Effect of silencing TEM8 gene on proliferation, apoptosis, migration and invasion of XWLC‑05 lung cancer cells

Gong, Quan; Liu, Chao; Wang, Cunde; Li, Zhuang; Zhang, Lijuan; Wang, Xicai

doi:10.3892/mmr.2017.7959

Cited by 10 publications

(16 citation statements)

References 31 publications

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“…Since angiogenesis is a major hallmark of cancer, researchers have investigated the roles of CMG2 and TEM8 in cancer since their initial discovery. For TEM8, the literature is consistent in that its overexpression results in more aggressive cancer, especially for osteosarcomas 52 , gallbladder carcinomas 53 , melanomas 42 , and lung 54 , breast 55, 56 , and colorectal 57 cancers. However, for CMG2, there are mixed reports of the effect of its overexpression on cancer progression; some show that lower CMG2 correlated with a more aggressive soft-tissue sarcoma 58 and breast cancer 59 , and others reveal that higher CMG2 resulted in a worse survival rate in patients with gastric cancer 60 and glioblastoma 61 .…”

Section: Converging Physiological Functions Of Anthrax Toxin Receptorsmentioning

confidence: 78%

Converging physiological roles of the anthrax toxin receptors

Sergeeva

Goot

2019

F1000Res

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The anthrax toxin receptors—capillary morphogenesis gene 2 (CMG2) and tumor endothelial marker 8 (TEM8)—were identified almost 20 years ago, although few studies have moved beyond their roles as receptors for the anthrax toxins to address their physiological functions. In the last few years, insight into their endogenous roles has come from two rare diseases: hyaline fibromatosis syndrome, caused by mutations in CMG2, and growth retardation, alopecia, pseudo-anodontia, and optic atrophy (GAPO) syndrome, caused by loss-of-function mutations in TEM8. Although CMG2 and TEM8 are highly homologous at the protein level, the difference in disease symptoms points to variations in the physiological roles of the two anthrax receptors. Here, we focus on the similarities between these receptors in their ability to regulate extracellular matrix homeostasis, angiogenesis, cell migration, and skin elasticity. In this way, we shed light on how mutations in these two related proteins cause such seemingly different diseases and we highlight the existing knowledge gaps that could form the focus of future studies.

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Section: Converging Physiological Functions Of Anthrax Toxin Receptorsmentioning

confidence: 78%

Converging physiological roles of the anthrax toxin receptors

Sergeeva

Goot

2019

F1000Res

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“…Therefore, the function of Antxr1 in the proliferation of endothelial cells differs between physiological conditions and cancer angiogenesis. Furthermore, knockdown of Antxr1 reduced the proliferation of osteosarcoma and XWLC05 lung adenocarcinoma cells [31,32]. Thus, Antxr1 positively regulates the proliferation of both endothelial cells in cancer and the cancer cells themselves but negatively regulates endothelial cell proliferation in physiological conditions.…”

Section: Discussionmentioning

confidence: 93%

Antxr1, Which is a Target of Runx2, Regulates Chondrocyte Proliferation and Apoptosis

Jiang

Qin

Yoshida

et al. 2020

IJMS

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Antxr1/Tem8 is highly expressed in tumor endothelial cells and is a receptor for anthrax toxin. Mutation of Antxr1 causes GAPO syndrome, which is characterized by growth retardation, alopecia, pseudo-anodontia, and optic atrophy. However, the mechanism underlying the growth retardation remains to be clarified. Runx2 is essential for osteoblast differentiation and chondrocyte maturation and regulates chondrocyte proliferation through Ihh induction. In the search of Runx2 target genes in chondrocytes, we found that Antxr1 expression is upregulated by Runx2. Antxr1 was highly expressed in cartilaginous tissues and was directly regulated by Runx2. In skeletal development, the process of endochondral ossification proceeded similarly in wild-type and Antxr1–/– mice. However, the limbs of Antxr1–/– mice were shorter than those of wild-type mice from embryonic day 16.5 due to the reduced chondrocyte proliferation. Chondrocyte-specific Antxr1 transgenic mice exhibited shortened limbs, although the process of endochondral ossification proceeded as in wild-type mice. BrdU-uptake and apoptosis were both increased in chondrocytes, and the apoptosis-high regions were mineralized. These findings indicated that Antxr1, of which the expression is regulated by Runx2, plays an important role in chondrocyte proliferation and that overexpression of Antxr1 causes chondrocyte apoptosis accompanied by matrix mineralization.

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“…Moreover, ANTXR1 has previously been found to be specifically expressed in the tumor microenvironment . In the context of cancer, ANTXR1 is upregulated in diverse cancer types and plays an important role in tumor development, such as lung cancer, breast cancer, and gallbladder carcinoma . In addition, Shukla et al observed that ANTXR1 was expressed in 10.4% of T2 tumors, 79.5% of T3 tumors, and 84.8% of T4 tumors .…”

Section: Discussionmentioning

confidence: 99%

Anthrax toxin receptor 1/tumor endothelial marker 8 promotes gastric cancer progression through activation of the PI3K/AKT/mTOR signaling pathway

et al. 2020

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Anthrax toxin receptor 1 (ANTXR1), a type I transmembrane protein, is one of the receptors that facilitates the entrance of anthrax toxin into cells. Previous studies have confirmed the pivotal role of ANTXR1 in progression and tumorigenesis of diverse cancer types. However, the biological function of ANTXR1 in gastric cancer (GC) is still unknown. The present study aimed to investigate the role of ANTXR1 in GC and illuminate the potential molecular mechanisms. Bioinformatics analysis found that ANTXR1 expression was significantly upregulated in GC tissue and its overexpression was associated with poor prognosis of GC patients. Moreover, we confirmed the upregulation of ANTXR1 in GC cell lines and GC tissue by quantitative PCR, western blot analysis, and immunohistochemical analysis. Additionally, high protein expression level of ANTXR1 was positively associated with several clinicopathological parameters in GC patients. In our study, a series of in vitro and in vivo assays were undertaken through strategies of loss/gain-of-function and rescue assays.Consequently, our results indicated that ANTXR1 induced proliferation, cell cycle progression, invasion and migration, and tumorigenicity and induced suppressed apoptosis in GC. Mechanistic investigation indicated that ANTXR1 exerted its promoting effects on GC through activation of the PI3K/AKT/mTOR signaling pathway. In conclusion, our findings suggested that ANTXR1 plays a crucial role in the development and progression of GC and could serve as a novel prognostic biomarker and potential therapeutic target for GC. K E Y W O R D S ANTXR1, EMT, gastric cancer, metastasis, proliferation | 1133 CAI et Al.

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Effect of silencing TEM8 gene on proliferation, apoptosis, migration and invasion of XWLC‑05 lung cancer cells

Cited by 10 publications

References 31 publications

Converging physiological roles of the anthrax toxin receptors

Converging physiological roles of the anthrax toxin receptors

Antxr1, Which is a Target of Runx2, Regulates Chondrocyte Proliferation and Apoptosis

Anthrax toxin receptor 1/tumor endothelial marker 8 promotes gastric cancer progression through activation of the PI3K/AKT/mTOR signaling pathway

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