ArticleExperimental and therapeutic medicine2018
Mixed lineage kinase-4 promotes gastric carcinoma tumorigenesis through suppression of the c-Jun N-terminal kinase signaling pathway.
Article in Experimental and therapeutic medicine, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 1 paper.
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
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1 citing paper in PubMed, 2 citations in OpenAlex.
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6 authors at 2 institutions in 1 country.
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Abstract
Mixed lineage kinase-4 (MLK-4) is an important member of the mixed-lineage family of kinases that regulates the extracellular signal-regulated kinases and c-Jun N-terminal kinase (JNK) signaling pathways. The functions and mechanisms of MLK-4 in cancer initiation and progression have not been well understood. The present study investigated the expression, function and regulatory mechanism of MLK-4 in gastric carcinoma cells. Biochemical data indicated that normal MLK-4 was downregulated, which exerted dominant negative effects on gastric carcinoma cell viability, migration and invasion. The experimental data demonstrated that MLK-4 supplement abrogated activity of these mutants and induced inhibitory effects on gastric carcinoma cell viabilty, migration and invasion
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