GALNT6 Promotes Tumorigenicity and Metastasis of Breast Cancer Cell via β-catenin/MUC1-C Signaling Pathway

Mao, Yihua; Zhang, Yuqi; Fan, Sairong; Chen, Lvao; Tang, Lili; Chen, Xiaoming; Lyu, Jianxin

doi:10.7150/ijbs.29048

Cited by 27 publications

(23 citation statements)

References 38 publications

(40 reference statements)

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“…The culture medium was supplemented with 10% FBS. When the cells reached a confluence of 90%, the blocks were removed and the width was photographed using an optical microscope (Leica Microsystems GmbH; magnification, ×40) and measured at 24, 48 and 72 h. The gap closure values were calculated as follows: Percentage of gap closure= 1 -(width t /width 0 ) ×100% (36).…”

Section: Methodsmentioning

confidence: 99%

Amyloid precursor protein promotes the migration and invasion of breast cancer cells by regulating the MAPK signaling pathway

Xiong

Chen

2019

Int J Mol Med

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To verify whether amyloid precursor protein (APP) affects the migration and invasion of breast cancer cell lines, and to understand its underlying mechanisms, epithelial-mesenchymal transition (EMT), the mitogen-activated protein kinase (MAPK) signaling pathway and the matrix metalloproteinase (MMP) family were investigated in MDA-MB-231, MCF-7 and BT474 human breast cancer cells. Breast cancer cell lines were transfected with plasmids containing APP coding sequences (pEGFP-n1-APP) and APP short hairpin RNA (pENTR APP shRNA). APP overexpres-sion efficiency, knockout efficiency and the expression levels of related genes were tested using reverse transcription-quantitative PCR (RT-qPCR) and western blot analyses. The effects of APP and mitogen-activated protein kinase kinase (MEK) inhibitor on cell migration and invasion were examined using Transwell assays. The results demonstrated that APP was significantly upregulated in the pEGFP-n1-APP group (P<0.05), and significantly downregulated in the pENTR APP shRNA group (P<0.05), compared with the control group. APP overexpression increased the migratory and invasive ability of human breast cancer cells (P<0.05), whereas APP silencing significantly inhibited cell migration and invasion (P<0.05). RT-qPCR and western blot analysis results suggested that APP overexpression significantly increased the expression of MMP-9, MMP-2, MMP-3, N-cadherin and vimentin (P<0.05). In addition, the enhanced expression of APP markedly affected the phosphorylation of mitogen-activated protein kinase kinase kinase 11 (MLK3), mitogen-activated protein kinase kinase 4 (MEK4) and mitogen-activated protein kinase 10 (JNK3; P<0.05). Additionally, APP overexpression had no effect on the total expression levels of MLK3, MEK4, and JNK3; however, APP overexpression significantly decreased the expression levels of E-cadherin and cytokeratin (P<0.05). Conversely, APP silencing had the opposite effects. When cells were treated with the MEK inhibitor PD0325901, the expression of APP was not altered, nor was the expression levels of MEK and its upstream signaling molecules. Taken together, the present findings suggested that APP could affect the migration and invasion of human breast cancer cells by mediating the activation of the MAPK signaling pathway, thereby promoting the EMT process.

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Section: Methodsmentioning

confidence: 99%

Amyloid precursor protein promotes the migration and invasion of breast cancer cells by regulating the MAPK signaling pathway

Xiong

Chen

2019

Int J Mol Med

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“…CREB mediates the activation of cAMP-responsive genes by binding as a dimer to a conserved cAMP-responsive element (CRE), TGACGTCA [37,38] .Mayr and Marc Montminy had predicted that PCNA is one of the target genes containing consensus sites for CREB binding [34]. PCNA is a kind of cycle-related protein that is an indicator of tumour proliferation and is related to the occurrence of early cancer and tumour progression [39,40]. Its main function is to participate in DNA replication, and it is also involved in DNA excision repair cell cycle control chromatin assembly and RNA transcription [41].…”

Section: Discussionmentioning

confidence: 99%

The Novel Transcription Factor CREB3L4 Contributes to the Progression of Human Breast Carcinoma

Qian

Wang

et al. 2020

J Mammary Gland Biol Neoplasia

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Breast carcinoma(BC)is the most common cancer type among females globally. Understanding the molecular pathways that trigger the development of BC is crucial for both prevention and treatment. As such, the role of transcription factors (TFs) in the development of BC is a focal point in this field. CREB3s play a critical role in initiating the unfolded protein response (UPR); however, the role of CREB3 family members in breast cancer development remains largely unknown. Here, we mined the ONCOMINE database for the transcriptional data of CREB3s in patients with BC. Then, the regulatory functions of a novel TF, CREB3L4, were investigated. CREB3L4 knockdown in MDA-MB-231 and MCF-7 cells suppressed proliferation and promoted apoptosis and cell cycle arrest. ChIP assays confirmed that CREB3L4 can directly bind to the PCNA promoter region, suggesting that the PCNA protein may be functionally downstream of CREB3L4. Additionally, the expression level of CREB3L4 was assessed using our cohort. CREB3L4 is upregulated in breast cancer tissues and is significantly associated with histological grade and tumour size (P = 0.001 and P < 0.001, respectively). Furthermore, PCNA expression was upregulated in breast cancer tissues and positively correlated with CREB3L4. In summary, CREB3L4 may play an important role in the progression of human BC and may serve as a therapeutic target.

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“…These forms are combined with decreased levels of core 3 and core 4 structures (6,69,70) (Fig. 2); their presence is predominantly associated with changes in the expression levels of different glycosyltransferases (71,72). For example, the activity of The reaction is catalyzed by ppGalNAcT enzymes and results in the formation of the Tn antigen (GalNAcα1-O-Ser/Thr).…”

Section: Muc1 In Cancermentioning

confidence: 99%

MUC1 is an oncoprotein with a significant role in apoptosis (Review)

Supruniuk

Radziejewska

2021

Int J Oncol

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Mucin 1 (MUC1) is a membrane-bound, highly glycosylated protein that is overexpressed in all stages of malignant transformation. Overexpression of MUC1 together with loss of polarization and hypoglycosylation are associated with resistance to apoptosis, which is the process that results in efficient removal of damaged cells. Inhibition of the apoptotic process is responsible for tumor development, tumor progression and drug resistance. MUC1 is considered as an oncogenic molecule that is involved in various signaling pathways responsible for the regulation of apoptosis. Based on this, the aim of the present study was to discuss the involvement of MUC1 in the divergent mechanisms regulating programmed cell death. Contents 1. Introduction 2. Apoptosis 3. MUC1 as a cancer-associated membrane-bound molecule 4. Role of MUC1 in apoptosis 5. Conclusions

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GALNT6 Promotes Tumorigenicity and Metastasis of Breast Cancer Cell via β-catenin/MUC1-C Signaling Pathway

Cited by 27 publications

References 38 publications

Amyloid precursor protein promotes the migration and invasion of breast cancer cells by regulating the MAPK signaling pathway

Amyloid precursor protein promotes the migration and invasion of breast cancer cells by regulating the MAPK signaling pathway

The Novel Transcription Factor CREB3L4 Contributes to the Progression of Human Breast Carcinoma

MUC1 is an oncoprotein with a significant role in apoptosis (Review)

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