Tumor Cell Transformation Using Antisense Oligonucleotide

2014 ◽  
pp. 259-268 ◽  
Author(s):  
Mohamed R. Akl ◽  
Nehad M. Ayoub
Keyword(s):  
Tumor Cell ◽  
Antisense Oligonucleotide ◽  
Cell Transformation

Expression of FOXP1 in mucosa-associated lymphoid tissue lymphoma suggests a large tumor cell transformation and predicts a poorer prognosis in the positive thyroid patients

2012 ◽  
Vol 29 (5) ◽  
pp. 3352-3359 ◽  
Author(s):  
Wei Jiang ◽  
Lei Li ◽  
Yuan Tang ◽  
Wen-yan Zhang ◽  
Wei-ping Liu ◽  
...  
Keyword(s):  
Tumor Cell ◽  
Lymphoid Tissue ◽  
Cell Transformation ◽  
Large Tumor

scholarly journals 2165 Vesicular secretion of suppressor of cytokine signaling 3 by alveolar macrophages is dysregulated in NSCLC patients and its provision inhibits epithelial cell transformation and tumor cell function

2018 ◽  
Vol 2 (S1) ◽  
pp. 36-36
Author(s):  
Jennifer Speth ◽  
Loka R. Penke ◽  
Joseph Bazzill ◽  
Douglas A. Arenberg ◽  
James J. Moon ◽  
...  
Keyword(s):  
Lung Cancer ◽  
Tumor Cell ◽  
Alveolar Macrophages ◽  
Cell Transformation ◽  
Soft Agar ◽  
Cigarette Smoke Extract ◽  
Cytokine Signaling ◽  
Suppressor Of Cytokine Signaling ◽  
Induced Apoptosis ◽  
Nsclc Patients

OBJECTIVES/SPECIFIC AIMS: Insufficient endogenous expression of suppressor of cytokine signaling 3 (SOCS3) with subsequent over-activation of its target, the transcription factor STAT3, has been associated with tumorigenesis and cancer development in the lung and other organs. We have observed that a “backup” source of SOCS3 in the lung, namely that secreted in microvesicles (MVs) by alveolar macrophages, is reduced in the bronchoalveolar lavage fluid (BALF) of KRAS mutant mice harboring lung tumors. Here we sought to evaluate levels of SOCS3 in BALF of a cohort of non-small cell lung cancer (NSCLC) patients and to test the effects of vesicular SOCS3 administration on tumor cell transformation and function as potential therapeutic strategy. METHODS/STUDY POPULATION: In total, 22 BALF samples were obtained from healthy volunteers (n=11) as well as patients undergoing diagnostic bronchoscopies for suspected lung cancer (n=11). SOCS3 levels in the BALF were determined by ELISA after brief sonication to disrupt vesicles. In vitro experiments utilized the human adenocarcinoma cell line (A549) or human G12V mutant KRAS-expressing rat lung epithelial cells (RLE-G12V). Proliferation, Fas ligand (FasL)-induced apoptosis, and chemical transformation with N-methyl-N′-nitro-N-nitrosoguanidine (MNNG) or cigarette smoke extract (CSE) were assessed by CyQuant assay, annexin V staining, and soft agar assay, respectively. For SOCS3 rescue, epithelial cells were treated with natural alveolar macrophages-derived MVs (isolated via ultracentrifugation) or synthetic unilamellar liposomes containing human recombinant SOCS3 for at least 1 hour before assay. RESULTS/ANTICIPATED RESULTS: SOCS3 levels were significantly reduced in BALF samples of patients determined to have NSCLC as compared with healthy volunteers (186.6±26.74 vs. 395.6±74.31 pg/mL, p=0.015, n=11). Addition of exogenous SOCS3-containing liposomes had the capacity to significantly inhibit MNNG and cigarette smoke extract-induced transformation and colony formation in soft agar. Exogenous SOCS3 provided in liposomes or in natural MVs significantly induced apoptosis (both in the presence and absence of FasL) and inhibited basal proliferation of A549 cells. DISCUSSION/SIGNIFICANCE OF IMPACT: These data identified a novel dysregulation of immune surveillance in the form of decreased SOCS3 secretion in the tumor-bearing lung that may contribute to tumorigenesis via sustained STAT3 activation. Future studies will focus on the mechanism underlying this defect and whether rescuing SOCS3 secretion can inhibit cancer progression in vivo.

scholarly journals Hypermethylation of the 5' region of the calcitonin gene is a property of human lymphoid and acute myeloid malignancies

Blood ◽  
1987 ◽  
Vol 70 (2) ◽  
pp. 412-417 ◽  
Author(s):  
SB Baylin ◽  
ER Fearon ◽  
B Vogelstein ◽  
A de Bustros ◽  
SJ Sharkis ◽  
...  
Keyword(s):  
Tumor Cell ◽  
Progenitor Cells ◽  
Cell Transformation ◽  
Lymphoid Hyperplasia ◽  
Myelogenous Leukemia ◽  
Human Calcitonin ◽  
Barr Virus ◽  
Myeloid Progenitor ◽  
Myeloid Progenitor Cells ◽  
Epstein Barr

An abnormal increase in numbers of CCGG sites methylated in the 5′ region of the human calcitonin (CT) gene occurred in tumor cell DNA samples from 90% (17 of 19) of patients with non-Hodgkin's T and B cell lymphoid neoplasms and in 95% (21 of 22) of tumor cell DNA samples from patients with acute nonlymphocytic leukemia (ANLL). The changes were not seen in patients with chronic myelogenous leukemia (0 of 9). The abnormal methylation patterns appear to be a property only of transformed or malignant cells since they were not found in DNA from nonneoplastic adult tissues including sperm, early myeloid progenitor cells, benign lymphoid hyperplasia, peripheral lymphocytes stimulated to divide, or early myeloid progenitor cells (obtained by immunoaffinity using anti-My-10 antibody), but they did appear after Epstein-Barr virus transformation of lymphocytes. Moreover, during the course of therapy in patients with ANLL, the hypermethylation pattern reflects the presence of the leukemic clone even in normal-appearing granulocytes derived from this clone. The increased methylation of the CT gene may then provide an important molecular marker for biologic events in human cell transformation or tumor progression and may prove clinically useful in monitoring patients with lymphoid and acute myelogenous neoplasms.

scholarly journals Abstract 4790: Let-7 mediates sulindac inhibition of tumor cell transformation

2017 ◽  
Author(s):  
Zhipin Liang ◽  
Bin Yi ◽  
Hongyou Zhao ◽  
Ruixia Ma ◽  
Yaguang Xi
Keyword(s):  
Tumor Cell ◽  
Cell Transformation

A Functionally Improved Locked Nucleic Acid Antisense Oligonucleotide Inhibits Bcl-2 and Bcl-xL Expression and Facilitates Tumor Cell Apoptosis

2004 ◽  
Vol 14 (3) ◽  
pp. 199-209 ◽  
Author(s):  
A. Paula Simões-Wüst ◽  
Sally Hopkins-Donaldson ◽  
Brigitte Sigrist ◽  
Larisa Belyanskaya ◽  
Rolf A. Stahel ◽  
...  
Keyword(s):  
Nucleic Acid ◽  
Tumor Cell ◽  
Cell Apoptosis ◽  
Antisense Oligonucleotide ◽  
Locked Nucleic Acid ◽  
Tumor Cell Apoptosis

scholarly journals Kinase Suppressor of Ras 2 (KSR2) Regulates Tumor Cell Transformation via AMPK

2012 ◽  
Vol 32 (18) ◽  
pp. 3718-3731 ◽  
Author(s):  
M. R. Fernandez ◽  
M. D. Henry ◽  
R. E. Lewis
Keyword(s):  
Tumor Cell ◽  
Cell Transformation ◽  
Kinase Suppressor Of Ras

scholarly journals MicroRNAs as regulators of apoptosis mechanisms in cancer

2016 ◽  
Vol 89 (1) ◽  
pp. 50-55 ◽  
Author(s):  
Valentina Pileczki ◽  
Roxana Cojocneanu-Petric ◽  
Mahafarin Maralani ◽  
Ioana Berindan Neagoe ◽  
Robert Sandulescu
Keyword(s):  
Tumor Cell ◽  
Cell Transformation ◽  
Cancer Development ◽  
Biological Processes ◽  
Cell Resistance ◽  
Regulate Gene Expression ◽  
Resistance To Treatment ◽  
New Knowledge ◽  
Non Coding Rnas ◽  
Tumor Cell Resistance

MicroRNAs or miRNAs are small non-coding RNAs that regulate gene expression. Their discovery has brought new knowledge in biological processes of cancer. Involvement of miRNAs in cancer development includes several major pathways from cell transformation to tumor cell development, metastasis and resistance to treatment. The first part of this review discusses miRNAs function in the intrinsic and extrinsic pathways of apoptosis. Due to the fact that many miRNAs that regulate apoptosis have been shown to play a major role in tumor cell resistance to treatment, in the second part of the review we aim at discussing miRNAs potential in becoming curative molecules.       

scholarly journals Deregulation of Ribosomal Proteins in Human Cancers

2021 ◽  
Author(s):  
Wendy El Khoury ◽  
Zeina Nasr
Keyword(s):  
Protein Synthesis ◽  
Tumor Cell ◽  
Cell Fate ◽  
Ribosomal Proteins ◽  
Cell Transformation ◽  
Ribosomal Rnas ◽  
Human Cancers ◽  
Recent Advances ◽  
Different Types ◽  
Shed Light

The ribosome, the site for protein synthesis, is composed of ribosomal RNAs (rRNAs) and ribosomal proteins (RPs). The latter have been shown to have many ribosomal and extra-ribosomal functions. RPs are implicated in a variety of pathological processes, especially tumorigenesis and cell transformation. In this review, we will focus on the recent advances that shed light on the effects of RPs deregulation in different types of cancer and their roles in regulating the tumor cell fate.

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