Angiotensin II type 2 receptor-interacting protein 3a suppresses proliferation, migration and invasion in tongue squamous cell carcinoma via the extracellular signal-regulated kinase-Snai2 pathway

Zhao, Tingting; He, Qiuming; Z, Liu; Ding, Xiaoyun; Zhou, Xiaofeng; Wang, Anxun

doi:10.3892/ol.2015.3898

Cited by 19 publications

(18 citation statements)

References 27 publications

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“…The function of ATIP1 as a TSG in glioma is substantiated by our observation that in glioma cells, elevated ATIP1 expression mitigates proliferation and clonogenic outgrowth as well as migration and invasion ( Figure 3 a–f) as has been demonstrated for several other tumors [ 31 , 32 , 33 ]. ATIP1 dramatically reduced glioma cell motility and enhanced cell adhesion at least partially by the construction of LFACs ( Figure 3 e,f).…”

Section: Discussionsupporting

confidence: 71%

The Tumor Suppressor MTUS1/ATIP1 Modulates Tumor Promotion in Glioma: Association with Epigenetics and DNA Repair

Ranjan

Pandey

Panigrahi

et al. 2021

Cancers

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Glioblastoma (GBM) is a highly aggressive brain tumor. Resistance mechanisms in GBM present an array of challenges to understand its biology and to develop novel therapeutic strategies. We investigated the role of a TSG, MTUS1/ATIP1 in glioma. Glioma specimen, cells and low passage GBM sphere cultures (GSC) were analyzed for MTUS1/ATIP1 expression at the RNA and protein level. Methylation analyses were done by bisulfite sequencing (BSS). The consequence of chemotherapy and irradiation on ATIP1 expression and the influence of different cellular ATIP1 levels on survival was examined in vitro and in vivo. MTUS1/ATIP1 was downregulated in high-grade glioma (HGG), GSC and GBM cells and hypermethylation at the ATIP1 promoter region seems to be at least partially responsible for this downregulation. ATIP1 overexpression significantly reduced glioma progression by mitigating cell motility, proliferation and facilitate cell death. In glioma-bearing mice, elevated MTUS1/ATIP1 expression prolonged their survival. Chemotherapy, as well as irradiation, recovered ATIP1 expression both in vitro and in vivo. Surprisingly, ATIP1 overexpression increased irradiation-induced DNA-damage repair, resulting in radio-resistance. Our findings indicate that MTUS1/ATIP1 serves as TSG-regulating gliomagenesis, progression and therapy resistance. In HGG, higher MTUS1/ATIP1 expression might interfere with tumor irradiation therapy.

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Section: Discussionsupporting

confidence: 71%

The Tumor Suppressor MTUS1/ATIP1 Modulates Tumor Promotion in Glioma: Association with Epigenetics and DNA Repair

Ranjan

Pandey

Panigrahi

et al. 2021

Cancers

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“…DN is overexpressed in ovarian tumors, and contributes to local migration and long-distance metastasis of tumor cells ( 36 ). Additionally, previous reports have indicated that high HMGA2 and ATIP3a expression levels negatively affect the prognosis of patients with ovarian cancer ( 37 , 38 ). The present study demonstrated that matrine significantly suppressed ovarian cancer cell viability, migration and invasion by downregulating MTA-1, FN, ATIP3a and HMGA2 expression levels compared with the control group.…”

Section: Discussionmentioning

confidence: 96%

Matrine inhibits ovarian cancer cell viability and promotes apoptosis by regulating the ERK/JNK signaling pathway via p38MAPK

Liang

Jian-xin

2021

Oncol Rep

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Ovarian cancer displays the highest mortality rate among all types of gynecological cancer worldwide. The survival of patients with ovarian cancer remains poor due to poor responses to anticancer treatments. The present study aimed to investigate the therapeutic effects and potential mechanism underlying matrine in ovarian cancer tissues, ovarian cancer cells and a CAOV-3-derived tumor-bearing mouse model. MTT, migration, invasion, flow cytometry, immunofluorescence and immunohistochemistry assays were performed to assess the inhibitory effects of matrine on ovarian cancer. A xenograft ovarian cancer mouse model was established and treated with matrine or PBS. The results demonstrated that compared with the control group, matrine significantly induced ovarian cancer cell apoptosis by upregulating caspase-8 and Fas cell surface death receptor (Fas) expression levels, and downregulating Bcl-2 and Bcl-xl expression levels. Moreover, compared with the control group, matrine significantly inhibited ovarian cancer cell viability, migration and invasion by downregulating metastasis associated protein-1, fibronectin, angiotensin II type 2 receptor-interacting protein 3a and H high mobility group AT-hook 2 expression levels. Compared with the control group, matrine significantly increased p38MAPK, phosphorylated (p)ERK/ERK and pJNK/JNK expression levels in ovarian cancer cells. p38MAPK knockdown significantly downregulated p38MAPK, pERK/ERK and pJNK/JNK expression levels compared with the control group, which significantly promoted ovarian cancer cell viability, migration and invasion. In vivo experiments demonstrated that compared with the control group, matrine significantly suppressed tumor growth by markedly upregulating p38MAPK, ERK and JNK expression levels. The immunohistochemistry results demonstrated that caspase-8 and Fas expression levels were notably increased, whereas Bcl-2 and Bcl-xl expression levels were obviously decreased in matrine-treated tumors compared with PBS-treated tumors. In conclusion, the present study demonstrated that matrine inhibited ovarian cancer cell viability, migration and invasion, but induced cell apoptosis, suggesting that matrine may serve as a promising anticancer agent for the treatment of ovarian cancer.

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“…30 ATIP3a is also reported to involve ERK signaling pathway that belongs to the family of MAPKs and is downregulated after reconstitution of ATIP3a. 24 In addition, EMT pathway is also associated with ATIP3a-mediated inhibition of tumor growth and progression. 31 In this study, our findings show that reconstitution of ATIP3a inhibits ovarian cancer growth and promotes apoptosis induced by cisplatin.…”

Section: Discussionmentioning

confidence: 99%

“…Lower expression of ATIP3a has been reported in various human cancers. 23,24 We showed that ovarian tumor tissue presented lower ATIP3a expression compared to normal ovarian tissue (Additional file 1-Supplementary Material). This study also investigated the ATIP3a expression in ovarian cancer cells determined by western blotting and RT-qPCR to quantify the expression level.…”

Section: Atip3a Inhibits the Proliferation And Aggressiveness Of Ovarmentioning

confidence: 97%

Angiotensin II type 2 receptor–interacting protein 3a inhibits ovarian carcinoma metastasis via the extracellular HMGA2-mediated ERK/EMT pathway

Huang

Guo

et al. 2017

Tumour Biol.

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Local migration and long-distance metastasis is the main reason for higher mortality of ovarian cancer. Microtubule-associated tumor suppressor 1/angiotensin II type 2 receptor-interacting protein is associated with tumor initiation and progression and exerts anti-tumor effects. High mobility group AT-hook 2 is overexpressed in majority of metastatic carcinomas, which contributes to carcinomas metastasis through Snail-induced epithelial-to-mesenchymal transition signal pathway. The purpose of this study was to investigate the signal pathway of microtubule-associated tumor suppressor 1/angiotensin II type 2 receptor-interacting protein-mediated anti-tumor effects. Our data observed that ovarian carcinoma cells exhibited lower expression of angiotensin II type 2 receptor-interacting protein 3a and higher expression of high mobility group AT-hook 2 compared to normal ovarian cells. Restoration of angiotensin II type 2 receptor-interacting protein 3a expression in ovarian carcinoma cells inhibited high mobility group AT-hook 2 expression and exhibited anti-proliferative effects. In addition, angiotensin II type 2 receptor-interacting protein 3a treatment suppressed the phosphorylation of epithelial-to-mesenchymal transition and extracellular signal-regulated kinase in ovarian carcinoma cells. We also observed that angiotensin II type 2 receptor-interacting protein 3a restoration downregulated expression of Snail, E-Cadherin, N-Cadherin, and Vimentin in ovarian carcinoma cells, whereas angiotensin II type 2 receptor-interacting protein 3a knockdown enhanced the phosphorylation of extracellular signal-regulated kinase and epithelial-to-mesenchymal transition. In vivo assay indicated that angiotensin II type 2 receptor-interacting protein 3a inhibited ovarian tumor growth and elevated survival of tumor-bearing immunodeficient mice. Tumor histological analysis indicated that Snail, E-Cadherin, N-Cadherin, and Vimentin expression levels were downregulated via decreasing high mobility group AT-hook 2 expression. Furthermore, upregulation of angiotensin II type 2 receptor-interacting protein 3a impaired the phenotype of extracellular signal-regulated kinase and epithelial-to-mesenchymal transition in ovarian carcinoma cells and tumor tissues. Taken together, angiotensin II type 2 receptor-interacting protein 3a presents potential in suppressing the proliferation and aggressiveness of ovarian carcinoma cells through the high mobility group AT-hook 2-mediated extracellular signal-regulated kinase/epithelial-to-mesenchymal transition signal pathway.

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Angiotensin II type 2 receptor-interacting protein 3a suppresses proliferation, migration and invasion in tongue squamous cell carcinoma via the extracellular signal-regulated kinase-Snai2 pathway

Cited by 19 publications

References 27 publications

The Tumor Suppressor MTUS1/ATIP1 Modulates Tumor Promotion in Glioma: Association with Epigenetics and DNA Repair

The Tumor Suppressor MTUS1/ATIP1 Modulates Tumor Promotion in Glioma: Association with Epigenetics and DNA Repair

Matrine inhibits ovarian cancer cell viability and promotes apoptosis by regulating the ERK/JNK signaling pathway via p38MAPK

Angiotensin II type 2 receptor–interacting protein 3a inhibits ovarian carcinoma metastasis via the extracellular HMGA2-mediated ERK/EMT pathway

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