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Phosphoproteome of NSCLC patient–derived cells.

ABSTRACT: Phosphoproteome of anaplastic lymphoma kinase–positive non-small cell lung cancer (ALK+ NSCLC) patient–derived cells.

ORGANISM(S): Homo Sapiens (human)

SUBMITTER: Ryohei Katayama

PROVIDER: PXD050973 | JPOST Repository | Tue Nov 19 00:00:00 GMT 2024

REPOSITORIES: jPOST

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			Action	DRS
	240301_4N_pSTY_Fr1.raw	Raw
	240301_4N_pSTY_Fr2.raw	Raw
	240301_4N_pSTY_Fr3.raw	Raw
	240301_4N_pSTY_Fr4.raw	Raw
	240301_4N_pSTY_Fr5.raw	Raw

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Publications

Targeting ErbB and tankyrase1/2 prevent the emergence of drug-tolerant persister cells in ALK-positive lung cancer.

Fujimura Takaaki T Furugaki Koh K Mizuta Hayato H Muraoka Satoshi S Nishio Makoto M Adachi Jun J Uchibori Ken K Miyauchi Eisaku E Hayashi Hidetoshi H Katayama Ryohei R Yoshiura Shigeki S

NPJ precision oncology 20241117 1

Targeting the drug tolerant persister (DTP) state in cancer cells should prevent further development of resistance mechanisms. This study explored combination therapies to inhibit alectinib-induced DTP cell formation from anaplastic lymphoma kinase-positive non-small cell lung cancer (ALK + NSCLC) patient-derived cells. After drug-screening 3114 compounds, pan-HER inhibitors (ErbB pathway) and tankyrase1/2 inhibitors (Wnt/β-catenin signaling) emerged as top candidates to inhibit alectinib-induce ...[more]

PMID: 39551860

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Analysis of the genomic landscape in ALK+ NSCLC patients identifies novel aberrations associated with clinical outcomes

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ALK fusion NSCLC oncogenes promote survival and inhibit NK cell responses via SERPINB4 expression

Project description:Anaplastic lymphoma kinase (ALK) fusion variants in non-small-cell-lung cancer (NSCLC) consist of numerous dimerising fusion partners, with the most common being EML4. Clinical data suggests that the degree of treatment benefit in response to ALK tyrosine kinase inhibitors (TKIs) differs among the variant present in the patient tumor. Therefore, a better understanding the oncogenic signaling networks driven by different ALK-fusion variants is important. Here, we developed highly controlled doxycycline-inducible cell models bearing four different ALK fusion proteins, namely EML4-ALK-V1, EML4-ALK-V3, KIF5B-ALK, and TFG-ALK, in the context of non-tumorigenic NL20 human bronchial epithelial cells. These were complimented by patient-derived NSCLC cell lines harboring either EML4-ALK-V1 or EML4-ALK-V3 fusions. RNAseq and phosphoproteomics analysis were employed to identify dysregulated genes and hyper/hypo-phosphorylated proteins associated with ALK fusion expression. Among ALK fusion induced responses, we noted a robust inflammatory signature that included up-regulation of the Serpin B4 serine protease inhibitor in both NL20-inducible cell models and ALK-positive NSCLC patient-derived cell lines. We show that STAT3 is a major transcriptional regulator of SERPINB4 downstream of ALK fusions, along with NF-B and AP1. The upregulation of SERPINB4 promotes survival of ALK fusion expressing cells and inhibits natural killer (NK) cell-mediated cytotoxicity. In conclusion, our study reveals a novel ALK downstream survival axis that regulates Serpin B4 expression and identifies a molecular target that has potential for therapeutic impact targeting the immune response together with ALK TKIs in NSCLC.

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Korean NSCLC Phosphoproteome Subtype Analysis

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