scholarly journals Transcription Factor KLLN Inhibits Tumor Growth byARSuppression, Induces Apoptosis byTP53/TP73Stimulation in Prostate Carcinomas, and Correlates With Cellular Differentiation

2013 ◽  
Vol 98 (3) ◽  
pp. E586-E594 ◽  
Author(s):  
Yu Wang ◽  
Deepa Radhakrishnan ◽  
Xin He ◽  
Donna M. Peehl ◽  
Charis Eng
Keyword(s):  
Transcription Factor ◽  
Tumor Growth ◽  
Cellular Differentiation ◽  
Prostate Carcinomas

Transcription factor Egr-1 supports FGF-dependent angiogenesis during neovascularization and tumor growth

10.1038/nm905 ◽  
2003 ◽  
Vol 9 (8) ◽  
pp. 1026-1032 ◽  
Author(s):  
Roger G Fahmy ◽  
Crispin R Dass ◽  
Lun-Quan Sun ◽  
Colin N Chesterman ◽  
Levon M Khachigian
Keyword(s):  
Transcription Factor ◽  
Tumor Growth

scholarly journals Cisplatin-mediated activation of glucocorticoid receptor induces platinum resistance via MAST1

2021 ◽  
Vol 12 (1) ◽  
Author(s):  
Chaoyun Pan ◽  
JiHoon Kang ◽  
Jung Seok Hwang ◽  
Jie Li ◽  
Austin C. Boese ◽  
...  
Keyword(s):  
Transcription Factor ◽  
Glucocorticoid Receptor ◽  
Tumor Growth ◽  
Nuclear Translocation ◽  
Mapk Pathway ◽  
Underlying Mechanism ◽  
Patient Treatment ◽  
Platinum Resistance ◽  
Platinum Based Chemotherapy

AbstractAgonists of glucocorticoid receptor (GR) are frequently given to cancer patients with platinum-containing chemotherapy to reduce inflammation, but how GR influences tumor growth in response to platinum-based chemotherapy such as cisplatin through inflammation-independent signaling remains largely unclear. Combined genomics and transcription factor profiling reveal that MAST1, a critical platinum resistance factor that reprograms the MAPK pathway, is upregulated upon cisplatin exposure through activated transcription factor GR. Mechanistically, cisplatin binds to C622 in GR and recruits GR to the nucleus for its activation, which induces MAST1 expression and consequently reactivates MEK signaling. GR nuclear translocation and MAST1 upregulation coordinately occur in patient tumors collected after platinum treatment, and align with patient treatment resistance. Co-treatment with dexamethasone and cisplatin restores cisplatin-resistant tumor growth, whereas addition of the MAST1 inhibitor lestaurtinib abrogates tumor growth while preserving the inhibitory effect of dexamethasone on inflammation in vivo. These findings not only provide insights into the underlying mechanism of GR in cisplatin resistance but also offer an effective alternative therapeutic strategy to improve the clinical outcome of patients receiving platinum-based chemotherapy with GR agonists.

scholarly journals Interplay among SNAIL Transcription Factor, MicroRNAs, Long Non-Coding RNAs, and Circular RNAs in the Regulation of Tumor Growth and Metastasis

Cancers ◽  
2020 ◽  
Vol 12 (1) ◽  
pp. 209 ◽  
Author(s):  
Klaudia Skrzypek ◽  
Marcin Majka
Keyword(s):  
Transcription Factor ◽  
Tumor Growth ◽  
Epithelial To Mesenchymal Transition ◽  
Cell Metabolism ◽  
Circular Rnas ◽  
Mesenchymal Transition ◽  
Expression Of Genes ◽  
Non Coding Rnas ◽  
Tumor Growth And Metastasis ◽  
Novel Therapeutic Strategies

SNAIL (SNAI1) is a zinc finger transcription factor that binds to E-box sequences and regulates the expression of genes. It usually acts as a gene repressor, but it may also activate the expression of genes. SNAIL plays a key role in the regulation of epithelial to mesenchymal transition, which is the main mechanism responsible for the progression and metastasis of epithelial tumors. Nevertheless, it also regulates different processes that are responsible for tumor growth, such as the activity of cancer stem cells, the control of cell metabolism, and the regulation of differentiation. Different proteins and microRNAs may regulate the SNAIL level, and SNAIL may be an important regulator of microRNA expression as well. The interplay among SNAIL, microRNAs, long non-coding RNAs, and circular RNAs is a key event in the regulation of tumor growth and metastasis. This review for the first time discusses different types of regulation between SNAIL and non-coding RNAs with a focus on feedback loops and the role of competitive RNA. Understanding these mechanisms may help develop novel therapeutic strategies against cancer based on microRNAs.

Abstract C57: Snail transcription factor can regulate cathepsin L activity in prostate carcinomas

2014 ◽  
Author(s):  
Liza Burton ◽  
Peri Nappagan ◽  
Basil Smith ◽  
Manu Platt ◽  
Camille Ragin ◽  
...  
Keyword(s):  
Transcription Factor ◽  
Cathepsin L ◽  
Prostate Carcinomas

scholarly journals Cellular differentiation and the NtcA transcription factor in filamentous cyanobacteria

2004 ◽  
Vol 28 (4) ◽  
pp. 469-487 ◽  
Author(s):  
Antonia Herrero ◽  
Alicia M. Muro-Pastor ◽  
Ana Valladares ◽  
Enrique Flores
Keyword(s):  
Transcription Factor ◽  
Cellular Differentiation ◽  
Filamentous Cyanobacteria

scholarly journals Forkhead Box Transcription Factor (FOXO3a) mediates the cytotoxic effect of vernodalin in vitro and inhibits the breast tumor growth in vivo

2015 ◽  
Vol 34 (1) ◽  
Author(s):  
Suresh Kumar Ananda Sadagopan ◽  
Nooshin Mohebali ◽  
Chung Yeng Looi ◽  
Mohadeseh Hasanpourghadi ◽  
Ashok Kumar Pandurangan ◽  
...  
Keyword(s):  
Transcription Factor ◽  
Tumor Growth ◽  
Breast Tumor ◽  
Cytotoxic Effect ◽  
Forkhead Box

scholarly journals Suppression of Breast Tumor Growth and Metastasis by an Engineered Transcription Factor

PLoS ONE ◽  
2011 ◽  
Vol 6 (9) ◽  
pp. e24595 ◽  
Author(s):  
Adriana S. Beltran ◽  
Angela Russo ◽  
Haydee Lara ◽  
Cheng Fan ◽  
Paul M. Lizardi ◽  
...  
Keyword(s):  
Transcription Factor ◽  
Tumor Growth ◽  
Breast Tumor ◽  
Tumor Growth And Metastasis

KLF9, a transcription factor induced in flutamide-caused cell apoptosis, inhibits AKT activation and suppresses tumor growth of prostate cancer cells

The Prostate ◽  
2014 ◽  
Vol 74 (9) ◽  
pp. 946-958 ◽  
Author(s):  
Pengliang Shen ◽  
Jiabin Sun ◽  
Guiqin Xu ◽  
Li Zhang ◽  
Zhaojuan Yang ◽  
...  
Keyword(s):  
Prostate Cancer ◽  
Transcription Factor ◽  
Tumor Growth ◽  
Cancer Cells ◽  
Cell Apoptosis ◽  
Prostate Cancer Cells ◽  
Akt Activation

scholarly journals Targeting MYC and HDAC8 with a Combination of siRNAs Inhibits Neuroblastoma Cells Proliferation In Vitro and In Vivo Xenograft Tumor Growth

2021 ◽  
Author(s):  
Nagindra Prashad
Keyword(s):  
Cell Proliferation ◽  
Tumor Growth ◽  
Cellular Differentiation ◽  
Tumor Model ◽  
Significant Inhibition ◽  
Luciferase Reporter Plasmid ◽  
Combination Of Sirnas ◽  
Proliferation In Vitro

HDAC8, c MYC and MYCN are involved in the tumorigenesis of neuroblastoma. A mouse Neuroblastoma (NB) tumor model was used to understand the role of miRNA, miR-665 in NB tumorigenesis and cellular differentiation. During cellular differentiation of NB cells there is an up regulated miRNA-665. We found that HDAC 8, c MYC and MYCN are the direct targets of mimic miR-665 which was validated by luciferase reporter plasmid with 3’ UTR and ELISA. Mimic miR-665 inhibited cell proliferation, arrested cells in G1 stage and decreased S Phase in cell cycle. miR-665 increased the acetylation of histones and activated Caspase 3. This is the first report to recognize miRNA 665 as a suppressor miRNA of NB. The effects of miR-665 were confirmed with the transfection of siRNA for HDAC8 and siRNA for MYC. Individual siRNA- HDAC8 or siRNA-MYC inhibited 40–50% of cell proliferation in vitro, however, the treatment with the combination of both siRNA-MYC + siRNA- HDAC8 inhibited 86% of cell proliferation. Indicating that both the targets c MYC and HDAC 8 should be reduced to obtain a significant inhibition of cell proliferation. Intratumoral treatment of xenograft tumors in mice with the combination of siRNA-MYC + siRNA- HDAC8 reduced the levels of target c-MYC protein by 64% and target HDAC 8 protein by 85% and the average tumor growth reduced by 80% compared to control tumors treated with NC-siRNA. Our results suggest the potential therapeutic effect of suppressor miR-665 and the combination of siRNA-MYC + siRNA-HDAC8 for neuroblastoma treatment.

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