scholarly journals Bortezomib Targets Sp Transcription Factors in Cancer Cells

2018 ◽  
Vol 94 (4) ◽  
pp. 1187-1196 ◽  
Author(s):  
Keshav Karki ◽  
Sneha Harishchandra ◽  
Stephen Safe
Keyword(s):  
Transcription Factors ◽  
Cancer Cells ◽  
Sp Transcription Factors

scholarly journals Pharmacologic Doses of Ascorbic Acid Repress Specificity Protein (Sp) Transcription Factors and Sp-Regulated Genes in Colon Cancer Cells

2011 ◽  
Vol 63 (7) ◽  
pp. 1133-1142 ◽  
Author(s):  
Satya S. Pathi ◽  
Ping Lei ◽  
Sandeep Sreevalsan ◽  
Gayathri Chadalapaka ◽  
Indira Jutooru ◽  
...  
Keyword(s):  
Colon Cancer ◽  
Ascorbic Acid ◽  
Transcription Factors ◽  
Cancer Cells ◽  
Colon Cancer Cells ◽  
Specificity Protein ◽  
Sp Transcription Factors

scholarly journals Specificity protein (Sp) transcription factors Sp1, Sp3 and Sp4 are non-oncogene addiction genes in cancer cells

Oncotarget ◽  
2016 ◽  
Vol 7 (16) ◽  
pp. 22245-22256 ◽  
Author(s):  
Erik Hedrick ◽  
Yating Cheng ◽  
Un-Ho Jin ◽  
Kyounghyun Kim ◽  
Stephen Safe
Keyword(s):  
Transcription Factors ◽  
Cancer Cells ◽  
Oncogene Addiction ◽  
Specificity Protein ◽  
Sp Transcription Factors

scholarly journals Albendazole Exhibits Anti-Neoplastic Actions against Gastric Cancer Cells by Affecting STAT3 and STAT5 Activation by Pleiotropic Mechanism(s)

Biomedicines ◽  
2021 ◽  
Vol 9 (4) ◽  
pp. 362
Author(s):  
Min Hee Yang ◽  
In Jin Ha ◽  
Jae-Young Um ◽  
Kwang Seok Ahn
Keyword(s):  
Gastric Cancer ◽  
Reactive Oxygen Species ◽  
Transcription Factors ◽  
Cancer Cells ◽  
Small Interfering Rna ◽  
Oxygen Species ◽  
Gastric Cancer Cells ◽  
Drug Induced ◽  
Cellular Apoptosis ◽  
Interfering Rna

Albendazole (ABZ) has been reported to display anti-tumoral actions against various maliganncies, but possible impact of ABZ on gastric cancer has not been deciphered. As aberrant phosphorylation of STAT3 and STAT5 proteins can regulate the growth and progression of gastric cancer, we postulated that ABZ may interrupt the activation of these oncogenic transcription factors. We found that ABZ exposure abrogated STAT3/5 activation, inhibited phosphorylation of Janus-activated kinases 1/2 and Src and enhanced the levels of SHP-1 protein. Silencing of SHP-1 gene by small interfering RNA (siRNA) reversed the ABZ-promoted attenuation of STAT3 as well as STAT5 activation and cellular apoptosis. In addition, these effects were noted to be driven by an augmented levels of reactive oxygen species caused by drug-induced GSH/GSSG imbalance. Thus, the data indicates that ABZ can modulate the activation of STAT3 and STAT5 by pleiotropic mechanisms in gastric cancer cells.

scholarly journals Distinct Ring1b complexes defined by DEAD-box helicases and EMT transcription factors synergistically enhance E-cadherin silencing in breast cancer

2021 ◽  
Vol 12 (2) ◽  
Author(s):  
Yawei Wang ◽  
Yingying Sun ◽  
Chao Shang ◽  
Lili Chen ◽  
Hongyu Chen ◽  
...  
Keyword(s):  
Breast Cancer ◽  
Transcription Factors ◽  
Cancer Cells ◽  
Epithelial Mesenchymal Transition ◽  
Epigenetic Mechanism ◽  
Regulation Mechanism ◽  
Rna Helicases ◽  
Mesenchymal Transition ◽  
Dead Box ◽  
E Cadherin

AbstractRing1b is a core subunit of polycomb repressive complex 1 (PRC1) and is essential in several high-risk cancers. However, the epigenetic mechanism of Ring1b underlying breast cancer malignancy is poorly understood. In this study, we showed increased expression of Ring1b promoted metastasis by weakening cell–cell adhesions of breast cancer cells. We confirmed that Ring1b could downregulate E-cadherin and contributed to an epigenetic rewiring via PRC1-dependent function by forming distinct complexes with DEAD-box RNA helicases (DDXs) or epithelial-mesenchymal transition transcription factors (EMT TFs) on site-specific loci of E-cadherin promoter. DDXs-Ring1b complexes moderately inhibited E-cadherin, which resulted in an early hybrid EMT state of epithelial cells, and EMT TFs-Ring1b complexes cooperated with DDXs-Ring1b complexes to further repress E-cadherin in mesenchymal-like cancer cells. Clinically, high expression of Ring1b with DDXs or EMT TFs predicted low levels of E-cadherin, metastatic behavior, and poor prognosis. These findings provide an epigenetic regulation mechanism of Ring1b complexes in E-cadherin expression. Ring1b complexes may be potential therapeutic targets and biomarkers for diagnosis and prognosis in invasion breast cancer.

scholarly journals Prevention of High Glucose-Mediated EMT by Inhibition of Hsp70 Chaperone

2021 ◽  
Vol 22 (13) ◽  
pp. 6902
Author(s):  
Alina D. Nikotina ◽  
Snezhana A. Vladimirova ◽  
Elena Y. Komarova ◽  
Dmitry Alexeev ◽  
Sergey Efremov ◽  
...  
Keyword(s):  
Colon Cancer ◽  
Transcription Factors ◽  
Cell Motility ◽  
Cancer Cells ◽  
High Glucose ◽  
Binding Capacity ◽  
Colon Cancer Cells ◽  
Mesenchymal Transition ◽  
Hsp70 Chaperone ◽  
Migration Capacity

Hyperglycemia may contribute to the progression of carcinomas by triggering epithelial-to-mesenchymal transition (EMT). Some proteostasis systems are involved in metastasis; in this paper, we sought to explore the mechanism of Hsp70 chaperone in EMT. We showed that knockdown of Hsp70 reduced cell migration capacity concomitantly with levels of mRNA of the Slug, Snail, and Twist markers of EMT, in colon cancer cells incubated in high glucose medium. Conversely, treatment of cells with Hsp70 inducer U-133 were found to elevate cell motility, along with the other EMT markers. To prove that inhibiting Hsp70 may reduce EMT efficiency, we treated cells with a CL-43 inhibitor of the HSF1 transcription factor, which lowered Hsp70 and HSF1 content in the control and induced EMT in carcinoma cells. Importantly, CL-43 reduced migration capacity, EMT-linked transcription factors, and increased content of epithelial marker E-cadherin in colon cancer cells of three lines, including one derived from a clinical sample. To prove that Hsp70 chaperone should be targeted when inhibiting the EMT pathway, we treated cancer cells with 2-phenylethynesulfonamide (PES) and demonstrated that the compound inhibited substrate-binding capacity of Hsp70. Furthermore, PES suppressed EMT features, cell motility, and expression of specific transcription factors. In conclusion, the Hsp70 chaperone machine efficiently protects mechanisms of the EMT, and the safe inhibitors of the chaperone are needed to hamper metastasis at its initial stage.

scholarly journals High copy number variations, particular transcription factors, and low immunity contribute to the stemness of prostate cancer cells

2021 ◽  
Vol 19 (1) ◽  
Author(s):  
Zao Dai ◽  
Ping Liu
Keyword(s):  
Prostate Cancer ◽  
Transcription Factors ◽  
Copy Number Variation ◽  
Cancer Cells ◽  
Immune Cells ◽  
Copy Number ◽  
Tumor Metastasis ◽  
Prostate Cancer Cells ◽  
Immune Microenvironment ◽  
Number Variation

Abstract Background Tumor metastasis is the main cause of death of cancer patients, and cancer stem cells (CSCs) is the basis of tumor metastasis. However, systematic analysis of the stemness of prostate cancer cells is still not abundant. In this study, we explore the effective factors related to the stemness of prostate cancer cells by comprehensively mining the multi-omics data from TCGA database. Methods Based on the prostate cancer transcriptome data in TCGA, gene expression modules that strongly relate to the stemness of prostate cancer cells are obtained with WGCNA and stemness scores. Copy number variation of stemness genes of prostate cancer is calculated and the difference of transcription factors between prostate cancer and normal tissues is evaluated by using CNV (copy number variation) data and ATAC-seq data. The protein interaction network of stemness genes in prostate cancer is constructed using the STRING database. Meanwhile, the correlation between stemness genes of prostate cancer and immune cells is analyzed. Results Prostate cancer with higher Gleason grade possesses higher cell stemness. The gene set highly related to prostate cancer stemness has higher CNV in prostate cancer samples than that in normal samples. Although the transcription factors of stemness genes have similar expressions, they have different contributions between normal and prostate cancer tissues; and particular transcription factors enhance the stemness of prostate cancer, such as PUM1, CLOCK, SP1, TCF12, and so on. In addition, the lower tumor immune microenvironment is conducive to the stemness of prostate cancer. CD8 + T cells and M1 macrophages may play more important role in the stemness of prostate cancer than other immune cells in the tumor microenvironment. Finally, EZH2 is found to play a central role in stemness genes and is negatively correlated with resting mast cells and positively correlated with activated memory CD4 + T cells. Conclusions Based on the systematic and combined analysis of multi-omics data, we find that high copy number variation, specific transcription factors, and low immune microenvironment jointly contribute to the stemness of prostate cancer cells. These findings may provide us new clues and directions for the future research on stemness of prostate cancer.

scholarly journals Resveratrol Induces Growth Arrest and Apoptosis through Activation of FOXO Transcription Factors in Prostate Cancer Cells

PLoS ONE ◽  
2010 ◽  
Vol 5 (12) ◽  
pp. e15288 ◽  
Author(s):  
Qinghe Chen ◽  
Suthakar Ganapathy ◽  
Karan P. Singh ◽  
Sharmila Shankar ◽  
Rakesh K. Srivastava
Keyword(s):  
Prostate Cancer ◽  
Transcription Factors ◽  
Cancer Cells ◽  
Growth Arrest ◽  
Prostate Cancer Cells ◽  
Foxo Transcription Factors

scholarly journals How cancer cells remodel lipid metabolism: strategies targeting transcription factors

2021 ◽  
Vol 20 (1) ◽  
Author(s):  
Do-Won Jeong ◽  
Seulbee Lee ◽  
Yang-Sook Chun
Keyword(s):  
Transcription Factor ◽  
Transcription Factors ◽  
Lipid Metabolism ◽  
Cancer Cells ◽  
Cancer Biology ◽  
Factors Associated ◽  
Modeling Techniques ◽  
Related Enzyme ◽  
Potential Strategy

AbstractReprogramming of lipid metabolism has received increasing recognition as a hallmark of cancer cells because lipid dysregulation and the alteration of related enzyme profiles are closely correlated with oncogenic signals and malignant phenotypes, such as metastasis and therapeutic resistance. In this review, we describe recent findings that support the importance of lipids, as well as the transcription factors involved in cancer lipid metabolism. With recent advances in transcription factor analysis, including computer-modeling techniques, transcription factors are emerging as central players in cancer biology. Considering the limited number and the crucial role of transcription factors associated with lipid rewiring in cancers, transcription factor targeting is a promising potential strategy for cancer therapy.

scholarly journals The Expression of Transcription Factors is Different in Papillary Thyroid Cancer Cells during TNF - α induced EMT

2021 ◽  
Vol 12 (9) ◽  
pp. 2777-2786
Author(s):  
Nannan Lv ◽  
Fei Liu ◽  
Lan Cheng ◽  
Feng Liu ◽  
Jinsong Kuang
Keyword(s):  
Transcription Factors ◽  
Thyroid Cancer ◽  
Cancer Cells ◽  
Papillary Thyroid Cancer ◽  
Papillary Thyroid ◽  
Tnf Α ◽  
Thyroid Cancer Cells
Sign in / Sign up

Export Citation Format

Share Document