S100A2 protein and non-small cell lung cancer. The dual role concept

Hountis, Panagiotis; Matthaios, Dimitrios; Froudarakis, Marios; Bouros, Demosthenes; Kakolyris, Stylianos

doi:10.1007/s13277-014-2117-4

Cited by 24 publications

(16 citation statements)

References 38 publications

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“…In contrast, Heighway et al demonstrated that S100A2 was strongly expressed in primary NSCLC tissue [112], and Bulk et al later showed that S100A2 acts as a metastasis inducer in mouse models [113]. In 2014, Hountis et al introduced a dual role concept for S100A2 in lung cancer, implicating that S100A2 is primarily expressed in the nucleus at an early stage of NSCLC, where it mediates resistance to p53-dependent apoptosis and inhibits tumour-promoting genes (e.g., PA1-1 and vimentin) and in later stages relocates to the cytoplasm in a Ca 2+ -dependent manner [114]. S100A4 seems to be an important player in the development and metastasis of lung cancer, promoting tumour cell proliferation and motility [115,116].…”

Section: S100 Proteins In Lung Cancermentioning

confidence: 99%

Friend or Foe: S100 Proteins in Cancer

Allgöwer

Kretz

Karstedt

et al. 2020

Cancers

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S100 proteins are widely expressed small molecular EF-hand calcium-binding proteins of vertebrates, which are involved in numerous cellular processes, such as Ca2+ homeostasis, proliferation, apoptosis, differentiation, and inflammation. Although the complex network of S100 signalling is by far not fully deciphered, several S100 family members could be linked to a variety of diseases, such as inflammatory disorders, neurological diseases, and also cancer. The research of the past decades revealed that S100 proteins play a crucial role in the development and progression of many cancer types, such as breast cancer, lung cancer, and melanoma. Hence, S100 family members have also been shown to be promising diagnostic markers and possible novel targets for therapy. However, the current knowledge of S100 proteins is limited and more attention to this unique group of proteins is needed. Therefore, this review article summarises S100 proteins and their relation in different cancer types, while also providing an overview of novel therapeutic strategies for targeting S100 proteins for cancer treatment.

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Section: S100 Proteins In Lung Cancermentioning

confidence: 99%

Friend or Foe: S100 Proteins in Cancer

Allgöwer

Kretz

Karstedt

et al. 2020

Cancers

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“…3c ) has been related to tumor promoting processes, such as the epithelial-mesenchymal transition. Initially, though, to act as a tumor suppressor, it probably plays a dual role in cancerogenesis [ 33 – 35 ]. In both cases, truncating mutations of TP53 appear to cause larger upregulation of the targets, supporting the notion that they possess a higher driver potential, with some missense mutations actually acting as passengers.…”

Section: Resultsmentioning

confidence: 99%

Circuits of cancer drivers revealed by convergent misregulation of transcription factor targets across tumor types

González-Pérez

2016

Genome Med

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BackgroundLarge tumor genome sequencing projects have now uncovered a few hundred genes involved in the onset of tumorigenesis, or drivers, in some two dozen malignancies. One of the main challenges emerging from this catalog of drivers is how to make sense of their heterogeneity in most cancer types. This is key not only to understand how carcinogenesis appears and develops in these malignancies to be able to early diagnose them, but also to open up the possibility to employ therapeutic strategies targeting a driver protein to counteract the alteration of another connected driver.MethodsHere, I focus on driver transcription factors and their connection to tumorigensis in several tumor types through the alteration of the expression of their targets. First, I explore their involvement in tumorigenesis as mutational drivers in 28 different tumor types. Then, I collect a list of downstream targets of the all driver transcription factors (TFs), and identify which of them exhibit a differential expression upon alterations of driver transcription factors.ResultsI identify the subset of targets of each TF most likely mediating the tumorigenic effect of their driver alterations in each tumor type, and explore their overlap. Furthermore, I am able to identify other driver genes that cause tumorigenesis through the alteration of very similar sets of targets.ConclusionsI thus uncover these circuits of connected drivers which cause tumorigenesis through the perturbation of overlapping cellular pathways in a pan-cancer manner across 15 malignancies. The systematic detection of these circuits may be key to propose novel therapeutic strategies indirectly targeting driver alterations in tumors.Electronic supplementary materialThe online version of this article (doi:10.1186/s13073-015-0260-1) contains supplementary material, which is available to authorized users.

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“…Therefore, it is assumed that telaprevir itself might have an unfavorable effect on the exacerbation of cutaneous drug response. S100 calcium-binding protein A2 (S100A2) is a member of the EF-hand motif family S100 7 . The S100 family comprises more than 20 members of highly conserved acidic calcium-binding proteins.…”

Section: High S100a2 Expression In Keratinocytes In Patients With Drumentioning

confidence: 99%

High S100A2 expression in keratinocytes in patients with drug eruption

Yoshioka

Sawada

Saito‐Sasaki

et al. 2021

Sci Rep

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Telaprevir used as a protease inhibitor against hepatitis C virus is frequently associated with cutaneous adverse reactions. To explore a histological biomarker of cutaneous adverse events induced by telaprevir, we systematically searched for genes that were dysregulated by telaprevir in normal human epidermal keratinocytes (NHEKs). Microarray analysis and real-time polymerase chain reaction (PCR) revealed the significant increase in the expression of S100 calcium-binding protein A2 (S100A2) gene following treatment of NHEKs with telaprevir. Immunohistochemical analysis demonstrated that the expression of S100A2 was dominant in the spinous layer of the epidermis in patients with telaprevir-mediated severe-type drug eruptions and limited to the basal layer of the epidermis in healthy subjects. Furthermore, S100A2 expression increased after treatment with trichloroethylene and other medications, and the degree of S100A2 expression correlated with the severity of cutaneous adverse events. S100A2 expression also significantly increased in the skin of patients with atopic dermatitis and psoriasis. Taken together, S100A2 is highly expressed in the epidermis under inflammatory conditions and drug eruptions and may serve as a marker for keratinocyte damage in response to any inflammatory or toxic condition.

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S100A2 protein and non-small cell lung cancer. The dual role concept

Cited by 24 publications

References 38 publications

Friend or Foe: S100 Proteins in Cancer

Friend or Foe: S100 Proteins in Cancer

Circuits of cancer drivers revealed by convergent misregulation of transcription factor targets across tumor types

High S100A2 expression in keratinocytes in patients with drug eruption

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