Tissue inhibitor of metalloproteinase 2 inhibits activation of the β-catenin signaling in melanoma cells

Xia, Yuxuan; Wu, Shaoping

doi:10.1080/15384101.2015.1030557

Cited by 22 publications

(17 citation statements)

References 60 publications

(45 reference statements)

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“…These findings are similar to the previously reported effects of NE and miR‐373 (Kohler et al , 2009; Lesko et al , 2014; Roose et al , 1999). In further support of our findings, previous studies have reported that TIMP2 inhibits Wnt/β‐catenin signaling in melanoma (Xia and Wu, 2015).…”

Section: Discussionsupporting

confidence: 92%

Norepinephrine‐CREB1‐miR‐373 axis promotes progression of colon cancer

Han

Jiang

et al. 2020

Molecular Oncology

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The adrenergic system contributes to the stress-induced onset and progression of cancer. Adrenergic fibers are the primary source of norepinephrine (NE). The underlying mechanisms involved in NE-induced colon cancer remain to be understood. In this study, we describe the function and regulatory network of NE in the progression of colon cancer. We demonstrate that NE-induced phosphorylation of cAMP response element-binding protein 1 (CREB1) promotes proliferation, migration, and invasion of human colon cancer cells. The downstream effector of NE, CREB1, bound to the promoter of miR-373 and transcriptionally activated its expression. miR-373 expression was shown to be necessary for NE-induced cell proliferation, invasion, and tumor growth. We confirmed that proliferation and invasion of colon cancer cells are regulated in vitro and in vivo by miR-373 through targeting of the tumor suppressors TIMP2 and APC. Our data suggest that NE promotes colon cancer cell proliferation and metastasis by activating the CREB1-miR-373 axis. The study of this novel signaling axis may provide mechanistic insights into the neural regulation of colon cancer and help in the design of future clinical studies on stress biology in colorectal cancer.Abbreviations APC, adenomatous polyposis coli; CRC, colorectal cancer; CREB1, cAMP response element-binding protein 1; NE, norepinephrine; qRT-PCR, quantitative real-time polymerase chain reaction; TCGA, The Cancer Genome Atlas; TH, tyrosine hydroxylase; TIMP2, tissue inhibitor of metalloproteinases 2.

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Section: Discussionsupporting

confidence: 92%

Norepinephrine‐CREB1‐miR‐373 axis promotes progression of colon cancer

Han

Jiang

et al. 2020

Molecular Oncology

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“…He et al [25] revealed that exendin-4 inhibit cell growth, migration, and invasion and enhanced apoptosis by inhibiting the PI3K/AKT pathway during OC progression. Additionally, phosphorylation of β-catenin by AKT increases its transcriptional activity, leading to the accumulation of β-catenin in the cytosol and nucleus, and resulting in the activation and expression of downstream target genes, such as MMP2/TIMP-2, which causes cell invasiveness and metastasis [26,27]. In condition, it was revealed that suppressing β-catenin resulted in the decreased expression of c-myc and cyclin D1, and induced antitumor growth effects in OC cells [28,29].…”

Section: Discussionmentioning

confidence: 99%

PRR11 Overexpression Facilitates Ovarian Carcinoma Cell Proliferation, Migration, and Invasion Through Activation of the PI3K/AKT/β-Catenin Pathway

Zhu

Wang

et al. 2018

Cell Physiol Biochem

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Background/Aims: Ovarian cancer (OC) is the most lethal gynecologic malignancy, mainly due to the advanced stage at diagnosis in most patients and high rate of relapse. Thus, it is still essential to elucidate the underlying mechanisms and explore the diagnostic and therapeutic targets of OC. Recent studies have revealed that proline-rich protein 11 (PRR11) is dysregulated in different cancers, participating in their initiation and progression; however, it remains unclear whether PRR11 is involved in OC. Methods: Immunohistochemical staining, quantitative reverse transcription PCR, and western blotting were performed to evaluate PRR11 expression in OC tissues and cells. The relationship between PRR11 expression and the clinicopathologic data of patients were analyzed. We upregulated and downregulated PRR11 expression using a PRR11 overexpression vector and PRR11-specifc small interfering RNA, respectively, to further clarify its role in the malignant biological behavior of OC in vitro. Results: Overexpression of PRR11 in OC tissues and cells significantly correlated with advanced FIGO stage, lymph node metastasis, and large tumor size. Downregulation of PRR11 inhibited cell proliferation and prevented the invasion and migration of HO-8910 OC cells, whereas opposite results were observed in Caov3 cells upon PRR11 upregulation. Further analyses showed that PRR11 positively regulated cell proliferation-related proteins, including c-myc and cyclin D1, and increased and decreased the expression of matrix metalloproteinase 2 and tissue inhibitor of metalloproteinase 2, respectively. Additionally, our preliminary results demonstrated that PRR11 expression was mediated by the phosphoinositide 3-kinase/AKT/β-catenin signaling pathway. Conclusion: The results of this study provide evidence that PRR11 plays a critical role in the progression and metastasis of OC, and as such, may serve as a potential prognostic and therapeutic target in OC.

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“… 50 TIMP-2 elevates E-cadherin expression and inhibits the Wnt/β-catenin pathway, thus suppressing the proliferation of melanoma cells with high activity of β-catenin. 51 In mammary epithelial cells, extracellular TIMP3 functions to inactivate the Wnt-β-catenin pathway, followed by increasing phosphorylated β-catenin levels and decreasing nuclear β-catenin levels. 52 In accord with the above studies, TIMP3, upregulated by BC032913, inhibits nuclear translocation of β-catenin, followed by inactivating the Wnt/β-catenin pathway in our research.…”

Section: Discussionmentioning

confidence: 99%

Long Noncoding RNA BC032913 as a Novel Therapeutic Target for Colorectal Cancer that Suppresses Metastasis by Upregulating TIMP3

Lin

Tan

Qiu

et al. 2017

Molecular Therapy - Nucleic Acids

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SummaryLong noncoding RNAs (lncRNAs) have been shown to play critical roles in the biology of various cancers. However, their expression patterns and biological functions in human colorectal cancer (CRC) remain largely unknown. The aim of this study was to explore lncRNA profiles in CRC and investigate key lncRNAs involved in CRC tumorigenesis and progression. The microarray data of six CRC and matched non-cancerous tissues revealed distinct lncRNA profiles, including 899 upregulated and 1,646 downregulated lncRNAs (p < 0.05, fold change > 2.0). Furthermore, we found that the lncRNA BC032913 was generally underexpressed in 115 CRC samples compared with normal tissues. Reduced BC032913 levels were significantly associated with an advanced tumor, lymph nodes, distant metastasis (TNM) stage and a higher risk of lymph node and distant metastases. BC032913 downregulation indicated poor overall survival in CRC patients. Moreover, BC032913 enhanced the mRNA and protein expression of TIMP3 and inhibited Wnt/β-catenin pathway activity, thus suppressing CRC metastasis in vitro and in vivo. Collectively, the obtained data show that BC032913 plays an inhibitory role in CRC aggression by upregulating TIMP3, followed by inactivation of the Wnt/β-catenin pathway. Our findings indicate that the novel lncRNA BC032913 could serve as a novel prognostic marker and effective therapeutic target for CRC.

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Tissue inhibitor of metalloproteinase 2 inhibits activation of the β-catenin signaling in melanoma cells

Cited by 22 publications

References 60 publications

Norepinephrine‐CREB1‐miR‐373 axis promotes progression of colon cancer

Norepinephrine‐CREB1‐miR‐373 axis promotes progression of colon cancer

PRR11 Overexpression Facilitates Ovarian Carcinoma Cell Proliferation, Migration, and Invasion Through Activation of the PI3K/AKT/β-Catenin Pathway

Long Noncoding RNA BC032913 as a Novel Therapeutic Target for Colorectal Cancer that Suppresses Metastasis by Upregulating TIMP3

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