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You searched for +publisher:"Virginia Commonwealth University" +contributor:("Dr. Devanand Sarkar"). Showing records 1 – 3 of 3 total matches.

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Virginia Commonwealth University

1. 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 January 15, 2021. 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. 15 Jan 2021.

Vancouver:

Jariwala N. SND1 mediated downregulation of PTPN23 in HCC. [Internet] [Thesis]. Virginia Commonwealth University; 2014. [cited 2021 Jan 15]. 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


Virginia Commonwealth University

2. Binion, Brittany. Sildenafil and celecoxib interact to kill breast cancer cells.

Degree: MS, Biochemistry, 2014, Virginia Commonwealth University

Breast cancer is the second most commonly diagnosed cancer among American women and is responsible for the second highest number of cancer-related deaths. Targeted therapeutic agents sildenafil, a phosphodiesterase type 5 inhibitor, and celecoxib, a cyclooxygenase-2 inhibitor, have been used individually in conjunction with other chemotherapeutic agents to enhance cell killing in a variety of cancers. Sildenafil when combined with traditional chemotherapeutic drugs, such as the taxanes and anthracyclines, or celecoxib combined with traditional hormone therapies have been used to increase cytotoxicity and cell killing. The data presented here demonstrates that the novel combination of sildenafil and celecoxib work together to enhance cell killing in both receptor positive and triple negative breast cancer through the induction of autophagy, ER stress, as well as both intrinsic and extrinsic apoptosis. Advisors/Committee Members: Dr. Paul Dent, Dr. Laurence Booth, Dr. Devanand Sarkar.

Subjects/Keywords: sildenafil; celcoxib; BT474; BT549; breast cancer; Cancer Biology; Neoplasms; Translational Medical Research

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

APA (6th Edition):

Binion, B. (2014). Sildenafil and celecoxib interact to kill breast cancer cells. (Thesis). Virginia Commonwealth University. Retrieved from https://doi.org/10.25772/TGYV-XE12 ; https://scholarscompass.vcu.edu/etd/3580

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):

Binion, Brittany. “Sildenafil and celecoxib interact to kill breast cancer cells.” 2014. Thesis, Virginia Commonwealth University. Accessed January 15, 2021. https://doi.org/10.25772/TGYV-XE12 ; https://scholarscompass.vcu.edu/etd/3580.

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

MLA Handbook (7th Edition):

Binion, Brittany. “Sildenafil and celecoxib interact to kill breast cancer cells.” 2014. Web. 15 Jan 2021.

Vancouver:

Binion B. Sildenafil and celecoxib interact to kill breast cancer cells. [Internet] [Thesis]. Virginia Commonwealth University; 2014. [cited 2021 Jan 15]. Available from: https://doi.org/10.25772/TGYV-XE12 ; https://scholarscompass.vcu.edu/etd/3580.

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

Council of Science Editors:

Binion B. Sildenafil and celecoxib interact to kill breast cancer cells. [Thesis]. Virginia Commonwealth University; 2014. Available from: https://doi.org/10.25772/TGYV-XE12 ; https://scholarscompass.vcu.edu/etd/3580

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


Virginia Commonwealth University

3. Kulkarni, Rewa M. CO-LOCALIZATION OF POLYCYSTIC OVARY SYNDROME CANDIDATE GENE PRODUCTS IN HUMAN THECA CELLS SUGGESTS NOVEL SIGNALING PATHWAYS.

Degree: MS, Human Genetics, 2019, Virginia Commonwealth University

Polycystic ovary syndrome (PCOS) is the leading cause of anovulatory infertility and the most common endocrinopathy of women of reproductive age. Genome-wide association studies (GWAS) identified a number of loci associated PCOS in different ethnic populations, including women with Asian and European ancestry. Replication studies have confirmed some of these associations. Among the loci identified are those located near the LH receptor gene (LHCGR), a clathrin-binding protein gene (DENND1A) that also functions as a guanine nucleotide exchange factor, and the gene encoding RAB5B, a GTPase and protein involved in vesicular trafficking. The functional significance of one of these GWAS candidates (DENND1A) was supported by our discovery that a truncated protein splice variant of DENND1A termed DENND1A.V2, is elevated in PCOS theca cells, and that forced expression of DENND1A.V2 in normal theca cells increased CYP11A1 and CYP17A1 expression and androgen synthesis, a hallmark of PCOS. We previously proposed that the PCOS GWAS loci could be assembled into a functional network that contributes to altered gene expression in ovarian theca cells, resulting in increased androgen synthesis. Here we demonstrate the localization of LHCGR, DENND1AV.2 and RAB5B proteins in various cellular compartments in normal and PCOS theca cells. hCG and forskolin stimulation affects the distribution and co-localization of DENND1A.V2 and RAB5B in various cellular compartments This cytological evidence supports our PCOS gene network concept, and raises the intriguing possibility that LHCGR activation, via a cAMP-mediated process, promotes the translocation of DENND1A.V2 and RAB5B-containing vesicles from the PCOS theca cell cytoplasm into the nucleus, resulting in increased transcription of genes involved in androgen synthesis. Advisors/Committee Members: Dr. Jerome F. Strauss III, Dr. Maria Teves, Dr. Devanand Sarkar.

Subjects/Keywords: DENND1A; LHCGR; RAB5B; Polycystic ovary syndrome; theca cells; androgens; Genetics

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

APA (6th Edition):

Kulkarni, R. M. (2019). CO-LOCALIZATION OF POLYCYSTIC OVARY SYNDROME CANDIDATE GENE PRODUCTS IN HUMAN THECA CELLS SUGGESTS NOVEL SIGNALING PATHWAYS. (Thesis). Virginia Commonwealth University. Retrieved from https://doi.org/10.25772/XK8A-2878 ; https://scholarscompass.vcu.edu/etd/5741

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):

Kulkarni, Rewa M. “CO-LOCALIZATION OF POLYCYSTIC OVARY SYNDROME CANDIDATE GENE PRODUCTS IN HUMAN THECA CELLS SUGGESTS NOVEL SIGNALING PATHWAYS.” 2019. Thesis, Virginia Commonwealth University. Accessed January 15, 2021. https://doi.org/10.25772/XK8A-2878 ; https://scholarscompass.vcu.edu/etd/5741.

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

MLA Handbook (7th Edition):

Kulkarni, Rewa M. “CO-LOCALIZATION OF POLYCYSTIC OVARY SYNDROME CANDIDATE GENE PRODUCTS IN HUMAN THECA CELLS SUGGESTS NOVEL SIGNALING PATHWAYS.” 2019. Web. 15 Jan 2021.

Vancouver:

Kulkarni RM. CO-LOCALIZATION OF POLYCYSTIC OVARY SYNDROME CANDIDATE GENE PRODUCTS IN HUMAN THECA CELLS SUGGESTS NOVEL SIGNALING PATHWAYS. [Internet] [Thesis]. Virginia Commonwealth University; 2019. [cited 2021 Jan 15]. Available from: https://doi.org/10.25772/XK8A-2878 ; https://scholarscompass.vcu.edu/etd/5741.

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

Council of Science Editors:

Kulkarni RM. CO-LOCALIZATION OF POLYCYSTIC OVARY SYNDROME CANDIDATE GENE PRODUCTS IN HUMAN THECA CELLS SUGGESTS NOVEL SIGNALING PATHWAYS. [Thesis]. Virginia Commonwealth University; 2019. Available from: https://doi.org/10.25772/XK8A-2878 ; https://scholarscompass.vcu.edu/etd/5741

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

.