FRAT1 expression regulates proliferation in colon cancer cells

Zhu, Kongxi; Guo, Jianqiang; Wang, Hongjuan; Yu, Weihua

doi:10.3892/ol.2016.5300

Cited by 6 publications

(5 citation statements)

References 39 publications

(33 reference statements)

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“…The primers were as follows: ARHGAP24, 5′-AACTCCTGTCGCTCTTCTACC-3′ and 5′-GCTGTTGCCCACAAATGTCTC-3′; p53, 5′-CCACCATCCACTACAACTAC-3′ and 5′-AAACACGCACCTCAAAGC −3′; GAPDH, 5′-CACCCACTCCTCCACCTTTG-3′ and 5′-CCACCACCCTGTTGCTGTAG-3′. The RT-qPCR was conducted as the following procedure: cycle 1, 95°C for 10 min; cycle 2 with 40 repeated cycles of 95°C for 15 sec, 60°C for 45 sec, and then 95°C for 15 sec, 60°C for 1 min for one cycle; 95°C for 15 sec, 60°C for 15 sec for one cycle ( 18 , 19 ).…”

Section: Methodsmentioning

confidence: 99%

ARHGAP24 regulates cell ability and apoptosis ofcolorectal cancer cells via the regulation of P53

et al. 2018

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Colorectal cancer is a human malignancy ranked the third highest of the global incidence of malignant tumors. Rho GTPase-activating proteins (RHOGAPs) were identified functional in several processes of tumors. In the present study, through reverse transcription-quantitative PCR (RT-qPCR) and western blot analysis, expression of Rho GTPase-activating protein 24 (ARHGAP24) and p53 was measured in colorectal cancer tissues, which was lower than that in adjacent normal tissues, revealing that ARHGAP24 may be implicated in the progress of colorectal cancer and in vitro, overexpression of ARHGAP24 in LoVo and HCT116 cells inhibited the cell ability and enhanced cell apoptosis, and accompanied with high protein expression of p53, p21 and Bax. Further, addition of p53 inhibitor PFT-α had an antagonistic effect on cell proliferation and apoptosis of LoVo and HCT116 cells induced by ARHGAP24 overexpression. In addition, the expression of p21 and Bax was positively correlated with p53 expression. All of the above data demonstrated that ARHGAP24 was likely to be a tumor suppressor in colorectal cancer and may function closely related to p53, p21 and Bax. We inferred that ARHGAP24 may be a novel target for in-depth study of colorectal cancer.

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Section: Methodsmentioning

confidence: 99%

ARHGAP24 regulates cell ability and apoptosis ofcolorectal cancer cells via the regulation of P53

et al. 2018

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“…The gene is involved in the process of carcinogenesis in CRC by the Wnt/β-catenin pathway. According to Zhu et al, FRAT1 regulates the proliferation in colon cancer cells and constitutes a potential target for the treatment of CRC (Zhu et al 2016 ).…”

Section: Discussionmentioning

confidence: 99%

SNP array genomic analysis of matched pairs of brain and liver metastases in primary colorectal cancer

Brandt,

Holland,

Wallenborn

et al. 2023

J Cancer Res Clin Oncol

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Purpose Brain metastasis formation is a rare and late event in colorectal cancer (CRC) patients and associated with poor survival. In contrast to other metastatic sites, the knowledge on chromosomal aberrations in brain metastases is very limited. Methods Therefore, we carried out single nucleotide polymorphism (SNP) array analyses on matched primary CRC and brain metastases of four patients as well as on liver metastases of three patients. Results Brain metastases showed more chromosomal aberrations than primary tumors or liver metastases. Commonly occurring aberrations were gain of 8q11.1-q24.3 (primary CRC), gain of 13q12.13-q12.3 (liver metastases), and gain of 20q11.1-q13.33 (brain metastases). Furthermore, we found one copy-neutral loss of heterozygosity (cn-LOH) region on chromosome 3 in primary CRC, three cn-LOH regions in liver metastases and 23 cn-LOH regions in brain metastases, comprising 26 previously undescribed sites. Conclusion The more frequent occurrence of cn-LOHs and subsequently affected genes in brain metastases shed light on the pathophysiology of brain metastasis formation. Further pairwise genetic analyses between primary tumors and their metastases will help to define the role of affected genes in cn-LOH regions.

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“…Therefore, the identification of novel biomarkers and an ------------------------------------------------------------------------------------------------------------------------------- The Wnt/β-catenin signaling pathway is highly conserved in metazoan organisms and serves a critical role in embryonic development and carcinogenesis (36,37). as a positive regulator of Wnt/β-catenin signaling, FraT1 is highly upregulated in various human cancers, such as non-small cell lung cancer (nSclc) (17,38), chondrosarcoma (39), ovarian cancer (18), colon cancer (19), gastric cancer (12) and esophageal cancer (20). This upregulation commonly leads to high malignant potential, growth to the point of lethality, and subsequently, poor patient prognosis in these diseases.…”

Section: Discussionmentioning

confidence: 99%

“…FraT1 positively regulates the Wnt/β-catenin signaling pathway by inhibiting the activity of GSK-3β toward β-catenin (14)(15)(16). aberrant activation of FraT1 promotes Wnt/β-catenin signaling pathway dysregulation and FraT1 is highly upregulated in a variety of human cancers (12,(17)(18)(19)(20). our previous study demonstrated that FraT1 is an important factor for the development of gliomas, as well as for predicting patient prognosis.…”

Section: Introductionmentioning

confidence: 98%

FRAT1 promotes the angiogenic properties of human glioblastoma cells via VEGFA

et al. 2022

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Glioblastoma is a common central nervous system tumor and despite considerable advancements in treatment patient prognosis remains poor. Angiogenesis is a significant prognostic factor in glioblastoma, anti-angiogenic treatments represent a promising therapeutic approach. Vascular endothelial growth factor a (VeGFa) is a predominant regulator of angiogenesis and mounting evidence suggests that the Wnt signaling pathway serves a significant role in tumor angiogenesis. as a positive regulator of the Wnt/β-catenin signaling pathway, frequently rearranged in advanced T-cell lymphomas-1 (FraT1) is highly expressed in human glioblastoma and is significantly associated with glioblastoma growth, invasion and migration, as well as poor patient prognosis. Bioinformatics analysis demonstrated that both VeGFa and FraT1 were highly expressed in most tumor tissues and associated with prognosis. However, whether and how FraT1 is involved in angiogenesis remains to be elucidated. in the present study, the relationship between FraT1 and VeGFa in angiogenesis was investigated using the human glioblastoma u251 cell line. Small interfering rnas (sirnas) were used to silence FraT1 expression in u251 cells, and the mrna and protein expression levels of VeGFa, as well as the concentration of VeGFa in u251 cell supernatants, were determined using reverse transcription-quantitative Pcr, western blotting and eliSa. a tube formation assay was conducted to assess angiogenesis. The results demonstrated that siRNA knockdown significantly decreased the protein expression levels of FraT1 in u251 cells and markedly decreased the mrna and protein expression levels of VeGFa. Furthermore, the concentration of VeGFa in the cell supernatant was significantly reduced and angiogenesis was suppressed. These results suggested that FraT1 may promote VeGFa secretion and angiogenesis in human glioblastoma cells via the Wnt/β-catenin signaling pathway, supporting the potential use of FraT1 as a promising therapeutic target in human glioblastoma.

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FRAT1 expression regulates proliferation in colon cancer cells

Cited by 6 publications

References 39 publications

ARHGAP24 regulates cell ability and apoptosis ofcolorectal cancer cells via the regulation of P53

ARHGAP24 regulates cell ability and apoptosis ofcolorectal cancer cells via the regulation of P53

SNP array genomic analysis of matched pairs of brain and liver metastases in primary colorectal cancer

FRAT1 promotes the angiogenic properties of human glioblastoma cells via VEGFA

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