Tumor Endothelial Marker 8 Overexpression In Breast Cancer Cells Enhances Tumor Growth And Metastasis

Opoku-Darko, Michael; Yuen, C.; Gratton, Kathy; Sampson, E.; Bathe, Oliver F.

doi:10.1016/j.jss.2010.11.555

Cited by 3 publications

(3 citation statements)

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“…although previous studies have confirmed that TeM8 knockdown can significantly inhibit tumor growth in numerous cancer types (10,37), the underlying mechanism remains poorly understood. TeM8 antibodies have been reported to reduce tumor growth in mice through an antibody-dependent cellular cytotoxicity mechanism (15).…”

Section: Discussionmentioning

confidence: 98%

Targeted silencing of TEM8 suppresses non‑small cell lung cancer tumor growth via the ERK/Bcl‑2 signaling pathway

et al. 2021

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non-small cell lung cancer (nSclc) is one of the most common malignancies with high rates of mortality. although great progress has been made with the development of novel immunotherapies and targeted therapeutic strategies, the 5-year total survival rate of lung cancer has remained unchanged over the past few decades. Therefore, more effective therapeutics are urgently needed. Tumor endothelial marker 8 (TeM8) is an integrin-like cell surface transmembrane protein that has been demonstrated to be upregulated in numerous cancer types and previously showed promise for targeted cancer therapy. However, the role of TeM8 in nSclc remains poorly understood. The present study aimed to investigate the effects of silencing TeM8 on expression and regulation of extracellular signal-regulated kinase (erK)1/2 signaling pathways in nSclc. in the present study, a lentiviral vector that encoded a short hairpin rna targeting TeM8 was designed and transfected into Xuanwei lung cancer (XWlc)-05 lung cancer cells to silence TeM8 expression. Male BalB/c-nu/nu mice were then given subcutaneous injections in the right dorsal flank with XWLC-05 cells. Microvessel density was measured using an anti-cd34 antibody. The mrna and protein levels of erK1/2 and Bcl-2 in XWlc-05 cells or xenograft tumor tissues were detected by reverse transcription-quantitative polymerase chain reaction and western blotting. TeM8 knockdown was found to significantly inhibit tumor growth and conferred an anti-angiogenic ability in vivo. Furthermore, TeM8 knockdown suppressed the expression of Bcl-2 mediated by erK1/2 activity in XWlc-05 cells or tissues from mice with nSclc. To conclude, these results suggest that the targeted silencing of TeM8 may serve as an effective method of treating nSclc.

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Section: Discussionmentioning

confidence: 98%

Targeted silencing of TEM8 suppresses non‑small cell lung cancer tumor growth via the ERK/Bcl‑2 signaling pathway

et al. 2021

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“…Some studies have shown that the vascular density in high-grade prostate cancer is signi cantly higher than that in low-grade prostate cancer tumors [11], which implicates angiogenesis as a mechanism of prostate cancer progression. TEM8 is speci cally expressed in tumor blood vessels and some tumor cells [12,13] suggesting its potential advantages as an anti-tumor angiogenesis target [14,15]. Even though TEM8 is associated with poor prognosis in several solid tumors [16][17][18][19], little is known about its role in prostate cancer.…”

Section: Introductionmentioning

confidence: 99%

N-Myc Promotes Angiogenesis and Therapeutic Resistance of Prostate Cancer by TEM8

Fang

et al. 2021

Preprint

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Although patients with early localized prostate cancer can achieve a longer survival, castration-resistant prostate cancer (CRPC) has gradually developed with the use of androgen deprivation therapy (ADT). N-Myc and TEM8 play an important role in the progression of several cancer types. However, the underlying mechanism of how N-Myc and TEM8 promote the progression of prostate cancer remains unclear. In this study, the expression of N-Myc and TEM8 were detected in benign prostatic hyperplasia (BPH) and prostate cancer (PCa) tissues by immunohistochemistry (IHC). To find the mechanism of prostate cancer resistance to treatment, LNCaP cell lines were maintained in RPMI 1640 medium supplemented with 10% Charcoal-stripped fetal Bovine Serum. Subsequently, R language software was used to verify our results. Tubule formation assay of human umbilical vein endothelial cell (HUVEC) was conducted to examine the effect of N-Myc and TEM8 overexpression on angiogenesis of prostate cancer cells.IHC results showed a positive correlation between the expression of N-Myc and TEM8 in prostate cancer tissues. Further analysis showed that N-Myc and TEM8 were associated with clinicopathological features and poor prognosis in prostate cancer patients. We found that the overexpression of N-Myc and TEM8 promotes proliferative ability and angiogenesis. Further, N-Myc and TEM8 overexpression was associated with therapeutic resistance. N-Myc promoted angiogenesis and therapeutic resistance in prostate cancer via TEM8. Hence, targeting N-Myc/TEM8 pathway in prostate cancer would be a novel therapeutic strategy to advance the treatment of prostate cancer patients.

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“…17 More recent studies have suggested that the level of TEM8 expression within breast cancer cell lines is correlated with their capacity for growth, invasion, and metastasis, with more aggressive basal-like cells expressing higher levels of TEM8 mRNA and protein. 18 The link between TEM8 and tumorigenesis has also led to interest in manipulating the tumor-specific expression of TEM8 for the selective delivery of toxic or vascular-disrupting agents to tumor sites. 19…”

Section: Introductionmentioning

confidence: 99%

Identification of Small Molecules That Inhibit the Interaction of TEM8 with Anthrax Protective Antigen Using a FRET Assay

et al. 2013

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Tumor marker endothelial 8 (TEM8) is a receptor for the Protective Antigen (PA) component of anthrax toxin. TEM8 is upregulated on endothelial cells lining the blood vessels within tumors, compared to normal blood vessels. A number of studies have demonstrated a pivotal role for TEM8 in developmental and tumor angiogenesis. We have also shown that targeting the anthrax receptors with a mutated form of PA inhibits angiogenesis and tumor formation in vivo. Here we describe the development and testing of a high-throughput fluorescence resonance energy transfer assay to identify molecules that strongly inhibit the interaction of PA and TEM8. The assay we describe is sensitive and robust, with a Z-prime value of 0.8. A preliminary screen of 2310 known bioactive library compounds identified ebselen and thimerosal as inhibitors of the TEM8-PA interaction. These molecules each contain a cysteine-reactive transition metal, and complimentary studies indicate that their inhibition of interaction is due to modification of a cysteine residue in the TEM8 extracellular domain. This is the first demonstration of a high-throughput screening assay that identifies inhibitors of TEM8, with potential application for anti-anthrax and anti-angiogenic diseases.

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Tumor Endothelial Marker 8 Overexpression In Breast Cancer Cells Enhances Tumor Growth And Metastasis

Cited by 3 publications

References 0 publications

Targeted silencing of TEM8 suppresses non‑small cell lung cancer tumor growth via the ERK/Bcl‑2 signaling pathway

Targeted silencing of TEM8 suppresses non‑small cell lung cancer tumor growth via the ERK/Bcl‑2 signaling pathway

N-Myc Promotes Angiogenesis and Therapeutic Resistance of Prostate Cancer by TEM8

Identification of Small Molecules That Inhibit the Interaction of TEM8 with Anthrax Protective Antigen Using a FRET Assay

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