to the human Snail promoter through the two proximal Pea3 binding sites and enhances Snail expression. In addition, knockdown of Pea3 in invasive breast cancer cells results in down-regulation of Snail, partial reversal of EMT, and reduced invasiveness in vitro. Moreover, knockdown of Snail partially rescues the phenotype induced by Pea3 overexpression, suggesting that Snail is one of the mediators bridging Pea3 and EMT, and thereby metastatic progression of the cancer cells. In four breast cancer patient cohorts whose microarray and survival data were obtained from the Gene Expression Omnibus database, Pea3 and Snail expression are significantly correlated with each other and with overall survival of breast cancer patients. We further demonstrate that nuclear localization of Pea3 is associated with Snail expression in breast cancer cell lines and is an independent predictor of overall survival in a Chinese breast cancer patient cohort. In conclusion, our results suggest that Pea3 may be an important prognostic marker and a therapeutic target for metastatic progression of human breast cancer.

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“…A study conducted by Lee et al reported that the positive expression regulation of Id‐1 can be combined with Ets and inhibit the activity of P16 INK4ɑ , while the latter can promote the phosphorylation of Rb protein. Id‐1 can also form heterodimers to inhibit E2A from activating p21 through specific binding with E2A, while the latter can activate CDK2 to phosphorylate Rb protein and guarantee the successful procession of the G 1 /S phase . In addition, it has been found in bone cell cancer that Id‐1 activates cell growth and promotes cell proliferation by activating the MAPK of Raf‐1 .…”

Section: Discussionmentioning

confidence: 99%

“…8,9 A study conducted by Lee et al 10 also form heterodimers to inhibit E2A from activating p21 through specific binding with E2A, while the latter can activate CDK2 to phosphorylate Rb protein and guarantee the successful procession of the G 1 /S phase. 11 In addition, it has been found in bone cell cancer that Id-1 activates cell growth and promotes cell proliferation by activating the MAPK of Raf-1. 12 Furthermore, it has been found in gastric cancer and pancreatic cancer cells that the Id-reverse target-nuclear factor κB (NF-κB) pathway is activated to promote the expression of Bcl-2, inhibit the TNF-ɑ pathway, decrease the expression level of caspase-3, and inhibit tumor cell death.…”

Section: Discussionmentioning

confidence: 99%

A study of the impact of inhibitors of DNA binding‐1 on proliferation and migration in human colon carcinoma cells

Wang

Xue

et al. 2019

The Kaohsiung J of Med Scie

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This study aims to explore the effect of an inhibitor of DNA binding‐1 (Id‐1) on the proliferation and migration of human colon carcinoma cell line SW480 and HT‐29. SW480 and HT‐29 cells transfected with Id‐1‐interference sequence were assigned to the experimental groups (inhibition groups 1 and 2), and SW480 and HT‐29 cells with blank interference sequence (blank groups) and blank load transfection (blank load groups) were assigned as the control groups. The expression of Id‐1 in six groups was detected by reverse transcription‐polymerase chain reaction (RT‐PCR) and Western blot. Cell proliferation in vitro was assessed by MTT assay. RT‐PCR and Western blot results demonstrated that the mRNA and protein expressions of Id‐1 in the inhibition group 1 were lower than those in the blank group 1 and blank load group 1. RT‐PCR and Western blot results revealed that the mRNA and protein expressions of Id‐1 were lower in the inhibition group 2 than in the blank group 2 and blank load group 2. The results of the growth curve revealed that proliferation ability was significantly weaker from the third day in the inhibition groups 1 and 2 than in the blank group and blank load group. Transwell chamber experiment and Matrigel invasion assay revealed that the number of Transwell cells significantly decreased in the inhibition groups 1 and 2 than in the blank groups and blank load groups (P < 0.01). Id‐1 significantly promotes the proliferation and migration of human colon carcinoma cell lines SW480 and HT‐29.

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Prostate cancer cells modulate osteoblast mineralisation and osteoclast differentiation through Id-1

Cited by 20 publications

References 56 publications

Tasquinimod inhibits prostate cancer growth in bone through alterations in the bone microenvironment

Tasquinimod inhibits prostate cancer growth in bone through alterations in the bone microenvironment

Polyomavirus enhancer activator 3 protein promotes breast cancer metastatic progression through Snail‐induced epithelial–mesenchymal transition

A study of the impact of inhibitors of DNA binding‐1 on proliferation and migration in human colon carcinoma cells

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