scholarly journals Olig2 regulates p53-mediated apoptosis, migration and invasion of melanoma cells

2021 ◽  
Vol 11 (1) ◽  
Author(s):  
Ji Eun Lee ◽  
Sungjin Ahn ◽  
Haengdueng Jeong ◽  
Seungchan An ◽  
Cheol Hwan Myung ◽  
...  
Keyword(s):  
Transcription Factor ◽  
Enzyme Activity ◽  
Malignant Cell ◽  
Melanoma Cells ◽  
Migration And Invasion ◽  
High Recurrence Rate ◽  
Metastatic Progression ◽  
Helix Loop Helix ◽  
The Central Nervous System

AbstractMelanoma is a disease with a high recurrence rate and poor prognosis; therefore, the need for targeted therapeutics is steadily increasing. Oligodendrocyte transcription factor2 (Olig2) is a basic helix-loop-helix transcription factor that is expressed in the central nervous system during embryonic development. Olig2 is overexpressed in various malignant cell lines such as lung carcinoma, glioma and melanoma. Olig2 is known as a key transcription factor that promotes tumor growth in malignant glioma. However, the role of Olig2 in melanoma is not well characterized. We analyzed the role of Olig2 in apoptosis, migration, and invasion of melanoma cells. We confirmed that Olig2 was overexpressed in melanoma cells and tissues. Reduction of Olig2 increased apoptosis in melanoma cells by increasing p53 level and caspase-3/-7 enzyme activity. In addition, downregulation of Olig2 suppressed migration and invasion of melanoma cells by inhibiting EMT. Reduction of Olig2 inhibited expression of MMP-1 and the enzyme activity of MMP-2/-9 induced by TGF-β. Moreover, Olig2 was involved in the downstream stages of MEK/ERK and PI3K/AKT, which are major signaling pathways in metastatic progression of melanoma. In conclusion, this study demonstrated the crucial roles of Olig2 in apoptosis, migration, and invasion of melanoma and may help to further our understanding of the relationship between Olig2 and melanoma progression.

Transcription factor STAT1 promotes the proliferation, migration and invasion of nasopharyngeal carcinoma cells by upregulating LINC01160

2020 ◽  
Author(s):  
Jingang Ai ◽  
Guolin Tan ◽  
Tiansheng Wang ◽  
Wei Li ◽  
Ru Gao ◽  
...  
Keyword(s):  
Transcription Factor ◽  
Nasopharyngeal Carcinoma ◽  
Chromatin Immunoprecipitation ◽  
Malignant Cell ◽  
Carcinoma Cells ◽  
Migration And Invasion ◽  
Cell Phenotype

Aim: To investigate the role of LINC01160 in nasopharyngeal carcinoma (NPC). Materials & methods: Using NPC cells CNE-2 and HNE-2 in vitro, we performed quantitative PCR to determine mRNA expression and western blotting to determine protein expression. CCK-8, transwell, flow cytometry and wound healing assays were done to examine the function of LINC01160 and STAT1. Chromatin immunoprecipitation PCR (ChIP-PCR) confirmed that STAT1 combines with the LINC01160 promoter region. Xenograft experiments were used to verify the role of STAT1 and LINC01160 in vivo. Results: LINC01160 is upregulated in NPC and can promote a malignant cell phenotype. STAT1 is a transcription factor of LINC01160 and can promote a malignant cell phenotype through upregulating LINC01160 expression. Conclusion: STAT1 can promote a malignant cell phenotype by upregulating LINC01160.

scholarly journals Drosophila Zic family member odd-paired is needed for adult post-ecdysis maturation

Open Biology ◽  
2019 ◽  
Vol 9 (12) ◽  
pp. 190245
Author(s):  
Eléanor Simon ◽  
Sergio Fernández de la Puebla ◽  
Isabel Guerrero
Keyword(s):  
Central Nervous System ◽  
Nervous System ◽  
Transcription Factor ◽  
Drosophila Melanogaster ◽  
Family Member ◽  
Ectopic Expression ◽  
Functional Conservation ◽  
The Central Nervous System ◽  
Behavioural Sequence

Specific neuropeptides regulate in arthropods the shedding of the old cuticle (ecdysis) followed by maturation of the new cuticle. In Drosophila melanogaster , the last ecdysis occurs at eclosion from the pupal case, with a post-eclosion behavioural sequence that leads to wing extension, cuticle stretching and tanning. These events are highly stereotyped and are controlled by a subset of crustacean cardioactive peptide (CCAP) neurons through the expression of the neuropeptide Bursicon (Burs). We have studied the role of the transcription factor Odd-paired (Opa) during the post-eclosion period. We report that opa is expressed in the CCAP neurons of the central nervous system during various steps of the ecdysis process and in peripheral CCAP neurons innerving the larval muscles involved in adult ecdysis. We show that its downregulation alters Burs expression in the CCAP neurons. Ectopic expression of Opa, or the vertebrate homologue Zic2 , in the CCAP neurons also affects Burs expression, indicating an evolutionary functional conservation. Finally, our results show that, independently of its role in Burs regulation, Opa prevents death of CCAP neurons during larval development.

scholarly journals Dual, enzymatic and non-enzymatic, function of ecto-5'-nucleotidase (eN, CD73) in migration and invasion of A375 melanoma cells.

2012 ◽  
Vol 59 (4) ◽  
Author(s):  
Rafal Sadej ◽  
Andrzej C Skladanowski
Keyword(s):  
Cell Interaction ◽  
Melanoma Cells ◽  
Migration And Invasion ◽  
Extracellular Adenosine ◽  
Enzymatic Function ◽  
Ecm Proteins ◽  
A375 Melanoma ◽  
Formation Of Complexes ◽  
Strength Of Adhesion

Ecto-5'-nucleotidase (eN, CD73) mediates extracellular adenosine production from 5'-AMP. Non-enzymatic functions of eN have also been reported. The aim of the study was to investigate the role of ecto-5'-nucleotidase in aggressive melanoma behaviour. Analysis of the involvement of eN in adhesion, migration and invasion revealed eN functions unknown to date. We found that following eN blockade by concanavalin A, the strength of adhesion to different ECM proteins was not altered, but at the same time the invasion ability of the cells was decreased. On the other hand, knocking down eN in melanoma cells did not influence cell invasion but abolished their migration on tenascin C (TnC). Ecto-5'-nucleotidase seems to fulfil a more distinct role as a receptor than as an enzyme in the cell interaction and mobility on TnC. Ecto-5'-nucleotidase activates also focal adhesion kinase and enhances the formation of complexes upon cell adhesion to TnC. All these observations prove that an eN-TnC complex is involved in cell migration and invasion and thus in the regulation of melanoma progression.

scholarly journals Multifaceted Functional Role of Semaphorins in Glioblastoma

2019 ◽  
Vol 20 (9) ◽  
pp. 2144 ◽  
Author(s):  
Cristiana Angelucci ◽  
Gina Lama ◽  
Gigliola Sica
Keyword(s):  
Axon Guidance ◽  
Treatment Options ◽  
Migration And Invasion ◽  
Tumor Type ◽  
Metastatic Progression ◽  
Oncogenic Pathways ◽  
Membrane Bound ◽  
Wide Group

Glioblastoma (GBM) is the most malignant tumor type affecting the adult central nervous system. Despite advances in therapy, the prognosis for patients with GBM remains poor, with a median survival of about 15 months. To date, few treatment options are available and recent trials based on the molecular targeting of some of the GBM hallmark pathways (e.g., angiogenesis) have not produced any significant improvement in overall survival. The urgent need to develop more efficacious targeted therapies has led to a better molecular characterization of GBM, revealing an emerging role of semaphorins in GBM progression. Semphorins are a wide group of membrane-bound and secreted proteins, originally identified as axon guidance cues, signaling through their receptors, neuropilins, and plexins. A number of semaphorin signals involved in the control of axonal growth and navigation during development have been found to furthermore participate in crosstalk with different dysfunctional GBM pathways, controlling tumor cell proliferation, migration, and invasion, as well as tumor angiogenesis or immune response. In this review, we summarize the regulatory activities mediated by semaphorins and their receptors on the oncogenic pathways implicated in GBM growth and invasive/metastatic progression.

Pharmacological Inhibition of USP7 Supresses Growth and Metastasis of Melanoma Cells in Vitro and in Vivo

2020 ◽  
Author(s):  
Minmin Xiang ◽  
Long Liang ◽  
Xinwei Kuang ◽  
Zuozhong Xie ◽  
Jing Liu ◽  
...  
Keyword(s):  
Scratch Test ◽  
Resistance Mechanisms ◽  
Melanoma Cells ◽  
Migration And Invasion ◽  
Western Blot Assay ◽  
Novel Therapeutic Strategies ◽  
Novel Therapeutic

Abstract Background: Melanoma is a highly aggressive type of skin cancer. Due to the development of diverse resistance mechanisms and severe adverse side effects, significantly limits the efficiency of current therapeutic approaches. Identification of the new therapeutic targets involved in the pathogenesis will benefit to develop novel therapeutic strategies. The deubiquitinase USP7(ubiquitin-specific protease-7) is deregulated in serval cancer types, as a potential target for cancer treatment, but its role in melanoma is still unclear. Here, we investigated the role of USP7 and its inhibitor P22077 in melanoma treatment.Methods: To explore the role of USP7 and the anti-tuomr effect of P22077 in melanma progression and metastasis, a series of cell biological, molecular and biochemical approaches were used for in vitro and in vivo investigations.These methods included RT-qPCR, Western blot assay, cell transfection, CCK8 assay, flow cytometry, scratch test, Transwell assay, mouse xenograft,TUNEL staining.Results:The USP7 inhibitor P22077 suppressed the growth of melanoma in vitro and in vivo. additionally, P22077 induction of cell cycle arrest and apoptosis via ROS(reactive oxygen species) accumulation-induced DNA damage. Furthermore, inhibition of USP7 also prevented migration and invasion of melanoma cells in vitro and in vivo by decrease the Wnt/β-catenin signal pathway. Conclusion: Our data indicated that USP7 acts as an oncogene involved in melanoma cell proliferation and metastasis and may provide a novel therapeutic target for melanoma treatment.

Elucidating the role of the FoxO3a transcription factor in the IGF-1-induced migration and invasion of uveal melanoma cancer cells

2016 ◽  
Vol 84 ◽  
pp. 1538-1550 ◽  
Author(s):  
Fengxia Yan ◽  
Rifang Liao ◽  
Mohd Farhan ◽  
Tinghuai Wang ◽  
Jiashu Chen ◽  
...  
Keyword(s):  
Transcription Factor ◽  
Cancer Cells ◽  
Uveal Melanoma ◽  
Migration And Invasion ◽  
Melanoma Cancer

scholarly journals Empty Spiracles Homeobox 2 (EMX2) Inhibits the Invasion and Tumorigenesis in Colorectal Cancer Cells

2017 ◽  
Vol 25 (4) ◽  
pp. 537-544 ◽  
Author(s):  
Yan Zhang ◽  
Gang Cao ◽  
Qing-gong Yuan ◽  
Jun-hui Li ◽  
Wen-Bin Yang
Keyword(s):  
Colorectal Cancer ◽  
Transcription Factor ◽  
Essential Role ◽  
Migration And Invasion ◽  
Human Colorectal Cancer ◽  
Potential Therapeutic Target ◽  
Colorectal Cancer Cells ◽  
Proliferation In Vitro

Empty spiracles homeobox 2 (EMX2) is a homeodomain-containing transcription factor that plays an essential role in tumorigenesis. However, to the best of our knowledge, the role of EMX2 in human colorectal cancer (CRC) is still unclear. Thus, the aim of this study was to investigate the expression and role of EMX2 in CRC. Our results demonstrated that the expression of EMX2 was greatly decreased in CRC tissues and cell lines. Overexpression of EMX2 significantly inhibited the proliferation in vitro and CRC tumor growth in nude mice. In addition, EMX2 also inhibited the migration and invasion of CRC cells. Mechanically, overexpression of EMX2 downregulated the expression levels of β-catenin, cyclin D1, and c-Myc in CRC cells. Taken together, our study demonstrates that EMX2 inhibits proliferation and tumorigenesis through inactivation of the Wnt/β-catenin pathway in CRC cells. Therefore, EMX2 may be a potential therapeutic target for the treatment of CRC.

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