HER3 in cancer: from the bench to the bedside

Gandullo-Sánchez, Lucía; Ocaña, Alberto; Pandiella, Atanasio

doi:10.1186/s13046-022-02515-x

Cited by 45 publications

(33 citation statements)

References 283 publications

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“…ERBB3 is rarely mutated in LUAD based on the cosmic database ( https://cancer.sanger.ac.uk ). ERBB3 encodes a member of the epidermal growth factor receptor family of receptor tyrosine kinases and plays an important role in several cancers ( Gandullo-Sanchez et al , 2022 ).…”

Section: Resultsmentioning

confidence: 99%

WMDS.net: a network control framework for identifying key players in transcriptome programs

et al. 2023

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Motivation Mammalian cells can be transcriptionally reprogrammed to other cellular phenotypes. Controllability of such complex transitions in transcriptional networks underlying cellular phenotypes is an inherent biological characteristic. This network controllability can be interpreted by operating a few key regulators to guide the transcriptional program from one state to another. Finding the key regulators in the transcriptional program can provide key insights into the network state transition underlying cellular phenotypes. Results To address this challenge, here we proposed to identify the key regulators in the transcriptional co-expression network as a minimum dominating set (MDS) of driver nodes that can fully control the network state transition. Based on the theory of structural controllability, we developed a weighted MDS network model (WMDS.net) to find the drive nodes of differential gene co-expression networks. The weight of WMDS.net integrates the degree of nodes in the network and the significance of gene co-expression difference between two physiological states into the measurement of node controllability of the transcriptional network. To confirm its validity, we applied WMDS.net to the discovery of cancer driver genes in RNA-seq datasets from The Cancer Genome Atlas. WMDS.net is powerful among various cancer datasets and outperformed the other top-tier tools with a better balance between precision and recall. Availability https://github.com/chaofen123/WMDS.net. Supplementary information Supplementary data are available at Bioinformatics online.

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Section: Resultsmentioning

confidence: 99%

WMDS.net: a network control framework for identifying key players in transcriptome programs

et al. 2023

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“…Given the importance of ERBB3 to be frequently upregulated in several cancers and its implication in drug-resistance, a huge effort has been put for the development of anti-ERBB3 therapies. Several monoclonal antibodies (mAbs) against ERBB3 are currently in clinical trials to assess their e cacy in several cancers including lung cancer [30]. A notable example of ERBB3 monoclonal antibody is the patritumab deruxtecan, which prevents the binding of HRG to ERBB3 leading to loss of ERBB3 expression [31,32].…”

Section: Discussionmentioning

confidence: 99%

Targeting ERBB3 and AKT to overcome adaptive resistance in EML4-ALK non-small cell lung cancer

Bayliss,

Sampson,

et al. 2024

Preprint

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The fusion event between EML4 and ALK drives a significant oncogenic activity in 5% of non-small cell lung cancer (NSCLC). Even though potent ALK-tyrosine kinase inhibitors (ALK-TKIs) are successfully used for the treatment of EML4-ALK-positive NSCLC patients, a subset of those patients eventually acquire resistance during their therapy. Here, we investigate the kinase responses in EML4-ALK V1 and V3 NSCLC cancer cells after acute inhibition with ALK TKI, lorlatinib. Using phosphopeptide chip array and upstream kinase prediction analysis, we identified a group of phosphorylated tyrosine peptides including ERBB and AKT proteins that are upregulated upon ALK-TKI treatment in EML4-ALK-positive NSCLC cell lines. Dual inhibition of ALK and ERBB receptors or AKT1 disrupts RAS/MAPK and AKT/PI3K signalling pathways, and enhances apoptosis in EML4-ALK NSCLC cancer cells. Heregulin, an ERBB3 ligand, differentially modulates the sensitivity of EML4-ALK cell lines to ALK inhibitors. These findings emphasize the important roles of AKT1 and ERBB3 to regulate signalling after acute lorlatinib treatment, identifying them as potential targets that may be beneficial to prevent adaptive resistance to EML4-ALK-targeted therapies in NSCLC.

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“…The activation of HER2 receptors can be induced by hetero- or homodimerization with HER2 ( Hsu and Hung, 2016 ) or other members of the ERbB/HER family, such as HER3 or EGFR, in both normal and tumor cells ( Altiok et al, 1995 , Gandullo Sánchez et al,2022 ). Each breast cancer cell line used in our study exhibits a distinct expression profile of various HER receptors ( Maadi et al,2018 ), which could significantly impact the binding preference of our HER2 DNA aptamer HMAP7.…”

Section: Discussionmentioning

confidence: 99%

Theranostic potential of a novel aptamer specifically targeting HER2 in breast cancer cells

KÜÇÜKCANKURT,

UÇAK,

ALTIOK

2024

Turkish Journal of Biology

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Background/aim The overexpression of HER2 is correlated with poorer outcomes and therapeutic resistance in breast cancer patients. While HER2-targeted therapies have shown improvement, prognosis remains poor for HER2-positive breast cancer patients, and these treatments have limitations. Therefore, it is crucial to explore effective molecular strategies for early detection and treatment of HER2-positive breast cancers. Materials and methods In this study, we employed the cell-SELEX method to generate a selective aptamer capable of recognizing HER2 in its native conformation within breast cancer cells, for theranostic applications. Utilizing an adherent cell-SELEX approach, we developed and explored a DNA aptamer, named HMAP7, which can specifically target HER2 in the MDA-MB-453 and SK-BR-3 human breast cancer cell lines. After sequencing, the binding affinities of 10 candidate aptamers to HER2 receptors were evaluated by measuring fluorescence intensities within intact cells using near-infrared optical imaging. The dissociation constant of HMAP7 was determined to be in the nanomolar range in both cell lines. Results The cell-SELEX-derived aptamer sequence, HMAP7 (41-mer), exhibited the highest binding affinity and specificity for HER2. HMAP7 was rapidly internalized into breast cancer cells overexpressing HER2 but showed no uptake in the HER2 receptor-deficient breast cancer cell line MDA-MB-231. Moreover, HMAP7 demonstrated remarkable selectivity for HER2, rendering it suitable for use in complex biological systems. Conclusions Our findings suggest that the novel DNA aptamer HMAP7 holds promise for both therapeutic and diagnostic applications, enabling selective delivery of therapeutic agents or imaging of HER2-positive breast tumors.

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HER3 in cancer: from the bench to the bedside

Cited by 45 publications

References 283 publications

WMDS.net: a network control framework for identifying key players in transcriptome programs

WMDS.net: a network control framework for identifying key players in transcriptome programs

Targeting ERBB3 and AKT to overcome adaptive resistance in EML4-ALK non-small cell lung cancer

Theranostic potential of a novel aptamer specifically targeting HER2 in breast cancer cells

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