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You searched for subject:( SND1). Showing records 1 – 3 of 3 total matches.

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Virginia Commonwealth University

1. Mckiver, Bryan D. SND1-Targeted Gene Therapy for Hepatocellular Carcinoma.

Degree: MS, Molecular Biology and Genetics, 2018, Virginia Commonwealth University

Staphylococcal nuclease and tudor-domain containing 1 (SND1) is an oncogene for a wide variety of cancers, including hepatocellular carcinoma (HCC). SND1 is a multifunctional protein regulating gene expression of proto-oncogenes and tumor suppressor genes, making SND1 a prime target for developing cancer therapeutics. This notion is especially attributed to HCC as most patients are diagnosed in advanced stages and the therapeutic options available for these patients are severely limited. In this study, we evaluated the therapeutic potential of a replication-defective adenovirus vector delivering SND1 shRNA (Ad.SND1sh) to human HCC cell lines, HepG3, HuH-7, and Hep3B. Adenovirus infection in HCC cells was confirmed by Western blotting and immunofluorescence. The efficacy of Ad.SND1sh to knockdown SND1 expression was confirmed via Western blot, qRT-PCR, and immunofluorescence. Ad.SND1sh did not significantly affect proliferation of the three human HCC cells but significantly inhibited their invasive and migratory capacities, as determined by wound healing and Matrigel invasion assays, respectively. As a corollary, Ad.SND1sh treatment resulted in a decrease in mesenchymal markers, such as N-cadherin, Twist, Snail, and Slug, without affecting levels of epithelial marker E-Cadherin, indicating that SND1 knockdown induces mesenchymal conversion in HCC cells. Additionally, reductions in liver cancer stem cell marker CD133 and HCC marker α-fetoprotein (AFP) were observed with SND1 knockdown. HCC cells with aberrant expression of these markers are associated with tumor initiation, recurrence, and multi-drug resistance. Our findings indicate that Ad.SND1sh may potentially be an effective therapy for advanced HCC and needs to be studied further for its clinical application. Advisors/Committee Members: Devanand Sarkar, Zheng Fu, Michael McVoy.

Subjects/Keywords: SND1; Hepatocellular Carcinoma; HCC; Gene Therapy; Tudor-SN; Genetics; Molecular Genetics

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APA · Chicago · MLA · Vancouver · CSE | Export to Zotero / EndNote / Reference Manager

APA (6th Edition):

Mckiver, B. D. (2018). SND1-Targeted Gene Therapy for Hepatocellular Carcinoma. (Thesis). Virginia Commonwealth University. Retrieved from https://doi.org/10.25772/MSEN-5231 ; https://scholarscompass.vcu.edu/etd/5676

Note: this citation may be lacking information needed for this citation format:
Not specified: Masters Thesis or Doctoral Dissertation

Chicago Manual of Style (16th Edition):

Mckiver, Bryan D. “SND1-Targeted Gene Therapy for Hepatocellular Carcinoma.” 2018. Thesis, Virginia Commonwealth University. Accessed December 05, 2020. https://doi.org/10.25772/MSEN-5231 ; https://scholarscompass.vcu.edu/etd/5676.

Note: this citation may be lacking information needed for this citation format:
Not specified: Masters Thesis or Doctoral Dissertation

MLA Handbook (7th Edition):

Mckiver, Bryan D. “SND1-Targeted Gene Therapy for Hepatocellular Carcinoma.” 2018. Web. 05 Dec 2020.

Vancouver:

Mckiver BD. SND1-Targeted Gene Therapy for Hepatocellular Carcinoma. [Internet] [Thesis]. Virginia Commonwealth University; 2018. [cited 2020 Dec 05]. Available from: https://doi.org/10.25772/MSEN-5231 ; https://scholarscompass.vcu.edu/etd/5676.

Note: this citation may be lacking information needed for this citation format:
Not specified: Masters Thesis or Doctoral Dissertation

Council of Science Editors:

Mckiver BD. SND1-Targeted Gene Therapy for Hepatocellular Carcinoma. [Thesis]. Virginia Commonwealth University; 2018. Available from: https://doi.org/10.25772/MSEN-5231 ; https://scholarscompass.vcu.edu/etd/5676

Note: this citation may be lacking information needed for this citation format:
Not specified: Masters Thesis or Doctoral Dissertation


Virginia Commonwealth University

2. Jariwala, Nidhi. SND1 mediated downregulation of PTPN23 in HCC.

Degree: MS, Human Genetics, 2014, Virginia Commonwealth University

SND1 MEDIATED DOWNREGULATION OF PTPN23 IN HEPATOCELLULAR CARCINOMA By Nidhi Jariwala, MS A thesis submitted in partial fulfillment of the requirements for the degree of Master of Science at Virginia Commonwealth University, 2014. ADVISOR: Dr. Devanand Sarkar Associate Professor, Department of Human and Molecular Genetics Blick Scholar Associate Scientific Director, Cancer Therapeutics VCU Institute of Molecular Medicine Massey Cancer Center ABSTRACT Staphyloccocal nuclease domain containing protein 1 (SND1) is identified as an oncogene in multiple cancers, including hepatocellular carcinoma (HCC). SND1 regulates gene expression at transcriptional as well as post-transcriptional level and mediates molecular pathways that culminate into carcinogenesis. SND1 is a component of RNA-induced silencing complex (RISC) and functions as a nuclease for RNAi-mediated mRNA degradation. On the other hand SND1 also binds to specific mRNAs, increasing their stability and hence expression. The aim of the present study is to identify mRNAs to which SND1 binds and modulates them either by degradation or increasing stability which might facilitate promotion of HCC by SND1. We performed RNA immunoprecipitation followed by RNA sequencing (RIP-Seq) using anti-SND1 antibody and human HCC cell line QGY-7703. More than 350 mRNAs were identified to be interacting with SND1, of which Protein tyrosine phosphatase non-receptor 23 (PTPN23) was of particular interest, since PTPN23 has been identified to be a tumor suppressor and its role in HCC has not been studied. We document that SND1 can bind to PTPN23 mRNA and induce its degradation. There is an inverse correlation between SND1 and PTPN23 levels in human HCC cell lines and PTPN23 level is downregulated in HCC. Our study thus identifies a novel mechanism by which SND1 promotes hepatocarcinogenesis and identifies PTPN23 as a potential tumor suppressor in HCC. Further studies need to be performed to explore the relationship of these two molecules in in vivo models and to develop PTPN23 overexpression as a potential therapeutic approach for HCC. Advisors/Committee Members: Dr. Devanand Sarkar.

Subjects/Keywords: HCC; liver cancer; SND1; PTPN23; Genetics; Molecular Genetics

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APA · Chicago · MLA · Vancouver · CSE | Export to Zotero / EndNote / Reference Manager

APA (6th Edition):

Jariwala, N. (2014). SND1 mediated downregulation of PTPN23 in HCC. (Thesis). Virginia Commonwealth University. Retrieved from https://doi.org/10.25772/HA1K-PJ68 ; https://scholarscompass.vcu.edu/etd/3648

Note: this citation may be lacking information needed for this citation format:
Not specified: Masters Thesis or Doctoral Dissertation

Chicago Manual of Style (16th Edition):

Jariwala, Nidhi. “SND1 mediated downregulation of PTPN23 in HCC.” 2014. Thesis, Virginia Commonwealth University. Accessed December 05, 2020. https://doi.org/10.25772/HA1K-PJ68 ; https://scholarscompass.vcu.edu/etd/3648.

Note: this citation may be lacking information needed for this citation format:
Not specified: Masters Thesis or Doctoral Dissertation

MLA Handbook (7th Edition):

Jariwala, Nidhi. “SND1 mediated downregulation of PTPN23 in HCC.” 2014. Web. 05 Dec 2020.

Vancouver:

Jariwala N. SND1 mediated downregulation of PTPN23 in HCC. [Internet] [Thesis]. Virginia Commonwealth University; 2014. [cited 2020 Dec 05]. Available from: https://doi.org/10.25772/HA1K-PJ68 ; https://scholarscompass.vcu.edu/etd/3648.

Note: this citation may be lacking information needed for this citation format:
Not specified: Masters Thesis or Doctoral Dissertation

Council of Science Editors:

Jariwala N. SND1 mediated downregulation of PTPN23 in HCC. [Thesis]. Virginia Commonwealth University; 2014. Available from: https://doi.org/10.25772/HA1K-PJ68 ; https://scholarscompass.vcu.edu/etd/3648

Note: this citation may be lacking information needed for this citation format:
Not specified: Masters Thesis or Doctoral Dissertation


Princeton University

3. Wan, Liling. Dissecting the roles of MTDH/AEG-1 during multiple steps of cancer development .

Degree: PhD, 2014, Princeton University

Growing clinical evidence indicates a strong correlation between MTDH expression and the pathogenesis of many human cancer types, underscoring the potentially broad importance of this molecule in cancer biology. However, fundamental understanding of MTDH in normal development and malignancy is hindered by the lack of physiologically relevant animal models, and the mechanisms of its action remain poorly understood. Here, by generating the first knockout/transgenic mouse models, I dissect Mtdh's function during cancer progression and explore the underlying mechanisms. First, we report that while whole-organism ablation of Mtdh has little effect on normal development in mice, it inhibits mammary tumor formation driven by diverse oncogenes and carcinogen, and this tumorigenic defect in Mtdh-KO mice can be rescued by mammary epithelial cell-specific re-expression of Mtdh. Furthermore, Mtdh is required for oncogene-induced expansion and activities of basal and luminal tumor-initiating cells (TICs) at early tumorigenesis, whereas it is dispensable for normal mammary stem cells. Second, we performed thorough clinical and functional investigation of MTDH in prostate cancer (PCa) progression and metastasis. We found MTDH levels are tightly correlated with human PCa progression, and genomic gain at 8q22, where MTDH resides, is also observed frequently in prostate tumors and is associated with adverse clinical outcome. Functionally, deletion of Mtdh in a PCa mouse model prolongs tumor latency, reduces tumor burden, arrests cancer progression at non-malignant stages, and finally, inhibits systemic metastasis. These clinical and functional data thus establish MTDH as a potential biomarker and therapeutic target for human PCa. Finally, we examined the functional dependency of MTDH on its interacting partner SND1. We solved the crystal structure of MTDH-SND1 complex and uncovered key residues critical for the interaction. Silencing MTDH or SND1 individually, or disrupting their interaction by mutagenesis, impairs the survival and tumorigenenic potential of TICs. Mechanistically, SND1 acts as a survival factor by regulating the expression of pro-survival genes under stress, and MTDH interaction is critical to stabilize SND1 and sustain SND1-dependent survival gene signature. Our study suggests that targeting the MTDH-SND1 interaction may offer an opportunity to control tumor initiation, recurrence and metastasis by regulating cellular survival and TIC activities. Advisors/Committee Members: Kang, Yibin (advisor).

Subjects/Keywords: AEG-1; breast cancer; Metadherin; MTDH; SND1; stem cell

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APA · Chicago · MLA · Vancouver · CSE | Export to Zotero / EndNote / Reference Manager

APA (6th Edition):

Wan, L. (2014). Dissecting the roles of MTDH/AEG-1 during multiple steps of cancer development . (Doctoral Dissertation). Princeton University. Retrieved from http://arks.princeton.edu/ark:/88435/dsp01k930bx182

Chicago Manual of Style (16th Edition):

Wan, Liling. “Dissecting the roles of MTDH/AEG-1 during multiple steps of cancer development .” 2014. Doctoral Dissertation, Princeton University. Accessed December 05, 2020. http://arks.princeton.edu/ark:/88435/dsp01k930bx182.

MLA Handbook (7th Edition):

Wan, Liling. “Dissecting the roles of MTDH/AEG-1 during multiple steps of cancer development .” 2014. Web. 05 Dec 2020.

Vancouver:

Wan L. Dissecting the roles of MTDH/AEG-1 during multiple steps of cancer development . [Internet] [Doctoral dissertation]. Princeton University; 2014. [cited 2020 Dec 05]. Available from: http://arks.princeton.edu/ark:/88435/dsp01k930bx182.

Council of Science Editors:

Wan L. Dissecting the roles of MTDH/AEG-1 during multiple steps of cancer development . [Doctoral Dissertation]. Princeton University; 2014. Available from: http://arks.princeton.edu/ark:/88435/dsp01k930bx182

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