Defining the Cancer Master Switch

Balentine, Courtney J.; Berger, David H.; Liu, Shi He; Chen, Changyi; Nemunaitis, John; Brunicardi, F. Charles

doi:10.1007/s00268-010-0941-2

Cited by 3 publications

(3 citation statements)

References 118 publications

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“…However, evidence exists, perhaps as expected of homeobox genes, for a causative role in cellular processes including proliferation, differentiation, apoptosis, angiogenesis, resistance to chemotherapies, invasion, and metastasis. These qualities are typically used to define candidate factors to serve as a "Master Switch" for the development and progression of cancer (65). Whether one or more RHOX factors serve as such a switch remains to be seen.…”

Section: Discussion and Future Directionsmentioning

confidence: 99%

“…The aberrant regulation of methylation may contribute in multiple tumorigenesis pathways as there is potential for both the derepression of oncogenes and silencing of anticancer genes (64). If the gene that is aberrantly activated is a "master switch" for cancer development (65), then a single misregulation event may lead to the acceleration of cancer development. The Rhox genes may be relevant to such a scenario as their expression is governed by the epigenome, and one gene that is normally silenced in non-reproductive tissues has recently been shown to actively organize the expression of other members of the cluster.…”

Section: Potential Mechanisms Of Rhox Gene Misregulationmentioning

confidence: 99%

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The role of Rhox homeobox factors in tumorigenesis

2013

Front Biosci

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Homeobox genes encode transcription factors that have well-established roles in embryonic development. We recently discovered the Rhox genes, a new family of homeobox genes, which are selectively expressed in the developing embryo, postnatal and adult gonads, and accessory tissues associated with mammalian reproduction. The largest and best-characterized Rhox cluster is found in mouse. However, all mammals examined to date possess a set of Rhox genes that, while they may vary in number by species, appear relevant to reproduction and are located in the syntenic region of the X chromosome. Rhox5, the founding member of the family, was initially cloned from a screen to identify tumorigenic antigens from T-cell lymphomas, and was later found to be widely expressed in tumors from tissues of diverse origins that do not normally express the Rhox genes. This aberrant upregulation appears to be a general feature of many Rhox genes, but the implications of this misexpression remain largely uninvestigated. In this review, we will discuss the latest findings on the normal and abnormal roles of the Rhox genes and their potential contributions to the formation and progression of tumors.

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Section: Discussion and Future Directionsmentioning

confidence: 99%

Section: Potential Mechanisms Of Rhox Gene Misregulationmentioning

confidence: 99%

The role of Rhox homeobox factors in tumorigenesis

2013

Front Biosci

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“…Cancer could be viewed as the result of switch like behavior of cells (Mills et al 2010, Balentine et al 2011, Torres et al 2018). Robustness is preserved, as cells transform from normal state to cancer state.…”

Section: Introductionmentioning

confidence: 99%

Mutually Antagonistic Protein Pairs of Cancer

Dalgıç

2021

Preprint

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Switch-like behavior of tumorigenesis could be governed by antagonistic gene and protein pairs with mutual inhibition. Unlike extensive analysis of gene expression, search for protein level antagonistic pairs has been limited. Here, potential cancer type specific antagonist protein pairs with mutual inhibition were obtained from large scale datasets. Cancer samples or cancer types were compared to retrieve potential protein pairs with contrasting differential expression patterns. Analysis of two different protein expression datasets showed that a few proteins participate in most of the mutually antagonistic relationships. Some proteins with highly antagonistic profile were identified, which could not be attained from a differential expression or a correlation based analysis. The antagonistic protein pairs are sparsely connected by molecular interactions. Glioma, melanoma, and cervical cancer, are more frequently associated with antagonistic proteins than most of the other cancer types. Integrative analysis of mutually antagonist protein pairs contributes to our understanding of systems level changes of cancer.

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Design, synthesis, and antiproliferative activity of new indole/1,2,4‐triazole/chalcone hybrids as EGFR and/or c‐MET inhibitors

Mahmoud,

Abdelhamid,

Youssif

et al. 2024

Archiv der Pharmazie

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A novel group of indolyl‐1,2,4‐triazole‐chalcone hybrids was designed, synthesized, and assessed for their anticancer activity. The synthesized compounds exhibited significant antiproliferative activity. Compounds 9a and 9e exhibited significant cancer inhibition with GI50 ranging from 3.69 to 20.40 µM and from 0.29 to >100 µM, respectively. Both compounds displayed a broad spectrum of anticancer activity with selectivity ratios ranging between 0.50–2.78 and 0.25–2.81 at the GI50 level, respectively. The synthesized compounds were also screened for their cytotoxicity by 3‐(4,5‐dimethylthiazole‐2‐yl)‐2,5‐diphenyltetrazol (MTT) assay and for inhibition of epidermal growth factor receptor (EGFR) and c‐MET (mesenchymal‐epithelial transition factor). Some of the tested compounds exhibited significant inhibition against EGFR and/or c‐MET. Compound 9b showed the highest c‐MET inhibition (IC50 = 4.70 nM) compared to foretinib (IC50 = 2.5 nM). Compound 9d showed equipotent activity compared with erlotinib against EGFR (IC50 = 0.052 µM) and displayed significant c‐MET inhibition with an IC50 value of 4.90 nM.

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Defining the Cancer Master Switch

Cited by 3 publications

References 118 publications

The role of Rhox homeobox factors in tumorigenesis

The role of Rhox homeobox factors in tumorigenesis

Mutually Antagonistic Protein Pairs of Cancer

Design, synthesis, and antiproliferative activity of new indole/1,2,4‐triazole/chalcone hybrids as EGFR and/or c‐MET inhibitors

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