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.

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 De-Ubiquitinating Enzymes USP21 Regulate MAPK1 Expression by Binding to Transcription Factor GATA3 to Regulate Tumor Growth and Cell Stemness of Gastric Cancer

2021 ◽  
Vol 9 ◽  
Author(s):  
Qingqu Guo ◽  
Dike Shi ◽  
Lele Lin ◽  
Hongbo Li ◽  
Yunhai Wei ◽  
...  
Keyword(s):  
Gastric Cancer ◽  
Cell Proliferation ◽  
Transcription Factor ◽  
Tumor Growth ◽  
Regulatory Mechanism ◽  
Malignant Progression ◽  
Transcriptional Level ◽  
Deubiquitinating Enzymes

USP21 is a kind of deubiquitinating enzymes involved in the malignant progression of various cancers, while its role in gastric cancer (GC) and the specific molecular mechanism are still unclear. This study probed into the function of USP21 in vitro and in vivo, and discussed the regulatory mechanism of USP21 in GC in vitro. We reported that USP21 promoted GC cell proliferation, migration, invasion, and stemness in vitro, and regulated GC tumor growth and cell stemness in mice in vivo. USP21 stabilized the expression of GATA3 by binding to GATA3. Besides, GATA3 also regulated the expression of MAPK1 at the transcriptional level. A series of in vitro experiments testified that USP21 regulated the expression of MAPK1 by binding to transcription factor GATA3, thereby regulating the tumor growth and cell stemness of GC. Overall, this study identified a new USP21/GATA3/MAPK1 axis, which plays a pivotal role in promoting the malignant progression of GC and might provide a potential target for treatment.

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